document_title: Cell cycle

question_text: when does the mass of dna increase in the cell cycle

text: Cell cycle

text: Phases[edit]

text: The cell cycle consists of four distinct phases: G1 phase, S phase (synthesis), G2 phase (collectively known as interphase) and M phase (mitosis). M phase is itself composed of two tightly coupled processes: karyokinesis, in which the cell's chromosomes are divided, and cytokinesis, in which the cell's cytoplasm divides forming two daughter cells. Activation of each phase is dependent on the proper progression and completion of the previous one. Cells that have temporarily or reversibly stopped dividing are said to have entered a state of quiescence called G0 phase.

text:
State
Phase
Abbreviation
Description

Resting
Gap 0
G0
A phase where the cell has left the cycle and has stopped dividing.

Interphase
Gap 1
G1
Cells increase in size in Gap 1. The G1 checkpoint control mechanism ensures that everything is ready for DNA synthesis.

Synthesis
S
DNA replication occurs during this phase.

Gap 2
G2
During the gap between DNA synthesis and mitosis, the cell will continue to grow. The G2 checkpoint control mechanism ensures that everything is ready to enter the M (mitosis) phase and divide.

Cell division
Mitosis
M
Cell growth stops at this stage and cellular energy is focused on the orderly division into two daughter cells. A checkpoint in the middle of mitosis (Metaphase Checkpoint) ensures that the cell is ready to complete cell division.

text: After cell division, each of the daughter cells begin the interphase of a new cycle. Although the various stages of interphase are not usually morphologically distinguishable, each phase of the cell cycle has a distinct set of specialized biochemical processes that prepare the cell for initiation of cell division.

text: G0 phase (quiescence)[edit]

text: G0 is a resting phase where the cell has left the cycle and has stopped dividing. The cell cycle starts with this phase. The word "post-mitotic" is sometimes used to refer to both quiescent and senescent cells. Non-proliferative (non-dividing) cells in multicellular eukaryotes generally enter the quiescent G0 state from G1 and may remain quiescent for long periods of time, possibly indefinitely (as is often the case for neurons). This is very common for cells that are fully differentiated. Cellular senescence occurs in response to DNA damage and external stress and usually constitutes an arrest in G1. Some cells enter the G0 phase semi-permanently and are considered post-mitotic, e.g., some liver, kidney, and stomach cells. Many cells do not enter G0 and continue to divide throughout an organism's life, e.g., epithelial cells.

text: Cellular senescence is also a state that occurs in response to DNA damage or degradation that would make a cell's progeny nonviable; it is often a biochemical alternative to the self-destruction of such a damaged cell by apoptosis.

text: Interphase (intermitosis)[edit]

text: Before a cell can enter cell division, it needs to take in nutrients. All of the preparations are done during interphase. Interphase is a series of changes that takes place in a newly formed cell and its nucleus, before it becomes capable of division again. It is also called preparatory phase or intermitosis. Previously it was called resting stage because there is no apparent activity related to cell division.Typically interphase lasts for at least 91% of the total time required for the cell cycle.

text: Interphase proceeds in three stages, G1, S, and G2, followed by the cycle of mitosis and cytokinesis. The cell's nuclear DNA contents are duplicated during S phase but may continue till G2 in case of heterochromatin.

text: G1 phase (First growth phase or Post mitotic gap phase)[edit]

text: The first phase within interphase, from the end of the previous M phase until the beginning of DNA synthesis, is called G1 (G indicating gap). It is also called the growth phase. During this phase, the biosynthetic activities of the cell, which are considerably slowed down during M phase, resume at a high rate. The duration of G1 is highly variable, even among different cells of the same species.[3] In this phase, the cell increases its supply of proteins, increases the number of organelles (such as mitochondria, ribosomes), and grows in size. In G1 phase, a cell has three options. (1) To continue cell cycle and enter S phase (2) Stop cell cycle and enter G0 phase for undergoing differentiation. (3) Get arrested in G1 phase hence it may enter G0 phase or re-enter cell cycle. The deciding factor is availability of nitrogens and storage of energy rich compounds at the deciding point called check point. This check point is called G1 cyclin or CG1. It causes transition of G1 to S phase. Once the check point of G1 phase is crossed, cell cycle will go uninterrupted till it is completed.

text: S phase (DNA replication)[edit]

text: The ensuing S phase starts when DNA synthesis commences; when it is complete, all of the chromosomes have been replicated, i.e., each chromosome has two (sister) chromatids. Thus, during this phase, the amount of DNA in the cell has effectively doubled, though the ploidy of the cell remains the same. Rates of RNA transcription and protein synthesis are very low during this phase. An exception to this is histone production, most of which occurs during the S phase.[4][5][6]

text: G2 phase (growth)[edit]

text: G2 phase occurs after DNA replication and is a period of protein synthesis and rapid cell growth to prepare the cell for mitosis. During this phase microtubules begin to reorganize to form a spindle.

text: Mitotic phase (chromosome separation)[edit]

text: The relatively brief M phase consists of nuclear division (karyokinesis). It is a relatively short period of the cell cycle. M phase is complex and highly regulated. The sequence of events is divided into phases, corresponding to the completion of one set of activities and the start of the next. These phases are sequentially known as:

text:
prophase,
metaphase,
anaphase,
telophase

text: Mitosis is the process by which a eukaryotic cell separates the chromosomes in its cell nucleus into two identical sets in two nuclei.[7] During the process of mitosis the pairs of chromosomes condense and attach to fibers that pull the sister chromatids to opposite sides of the cell.[8]

text: Mitosis occurs exclusively in eukaryotic cells, but occurs in different ways in different species. For example, animals undergo an "open" mitosis, where the nuclear envelope breaks down before the chromosomes separate, while fungi such as Aspergillus nidulans and Saccharomyces cerevisiae (yeast) undergo a "closed" mitosis, where chromosomes divide within an intact cell nucleus.[9] Prokaryotic cells, which lack a nucleus, divide by a process called binary fission.

text: Cytokinesis phase (separation of all cell components)[edit]

text: Mitosis is immediately followed by cytokinesis, which divides the nuclei, cytoplasm, organelles and cell membrane into two cells containing roughly equal shares of these cellular components. Mitosis and cytokinesis together define the division of the mother cell into two daughter cells, genetically identical to each other and to their parent cell. This accounts for approximately 10% of the cell cycle.

text: Because cytokinesis usually occurs in conjunction with mitosis, "mitosis" is often used interchangeably with "M phase". However, there are many cells where mitosis and cytokinesis occur separately, forming single cells with multiple nuclei in a process called endoreplication. This occurs most notably among the fungi and slime moulds, but is found in various groups. Even in animals, cytokinesis and mitosis may occur independently, for instance during certain stages of fruit fly embryonic development.[10] Errors in mitosis can either kill a cell through apoptosis or cause mutations that may lead to cancer.

text: The process of mitosis is complex and highly regulated. The sequence of events is divided into phases, corresponding to the completion of one set of activities and the start of the next. These stages are prophase, prometaphase, metaphase, anaphase and telophase. During the process of mitosis the pairs of chromosomes condense and attach to fibers that pull the sister chromatids to opposite sides of the cell. The cell then divides in cytokinesis, to produce two identical daughter cells.[8]

text: Regulation of eukaryotic cell cycle[edit]

text: Regulation of the cell cycle involves processes crucial to the survival of a cell, including the detection and repair of genetic damage as well as the prevention of uncontrolled cell division. The molecular events that control the cell cycle are ordered and directional; that is, each process occurs in a sequential fashion and it is impossible to "reverse" the cycle.

text: Role of cyclins and CDKs[edit]

text:
Nobel Laureate
Paul Nurse

Nobel Laureate
Tim Hunt

text: Two key classes of regulatory molecules, cyclins and cyclin-dependent kinases (CDKs), determine a cell's progress through the cell cycle.[11] Leland H. Hartwell, R. Timothy Hunt, and Paul M. Nurse won the 2001 Nobel Prize in Physiology or Medicine for their discovery of these central molecules.[12] Many of the genes encoding cyclins and CDKs are conserved among all eukaryotes, but in general more complex organisms have more elaborate cell cycle control systems that incorporate more individual components. Many of the relevant genes were first identified by studying yeast, especially Saccharomyces cerevisiae;[13] genetic nomenclature in yeast dubs many of these genes cdc (for "cell division cycle") followed by an identifying number, e.g. cdc25 or cdc20.

text: Cyclins form the regulatory subunits and CDKs the catalytic subunits of an activated heterodimer; cyclins have no catalytic activity and CDKs are inactive in the absence of a partner cyclin. When activated by a bound cyclin, CDKs perform a common biochemical reaction called phosphorylation that activates or inactivates target proteins to orchestrate coordinated entry into the next phase of the cell cycle. Different cyclin-CDK combinations determine the downstream proteins targeted. CDKs are constitutively expressed in cells whereas cyclins are synthesised at specific stages of the cell cycle, in response to various molecular signals.[14]

text: General mechanism of cyclin-CDK interaction[edit]

text: Upon receiving a pro-mitotic extracellular signal, G1 cyclin-CDK complexes become active to prepare the cell for S phase, promoting the expression of transcription factors that in turn promote the expression of S cyclins and of enzymes required for DNA replication. The G1 cyclin-CDK complexes also promote the degradation of molecules that function as S phase inhibitors by targeting them for ubiquitination. Once a protein has been ubiquitinated, it is targeted for proteolytic degradation by the proteasome. However, results from a recent study of E2F transcriptional dynamics at the single-cell level argue that the role of G1 cyclin-CDK activities, in particular cyclin D-CDK4/6, is to tune the timing rather than the commitment of cell cycle entry.[15]

text: Active S cyclin-CDK complexes phosphorylate proteins that make up the pre-replication complexes assembled during G1 phase on DNA replication origins. The phosphorylation serves two purposes: to activate each already-assembled pre-replication complex, and to prevent new complexes from forming. This ensures that every portion of the cell's genome will be replicated once and only once. The reason for prevention of gaps in replication is fairly clear, because daughter cells that are missing all or part of crucial genes will die. However, for reasons related to gene copy number effects, possession of extra copies of certain genes is also deleterious to the daughter cells.

text: Mitotic cyclin-CDK complexes, which are synthesized but inactivated during S and G2 phases, promote the initiation of mitosis by stimulating downstream proteins involved in chromosome condensation and mitotic spindle assembly. A critical complex activated during this process is a ubiquitin ligase known as the anaphase-promoting complex (APC), which promotes degradation of structural proteins associated with the chromosomal kinetochore. APC also targets the mitotic cyclins for degradation, ensuring that telophase and cytokinesis can proceed.[16]

text: Specific action of cyclin-CDK complexes[edit]

text: Cyclin D is the first cyclin produced in the cell cycle, in response to extracellular signals (e.g. growth factors). Cyclin D binds to existing CDK4, forming the active cyclin D-CDK4 complex. Cyclin D-CDK4 complex in turn phosphorylates the retinoblastoma susceptibility protein (Rb). The hyperphosphorylated Rb dissociates from the E2F/DP1/Rb complex (which was bound to the E2F responsive genes, effectively "blocking" them from transcription), activating E2F. Activation of E2F results in transcription of various genes like cyclin E, cyclin A, DNA polymerase, thymidine kinase, etc. Cyclin E thus produced binds to CDK2, forming the cyclin E-CDK2 complex, which pushes the cell from G1 to S phase (G1/S, which initiates the G2/M transition).[17] Cyclin B-cdk1 complex activation causes breakdown of nuclear envelope and initiation of prophase, and subsequently, its deactivation causes the cell to exit mitosis.[14] A quantitative study of E2F transcriptional dynamics at the single-cell level by using engineered fluorescent reporter cells provided a quantitative framework for understanding the control logic of cell cycle entry, challenging the canonical textbook model. Genes that regulate the amplitude of E2F accumulation, such as Myc, determine the commitment in cell cycle and S phase entry. G1 cyclin-CDK activities are not the driver of cell cycle entry. Instead, they primarily tune the timing of E2F increase, thereby modulating the pace of cell cycle progression.[15]

text: Inhibitors[edit]

text: Two families of genes, the cip/kip (CDK interacting protein/Kinase inhibitory protein) family and the INK4a/ARF (Inhibitor of Kinase 4/Alternative Reading Frame) family, prevent the progression of the cell cycle. Because these genes are instrumental in prevention of tumor formation, they are known as tumor suppressors.

text: The cip/kip family includes the genes p21, p27 and p57. They halt cell cycle in G1 phase, by binding to, and inactivating, cyclin-CDK complexes. p21 is activated by p53 (which, in turn, is triggered by DNA damage e.g. due to radiation). p27 is activated by Transforming Growth Factor of β (TGF β), a growth inhibitor.

text: The INK4a/ARF family includes p16INK4a, which binds to CDK4 and arrests the cell cycle in G1 phase, and p14ARF which prevents p53 degradation.

text: Synthetic inhibitors of Cdc25 could also be useful for the arrest of cell cycle and therefore be useful as antineoplastic and anticancer agents.[18]

text: Transcriptional regulatory network[edit]

text: Current evidence suggests that a semi-autonomous transcriptional network acts in concert with the CDK-cyclin machinery to regulate the cell cycle. Several gene expression studies in Saccharomyces cerevisiae have identified 800–1200 genes that change expression over the course of the cell cycle.[13][19][20] They are transcribed at high levels at specific points in the cell cycle, and remain at lower levels throughout the rest of the cycle. While the set of identified genes differs between studies due to the computational methods and criteria used to identify them, each study indicates that a large portion of yeast genes are temporally regulated.[21]

text: Many periodically expressed genes are driven by transcription factors that are also periodically expressed. One screen of single-gene knockouts identified 48 transcription factors (about 20% of all non-essential transcription factors) that show cell cycle progression defects.[22] Genome-wide studies using high throughput technologies have identified the transcription factors that bind to the promoters of yeast genes, and correlating these findings with temporal expression patterns have allowed the identification of transcription factors that drive phase-specific gene expression.[19][23] The expression profiles of these transcription factors are driven by the transcription factors that peak in the prior phase, and computational models have shown that a CDK-autonomous network of these transcription factors is sufficient to produce steady-state oscillations in gene expression).[20][24]

text: Experimental evidence also suggests that gene expression can oscillate with the period seen in dividing wild-type cells independently of the CDK machinery. Orlando et al. used microarrays to measure the expression of a set of 1,271 genes that they identified as periodic in both wild type cells and cells lacking all S-phase and mitotic cyclins (clb1,2,3,4,5,6). Of the 1,271 genes assayed, 882 continued to be expressed in the cyclin-deficient cells at the same time as in the wild type cells, despite the fact that the cyclin-deficient cells arrest at the border between G1 and S phase. However, 833 of the genes assayed changed behavior between the wild type and mutant cells, indicating that these genes are likely directly or indirectly regulated by the CDK-cyclin machinery. Some genes that continued to be expressed on time in the mutant cells were also expressed at different levels in the mutant and wild type cells. These findings suggest that while the transcriptional network may oscillate independently of the CDK-cyclin oscillator, they are coupled in a manner that requires both to ensure the proper timing of cell cycle events.[20] Other work indicates that phosphorylation, a post-translational modification, of cell cycle transcription factors by Cdk1 may alter the localization or activity of the transcription factors in order to tightly control timing of target genes.[22][25][26]

text: While oscillatory transcription plays a key role in the progression of the yeast cell cycle, the CDK-cyclin machinery operates independently in the early embryonic cell cycle. Before the midblastula transition, zygotic transcription does not occur and all needed proteins, such as the B-type cyclins, are translated from maternally loaded mRNA.[27]

text: DNA replication and DNA replication origin activity[edit]

text: Analyses of synchronized cultures of Saccharomyces cerevisiae under conditions that prevent DNA replication initiation without delaying cell cycle progression showed that origin licensing decreases the expression of genes with origins near their 3' ends, revealing that downstream origins can regulate the expression of upstream genes.[28] This confirms previous predictions from mathematical modeling of a global causal coordination between DNA replication origin activity and mRNA expression,[29][30][31] and shows that mathematical modeling of DNA microarray data can be used to correctly predict previously unknown biological modes of regulation.

text: Checkpoints[edit]

text: Cell cycle checkpoints are used by the cell to monitor and regulate the progress of the cell cycle.[32] Checkpoints prevent cell cycle progression at specific points, allowing verification of necessary phase processes and repair of DNA damage. The cell cannot proceed to the next phase until checkpoint requirements have been met. Checkpoints typically consist of a network of regulatory proteins that monitor and dictate the progression of the cell through the different stages of the cell cycle.

text: There are several checkpoints to ensure that damaged or incomplete DNA is not passed on to daughter cells. Three main checkpoints exist: the G1/S checkpoint, the G2/M checkpoint and the metaphase (mitotic) checkpoint.

text: G1/S transition is a rate-limiting step in the cell cycle and is also known as restriction point.[14] This is where the cell checks whether it has enough raw materials to fully replicate its DNA (nucleotide bases, DNA synthase, chromatin, etc.). An unhealthy or malnourished cell will get stuck at this checkpoint.

text: The G2/M checkpoint is where the cell ensures that it has enough cytoplasm and phospholipids for two daughter cells. But sometimes more importantly, it checks to see if it is the right time to replicate. There are some situations where many cells need to all replicate simultaneously (for example, a growing embryo should have a symmetric cell distribution until it reaches the mid-blastula transition). This is done by controlling the G2/M checkpoint.

text: The metaphase checkpoint is a fairly minor checkpoint, in that once a cell is in metaphase, it has committed to undergoing mitosis. However that's not to say it isn't important. In this checkpoint, the cell checks to ensure that the spindle has formed and that all of the chromosomes are aligned at the spindle equator before anaphase begins.[33]

text: While these are the three "main" checkpoints, not all cells have to pass through each of these checkpoints in this order to replicate. Many types of cancer are caused by mutations that allow the cells to speed through the various checkpoints or even skip them altogether. Going from S to M to S phase almost consecutively. Because these cells have lost their checkpoints, any DNA mutations that may have occurred are disregarded and passed on to the daughter cells. This is one reason why cancer cells have a tendency to exponentially accrue mutations. Aside from cancer cells, many fully differentiated cell types no longer replicate so they leave the cell cycle and stay in G0 until their death. Thus removing the need for cellular checkpoints. An alternative model of the cell cycle response to DNA damage has also been proposed, known as the postreplication checkpoint.

text: Checkpoint regulation plays an important role in an organism's development. In sexual reproduction, when egg fertilization occurs, when the sperm binds to the egg, it releases signalling factors that notify the egg that it has been fertilized. Among other things, this induces the now fertilized oocyte to return from its previously dormant, G0, state back into the cell cycle and on to mitotic replication and division.

text: p53 plays an important role in triggering the control mechanisms at both G1/S and G2/M checkpoints. In addition to p53, checkpoint regulators are being heavily researched for their roles in cancer growth and proliferation.

text: Fluorescence imaging of the cell cycle[edit]

text: Pioneering work by Atsushi Miyawaki and coworkers developed the fluorescent ubiquitination-based cell cycle indicator (FUCCI), which enables fluorescence imaging of the cell cycle. Originally, a green fluorescent protein, mAG, was fused to hGem(1/110) and an orange fluorescent protein (mKO2) was fused to hCdt1(30/120). Note, these fusions are fragments that contain a nuclear localization signal and ubiquitination sites for degradation, but are not functional proteins. The green fluorescent protein is made during the S, G2, or M phase and degraded during the G0 or G1 phase, while the orange fluorescent protein is made during the G0 or G1 phase and destroyed during the S, G2, or M phase.[34] A far-red and near-infrared FUCCI was developed using a cyanobacteria-derived fluorescent protein (smURFP) and a bacteriophytochrome-derived fluorescent protein (movie found at this link).[35]

text: Role in tumor formation[edit]

text: A disregulation of the cell cycle components may lead to tumor formation.[36] As mentioned above, when some genes like the cell cycle inhibitors, RB, p53 etc. mutate, they may cause the cell to multiply uncontrollably, forming a tumor. Although the duration of cell cycle in tumor cells is equal to or longer than that of normal cell cycle, the proportion of cells that are in active cell division (versus quiescent cells in G0 phase) in tumors is much higher than that in normal tissue[citation needed]. Thus there is a net increase in cell number as the number of cells that die by apoptosis or senescence remains the same.

text: The cells which are actively undergoing cell cycle are targeted in cancer therapy as the DNA is relatively exposed during cell division and hence susceptible to damage by drugs or radiation. This fact is made use of in cancer treatment; by a process known as debulking, a significant mass of the tumor is removed which pushes a significant number of the remaining tumor cells from G0 to G1 phase (due to increased availability of nutrients, oxygen, growth factors etc.). Radiation or chemotherapy following the debulking procedure kills these cells which have newly entered the cell cycle.[14]

text: The fastest cycling mammalian cells in culture, crypt cells in the intestinal epithelium, have a cycle time as short as 9 to 10 hours. Stem cells in resting mouse skin may have a cycle time of more than 200 hours. Most of this difference is due to the varying length of G1, the most variable phase of the cycle. M and S do not vary much.

text: In general, cells are most radiosensitive in late M and G2 phases and most resistant in late S phase.

text: For cells with a longer cell cycle time and a significantly long G1 phase, there is a second peak of resistance late in G1.

text: The pattern of resistance and sensitivity correlates with the level of sulfhydryl compounds in the cell. Sulfhydryls are natural substances that protect cells from radiation damage and tend to be at their highest levels in S and at their lowest near mitosis.


document_title: ComiXology

question_text: when do new comics come out on comixology

root

text: ComiXology

text: Products[edit]

text:
ComiXology.com was launched July 2007 as an online community for comic book fans; the website allows readers to identify upcoming releases and develop pull lists (individual pre-orders) from local brick-and-mortar comic shops. The website displays weekly listings of new titles that can be viewed by issue: displaying cover art, credits, description, price, page count, and other information; the site also includes weekly columns, blogs, news, and podcasts. Users can rate and comment on individual comic books. As of July 24, 2014, ComiXology offers DRM-free downloads (in PDF and CBZ formats) for the comics available from selected publishers on its online store.[10]
Pull List (launched December 2008), a mobile comic book store locater providing readers with a digital Pull List tool, allowing fans to pre-order comics for pick up from local stores through the app. This app has been replaced by the Comics by comiXology app and the web app have the retail store locator included.
Retailer Tools (launched February 2009), a suite of out-of-the-box web solutions for brick-and-mortar comic book retailers to optimize their presence online. Numerous retailers worldwide have integrated comiXology's Retailer Tools into their operations, representing about 2% of all pre-orders in the market.[citation needed]
Comics by ComiXology (launched July 2009), a digital comic book reader and store for mobile devices, including iOS (launched April 2010), Android, Windows 8 (via the Windows Store), and the Internet (web reader launched June 2010), that allows users to access their digital comic collection across multiple devices.

tag: ul

text: History[edit]

text: The company was founded in 2007 by CEO David Steinberger, CTO John D. Roberts, and Peter Jaffe. Subsequent to winning the business plan competition at New York University, the company received seed financing from Kit McQuiston, New York Angels and Rose Tech Ventures.[11]

tag: p

text: In May 2016, the company launched "comiXology Unlimited," a subscription service that gives access thousands of comics to read from most major publishers for a monthly fee of $5.99, however Marvel and DC are not included.[12]

text: ComiXology Unlimited[edit]

text: ComiXology Unlimited, is an online subscription service by ComiXology, a cloud based platform for digital comics The service offers more than four thousand issues to its subscribers and launched on May 24, 2016.[13]

text: ComiXology Unlimited contains a selection of titles from Image Comics, Dark Horse, IDW Publishing, BOOM! Studios, Dynamite Entertainment, Kodansha Comics, Oni Press, Valiant Entertainment, Archie Comics, Fantagraphics Books, Humanoids, Action Lab Entertainment, Aspen Comics, Magnetic Press, Zenescope Entertainment and more.[14] According to the company, ComiXology Unlimited offers the widest subscription selection of digital comics in the world. However, the service does not include Marvel (which has its own subscription[15] service) or DC Comics.[16]

text: For $5.99 a month customers can explore thousands of titles, like The Walking Dead, Attack on Titan, Hellboy, Adventure Time, Peanuts, Buffy the Vampire Slayer, Lumberjanes, Saga, The Umbrella Academy, Outcast, Transformers, and more.[17] ComiXology Unlimited is available on the comiXology app for Fire Tablet, Android, iOS and on the web at comixology.com. The company offers a free 30-day trial at comixology.com/unlimited.[18]

text: ComiXology Unlimited is currently available in the U.S.[19] and ComiXology plans to expand to other regions in the future.[20]

text: ComiXology updates the content included in the program on a monthly basis.[21]

text: The press reception for the launch was mostly positive, with journalists and bloggers focusing on the low price point, the 30-day free trial and the diverse collection of independent comics, graphic novels and manga available at launch.[22]

text: Some critics pointed out, however, that only some trades in the series are available in the program,[23] undermining the “unlimited” aspect of the subscription.

text: Patent[edit]

text: ComiXology's patent-pending Guided View technology allows readers to read through comics in full screen or from panel-to-panel, mimicking the natural movement of the eye as though readers were experiencing reading a print comic book.[24]

text: Content relationships[edit]

text:
ComiXology currently holds exclusive distribution rights on iOS to DC Comics digital content through branded apps and comics by comiXology.[citation needed]
ComiXology holds exclusive digital distribution rights to:

All of Robert Kirkman's titles - including The Walking Dead[25]
Youngblood and Armageddon Now from Rob Liefeld, original co-founder of Image Comics.[26]

ComiXology’s first original digital title, Box 13, has been acquired by Red 5 Comics for print distribution. ComiXology also commissioned a sequel to the comic, titled The Pandora Project. Both Box 13 titles were created by the Harvey Award-winning team behind the Zuda Comics title High Moon - David Gallaher and Steve Ellis[27]
Moon Girl is an original comic published by ComiXology, based on a public domain comics character. The creative team on Moon Girl is Tony Trov, Johnny Zito, and Rahzzah.[28]

text: Publishers[edit]

text: This section may require cleanup to meet Wikipedia's quality standards. The specific problem is: does every publisher need to be listed? Should this be rewritten to prose. How will this meet WP:NOTCATALOG? Please help improve this section if you can. (November 2015) (Learn how and when to remove this template message)

tag: table

text:
Publishers[29]

12-Gauge Comics
A Wave Blue World
AAM/Markosia
Aardvark-Vanaheim
Abrams ComicArts
Abstract Studio
Action Lab
Adhouse
Aelement
Akileos
Alterna Comics
Alternative Comics
Amigo Comics
Amulet Books
Andrews McMeel Publishing
Ankama
Antarctic Press
Ape Entertainment
Arcana Studio
Archaia Studios Press
Archie Comics
Aspen Comics
Astronaut Ink
Asylum Press
Avatar Press
Back Row Comics
Banana Tale Press
Blaze Comics
Blind Ferret Entertainment
Bongo Comics
BOOM! Studios
Bubble Comics
BughouseComics
C&W Creations
Çà et Là
Cartoon Books
Colring Book Press
Com.x
Comixheroes Universe
ComixTribe
ComiXology
Con Artist Entertainment

Creative Impulse Entertainment
Creator Owned Comics
Cryptozoic Entertainment
Dark Horse Comics
DC
Delcourt
Devil's Due
Digital Webbing
Disney
Digital Manga Publishing
Dynamite
EigoMANGA
Evil Twin
Fantagraphics
Fifth World
First Salvo
Galaxie Comics Studios
Glénat
Graphitti Designs
Graphix
GT Labs
Harlequin Comics
HarperCollins
Hermes Press
Hexagon Comics
HexComix
I CAN FLY Comics
Icon
IDW
Image Comics
Indeez
Ishimori
Keenspot
Kickstart
Kid Beowulf
Kingstone Comics
Kodansha
Kymera Press
Legendary
Los Brignolés
Marvel
MAX
MonkeyBrain
Monsterverse

Moonstone
MTV Comics
NBM
Oni Press
Panini Comics
Papercutz
R-Comics
Radical Comics
Raw Studios
Red 5 Comics
Red Circle Comics
Sandawe
Seven Seas
Shadowline

Silverline

Skybound
Slave Labor Graphics
Small Press
Soleil
Studio 407
Teshkeel
Th3rd World Studios
They Did This!
Thrillbent
TidalWave Productions
Titan
Todd McFarlane Productions
Tokyopop
Top Cow
Top Shelf
Trajectory - Classics Illustrated
Udon
Valiant Comics
Valve
Vents d'Quest
Yen Press
Vertigo
Viper Comics
VIZ Media
Virtual Graphics
Wanga Comics
WEBellipses
Zenescope

text: Controversies[edit]

text: In March 2013 during SXSW, an issue arose when Marvel Comics attempted to distribute over 700 comics for free via ComiXology for the Marvel #1 promotion.[30] The ComiXology servers were unable to keep up with user demand, preventing users from obtaining the promotional comics, as well as from reading comics they had purchased. This led to a formal apology and the promotions being delayed.[31] Soon afterward, the promotion was offered again and was reported to have "worked flawlessly".[32] In the aftermath of the ensuing difficulties some users have raised concerns regarding access to their files should the platform ever shut down.[33] To respond to this concern, in July 2014 selected publishers allow for DRM-free downloads of their comics.

text: On April 9, 2013, writer Brian K. Vaughan issued a statement[34] on Fiona Staples's blog that Apple Inc. had prohibited the sale of Saga #12 through iOS. This statement was quickly reported by the media, the impetus for the "ban" was speculated to be in response to two panels that depicted oral sex between men in a small, inset image violated Apple's restrictions on sexual content. The issue was available through the ComiXology and Image Comics digital comics website stores. The ban was criticized by artists and writers, who pointed to similarly explicit content in previous issues and in other works sold through iTunes. William Gibson and others suggested that the restriction could have occurred specifically because the drawings at issue involved gay sex.[35] A day later, Comixology announced that it had been they, not Apple, who had chosen not to make the issue available, based on their interpretation of Apple's rules, and that after receiving clarification from Apple, the issue would be sold on iOS devices.[36] Brian K. Vaughan then issued a statement apologizing for the miscommunication.[37]

text: After Amazon's controversial purchase of ComiXology, the company removed the option of purchasing comics inside the iOS app. This change resulted in immediate internet backlash from the comic book reader community, criticizing Amazon's acquisition of the distributor.[38] This change to ComiXology's structure has made readers concerned about the future of digital comic distribution.[39]

text: Reception[edit]

text: In September 2011, ComiXology's Comics application was the highest-grossing application in the App Store, and together with the branded applications for other comics publishers, accounted for a majority of the five top-grossing iPhone apps.

text: Having consistently ranked as one of the top-grossing iPad apps in iTunes, ComiXology was called the "iTunes of comics" by The New York Times in May 2012.[40] In 2011, comiXology ranked as number 10 in the top 20 grossing iPad apps for year and also powered two other apps in the top 20 — Marvel and DC.[41] In 2012, comiXology was ranked as the number 3 top grossing iPad app — the only app from 2011 to stay on the top ten list.[42]


document_title: The Good Doctor (TV series)

question_text: who plays dr kalu in the good doctor

question_tokens: who plays dr kalu in the good doctor

text: The Good Doctor (TV series)

text: Premise[edit]

text: The series follows Shaun Murphy, a young surgeon with autism and savant syndrome from the mid-size city of Casper, Wyoming, where he had a troubled childhood. He relocates to San Jose, California, to work at the prestigious San Jose St. Bonaventure Hospital.[2]

text: Cast and characters[edit]

text: Main[edit]

text:
Freddie Highmore as Dr. Shaun Murphy, a surgical resident with autism and savant syndrome.[3] His savant abilities include near-photographic recall and the ability to note minute details and changes. He is portrayed in flashbacks to his teen years by Graham Verchere.[4]
Nicholas Gonzalez as Dr. Neil Melendez: Attending Cardiothoracic surgeon in charge of surgical residents.[3] He is also engaged to Jessica Preston until episode 12.
Antonia Thomas as Dr. Claire Browne, a surgical resident who forms a special connection with Shaun.[5]
Chuku Modu as Dr. Jared Kalu, a surgical resident from a wealthy family.[6]
Beau Garrett as Jessica Preston: The hospital in-house attorney and Vice President of Risk Management. She is the granddaughter of the hospital founder and a friend of Dr. Glassman.[7]
Hill Harper as Dr. Marcus Andrews, Chief of Surgery, attending plastic surgeon, and board member.[8]
Richard Schiff as Dr. Aaron Glassman, President of the San Jose St. Bonaventure Hospital and attending neurosurgeon, who has been a mentor and good friend of Shaun since he was 14.[9][10]
Tamlyn Tomita as Allegra Aoki, Chairman of the San Jose St. Bonaventure Hospital Board and Vice President of the foundation that controls the hospital's funding.[11]

text: Recurring[edit]

text:
Dylan Kingwell as Steve Murphy: Shaun's younger brother (in flashbacks).[4] He also portrays Evan Gallico, a boy in the present that resembles Shaun's brother and is suffering from stage 4 osteosarcoma.
Graham Verchere as a young Shaun Murphy in flashbacks.
Paige Spara as Lea: Shaun's love interest/ former neighbor.
Christina Chang as Dr. Audrey Lim
Chris D'Elia as Kenny, Shaun's new neighbor, who moves into Lea's apartment.
Fiona Gubelmann as Dr. Morgan Reznick, a new resident (joins the cast for five episodes with the possibility of becoming a regular in season 2).[12] As a resident, Morgan will turn out to be a rival for Claire. (debuted in "She").[13]
Will Yun Lee as Dr. Alex Park, an ex-cop who decided to become a doctor (debuted in "Heartfelt").[14]

text: Notable guests[edit]

text:
Irene Keng as Dr. Elle McLean, a surgical resident (only appears in the pilot, however had series regular status for said episode) [8][15]
Jasika Nicole as Carly[16]
Eve Gordon as Nurse Fryday[16]
Eric Winter as Matt Coyle, a suave doctor who charms the hospital's staff, until he makes explicit advances towards one of them.[17]
Marsha Thomason as Dr. Isabel Barnes, Marcus' wife. [18]

text: Episodes[edit]

text:
No.
Title
Directed by
Written by
Original air date
U.S. viewers
(millions)

1
"Burnt Food"
Seth Gordon
David Shore
September 25, 2017 (2017-09-25)
11.22[19]

On the way to begin his surgical residency at San Jose St. Bonaventure Hospital, Dr. Shaun Murphy witnesses an airport sign fall and shatter glass onto a young boy. With his unique ability to visualize the internal body and using improvised methods and tools, Shaun is able to stabilize the boy. In a hospital board meeting, Dr. Aaron Glassman, president of the hospital, tries to convince the board to hire Shaun, despite his autism. Flashbacks give us a picture of Shaun's childhood and his motivation for becoming a doctor.

2
"Mount Rushmore"
Mike Listo
David Shore
October 2, 2017 (2017-10-02)
10.93[20]

Dr. Neil Melendez is doing rounds with Dr. Claire Browne and Dr. Jared Kalu. Melendez calls out Shaun for arriving late on his first full day. A middle aged woman is brought into the ER with abdominal pain. Shaun immediately diagnoses a malignant tumor. As punishment for lateness, Shaun is assigned 'scut work', where his attention to detail gets him in trouble. After rechecking a discharged young girl's test results, Shaun races to her home, annoying her parents over the late hour, but eventually saving the girl's life.

3
"Oliver"
John Dahl
William Rotko
October 9, 2017 (2017-10-09)
10.69[21]

Shaun and Claire fly to San Francisco Municipal Hospital to get a liver for a transplant patient. After learning the helicopter can't take off due to bad weather, they resort to a police escort. Meanwhile, at the Hospital, Chuck, the recipient of the liver, is discovered to have alcohol in his system, a development that could void his transplant eligibility. Chuck later confesses he had one drink at his daughter's graduation. In order to protect its reputation and ability to supply transplants to future patients, the hospital denies Chuck the liver. Shaun and Claire arrive back, having kept the liver viable, only to learn that it is to be taken to a patient at another hospital.

4
"Pipes"
Steven DePaul
Thomas L. Moran
October 16, 2017 (2017-10-16)
10.60[22]

Barb Allen, 22 weeks pregnant, and her husband arrive at St. Bonaventure, hoping the doctors can save their baby. A large non-cancerous tumor is growing on the fetus and must be removed in order to save his life. Despite the serious risks both to her and the baby, Barb insists on surgery. Meanwhile, Shaun and Claire are assigned a patient, Olivia, who has a boil in her genital area. However, when doctors attempt to drain it, a fibroid tumor is found to be wrapped around a nerve. The surgery to remove it will cut off all feeling in Olivia's genitals. Shaun comes up with a solution that allows her to keep feeling in her genital area.

5
"Point Three Percent"
Larry Teng
David Hoselton
October 23, 2017 (2017-10-23)
10.39[23]

Shaun notices a young boy, Evan, who has an uncanny resemblance to his deceased brother Steve. Evan was brought to the hospital by his parents for a possible fracture to his arm. However, we discover that he is actually suffering from bone cancer, a fact his parents have kept hidden from him. Meanwhile, the other members of the team try to diagnose an older man, brought in by his estranged son, with a severe allergy condition causing him to convulse violently. Claire and Jared determine that the man is suffering from a cystic form of tapeworms located in his skull. A successful surgery is performed by Dr. Glassman.

6
"Not Fake"
Michael Patrick Jann
Simran Baidwan
October 30, 2017 (2017-10-30)
10.60[24]

Shaun and the rest of the residents are working the graveyard shift when numerous casualties from a wedding bus crash come in. Among the victims are a woman with severe, visible burns, on whom Jared tries an experimental procedure, and a young man with a severely damaged leg. Tensions arise between the patients parents and fiancée over the best choice for treatment; his parents want to amputate the leg, his fiancée is in favour of an experimental bone-replacement procedure. After treating a patient, Claire realises that a woman has been left behind at the crash site.

7
"22 Steps"
David Straiton
Johanna Lee
November 13, 2017 (2017-11-13)
10.14[25]

Shaun encounters Liam, an autistic patient brought in to the hospital. Having to face prejudice from the young man's parents, Dr. Melendez defends him for the first time and acknowledges his exceptional abilities. On Dr. Glassman's directive, Claire continues with therapy sessions in order to curb her guilt over inadvertently causing the death of a patient. Jared deals with a 73-year-old man with severe chest pains thus needing urgent medical attention and a pacemaker; but the patient states his desire is to die.

8
"Apple"
Nestor Carbonell
David Renaud
November 20, 2017 (2017-11-20)
9.97[26]

While shopping at a grocery mart for apples, a robbery takes place. With Shaun's communication limitations, he puts the lives of two customers on a first date at risk, leading to a young woman getting shot. Shaun's neighbor Lea hugs him after he admits that he made a mistake with someone getting hurt. During surgery, Dr. Lim questions Claire's ability to not let her emotions get the better of her because of a racist patient. This leads to an argument between the two with Dr. Lim ordering Claire to leave the operating room. Claire puts her emotions in check to save the life of the racist patient much to the satisfaction and delight of Dr. Lim.

9
"Intangibles"
Bronwen Hughes
Karen Struck
November 27, 2017 (2017-11-27)
9.25[27]

The team takes on the case of a young boy from the Congo who has severe congenital heart anomalies; Murphy's latest encounter with his neighbor Lea has him confused. He takes flirting lessons from Claire and notes and charts what he sees in regards to the "flirting trifecta". Meanwhile, Claire along with a lab tech search for a misplaced tissue sample from a woman with possible throat cancer.

10
"Sacrifice"
Michael Patrick Jann
Lloyd Gilyard Jr.
December 4, 2017 (2017-12-04)
9.03[28]

Shaun has reluctantly agreed to Dr. Glassman's repeated suggestions to meet with a therapist, but ultimately changes his mind after a new patient, Bobby Otto, convinces Shaun to stop letting people tell him what to do. Claire runs into an uncomfortable situation with Dr. Matt Coyle, who makes unwanted sexual advances toward her during a patient consultation. Jared finds out and physically threatens him. As a result, Jared is fired. After a tense dinner with Jessica, her father and Dr. Melendez, Jessica states that she doesn't want to have children.

11
"Islands Part One"
Bill D'Elia
Thomas L. Moran & William Rotko
January 8, 2018 (2018-01-08)
8.30[29]

Shaun and Lea embark on an impromptu road trip. Shaun drives, drinks Tequila, sings karaoke, all for the first time, and experiences his first kiss with Lea. Melendez and Andrews operate on conjoined twins, one of whom needs a kidney. Complications develop and the operation to separate them, planned for six months after the kidney surgery, must be done immediately. The operation goes well until it's discovered the twins have not awakened from the surgery. Melendez decides it's more important to be with Jessica and that he can be a "father" in other ways.

12
"Islands Part Two"
Cherie Nowlan
Thomas L. Moran & William Rotko
January 15, 2018 (2018-01-15)
9.33[30]

Shaun returns to the hospital after his trip and gives Dr. Glassman his two weeks’ notice, intending on moving to Hershey to be with Lea. The twins suffer complications from their surgery; Katie is not getting enough blood flow to the brain, while Jenny’s heart is failing. Despite the doctors’ best efforts to save both twins, Jenny dies on the operating table. Jessica is forced to look into previous misconduct at the hospital in which white doctors were only warned instead of fired, after allegations of racism by Kalu’s lawyer; as a result, Jared is reinstated. Jessica tells Melendez that she wants to break up because she feels like she is standing in his way of being a father.

13
"Seven Reasons"
Mike Listo
David Shore & David Hoselton
January 22, 2018 (2018-01-22)
9.61[31]

While treating a Muslim patient, Shaun senses she is lying and makes controversial claims about how she sustained her injuries. Melendez punctures the bronchus of the patient during surgery and is put under investigation after Shaun questions if his personal life is affecting his work. While Claire assists in a surgery on a stroke patient who had an aneurysm with Dr. Lim, she learns that Coyle got a new job and a raise. They inform the patient's wife that he needs surgery or he will die, but she refuses to conset until Claire explains the reality of the situation. Shaun asks Glassman to be friends, but Glassman decides to give him his own space and not be friends, which upsets Shaun.

14
"She"
Seth Gordon
Simran Baidwan
February 5, 2018 (2018-02-05)
9.63[32]

The four residents including the new Dr. Morgan Reznick are paired off in competition; Reznick and Browne with Melendez, Murphy and Kalu with Lim. Murphy and Kalu are faced with a gender dysphoric patient, Quinn, which leads to friction when Murphy claims people can only be their biological gender. Murphy and Kalu determine that Quinn has testicular cancer along with fragile bones caused by puberty blockers. Browne and Reznick tend to a male patient that has contracted a superbug resistant to all medication, as a result of taking leftover persciption medication for the wrong purpose. Drs. Andrews and Barnes see a fertility specialist as they are having trouble concieving.

15
"Heartfelt"
Regina King
Thomas L. Moran & Johanna Lee
February 26, 2018 (2018-02-26)
7.82[33]

A female teen goes through a risky surgery to implant a sternum so she can live a normal life without being confined to her house. A young male teen initially rejects the idea of having a convicted killer's liver transplanted in him, but without it he has a day to live. A former 15 year veteran cop turned doctor, Alex Park, is skeptical of the convict, Boris's, motives. Allegra talks to Dr. Andrews about a young wealthy donor, Aidan Coulter, but Andrews says being involved with him might give people the wrong idea and that she used sex to solicit donations. At a fundraiser, Jared tells Claire he loved her and thought maybe she would one day love him, but came to the realization that isn't true leaving the status of their relationship unknown.

16
"Pain"
Allison Liddi-Brown
William L. Rotko & David Renaud
March 12, 2018 (2018-03-12)
9.88[34]

Shaun, Claire, and Alex assist Melendez with one of his first patients, a man named Hunter who was paralyzed in a motorcycle accident ten years prior. Jared, Morgan, and Andrews attend a patient who has an infection caused by plastic surgery. Claire's estranged mother shows up at the hospital in an attempt to reconnect. Andrews sees an infertility specialist that tells him there is a surgery that could help him with his sperm count, but that there is a risk of impotence. Alex does a background check on Kenny which sheds light on his criminal past leading him to suggest Shaun is being used by him.

17
"Smile"
Bill D'Elia
David Hoselton & Karen Struck
March 19, 2018 (2018-03-19)
9.03[35]

Shaun and Alex treat teenaged Gretchen's Mobius Syndrome, enabling her to smile; Andrews persuades an insurance executive to cover the surgery. Morgan and Claire's patient, "Lucy Callard," is actually an identity thief who let her insurance lapse to pay her son's college tuition and failed to fill her post-operative antibiotic prescription due to fear of discovery. Morgan convinces the real Lucy Callard, a painkiller addict, to enter rehab; Claire gains the trust of the imposter, Beatrice, who dies of an infection. Jared romantically pursues his burn-victim patient, Celez, after she completes her treatment; he is also offered a job in Denver. Kenny takes advantage of Shaun. Shaun urges Glassman to date hospital barista Debbie; they hit it off over their interest in classic cars, but Glassman suddenly experiences aphasia at the end of their dinner date.

18
"More"
Mike Listo
David Shore & Lloyd Gilyard, Jr.
March 26, 2018 (2018-03-26)
9.52[36]

Glassman tells Shaun that he has an inoperable glioma and eighteen months to live. Glassman accepts his death, but agrees to additional imaging for Shaun's sake; this yields a worse prognosis of four months to live. Glassman takes Shaun to a park his late daughter loved so they can enjoy the time Glassman has left. Shaun determines how a minimally invasive biopsy could be performed; Glassman is diagnosed with an operable form of cancer; he will pursue treatment. Collegiate patient Caden suffers a complication after treatment for a fraternity hazing injury. Jared and Alex question Caden's friend, but Jared is put off by Alex's distrustful nature. Shaun determines that he erred in clamping Caden's artery. He proposes a risky procedure to save Caden's life and offers to take full responsibility for performing it, but Melendez decides they will perform it together. Caden survives and Melendez invites the team out for drinks, which Morgan finds perverse; Melendez hopes a doctor supports her when she inevitably kills a patient. Shaun decides he must admit his mistake to Andrews, even though Glassman staked his position on Shaun's success; Glassman leaves the decision up to Shaun, and accompanies him to meet with Andrews.

text: Production[edit]

text: Development[edit]

text: In May 2014, CBS Television Studios began development on an American remake of the hit South Korean medical drama Good Doctor with Daniel Dae Kim as producer. Kim explained the appeal of adapting the series as "something that can fit into a recognizable world, with a breadth of characters that can be explored in the long run".[37] The story of a pediatric surgeon with autism was to be set in Boston and projected to air in August 2015.[38][39] However, CBS did not pick up the project and it moved to Sony Pictures Television, with a put pilot commitment from ABC in October 2016. The series is developed by David Shore, who is executive producing alongside Kim, Sebastian Lee, and David Kim.[40] ABC officially ordered the series to pilot in January 2017.[41]

text: On May 11, 2017, ABC ordered the show to series as a co-production with Sony Pictures Television and ABC Studios,[42] and it was officially picked up for a full season of 18 episodes on October 3, 2017.[43] On March 7, 2018, ABC renewed the series for a second season.[44] It will premiere in the fall of 2018.

text: Casting[edit]

text: On February 17, 2017, Antonia Thomas was cast as Dr. Claire Browne, a strong-willed and talented doctor who forms a special connection with Shaun.[5] A week later, Freddie Highmore was cast in the lead role as Dr. Shaun Murphy, a young surgeon with autism; and Nicholas Gonzalez was cast as Dr. Neil Melendez, the boss of the surgical residents at the hospital.[3] The next month, Chuku Modu was cast as resident Dr. Jared Kalu (originally Dr. Jared Unger);[6] Hill Harper as head of surgery Dr. Marcus Andrews (originally Dr. Horace Andrews); Irene Keng as resident Dr. Elle McLean;[8] and Richard Schiff was cast as Dr. Aaron Glassman (originally Dr. Ira Glassman), the hospital president and Shaun's mentor.[9][42] Schiff was shortly followed by Beau Garrett as hospital board member Jessica Preston and a friend of Dr. Glassman.[7] In September 2017, Tamlyn Tomita was promoted to the principal cast as Allegra Aoki.[11]

text: In April 2018, it was revealed that Will Yun Lee, Fiona Gubelmann, Christina Chang, and Paige Spara had been promoted to series regulars for the second season, after recurring in the first as Alex, Morgan, Audrey, and Lea, respectively.[45] In addition, it was announced that Chuku Modu would not return for the second season.[45]

text: Filming[edit]

text: Production on the pilot took place from March 21 to April 6, 2017 in Vancouver, British Columbia.[47][48] Filming for the rest of the season began on July 26, 2017, and concluded on March 1, 2018.[49]

text: Music[edit]

text: Dan Romer serves as the primary composer for the series.[50]

text: Release[edit]

text: Broadcast[edit]

text: The Good Doctor began airing on September 25, 2017, on ABC in the United States,[51] and on CTV in Canada.[52] Sky Living acquired the broadcast rights for the United Kingdom and Ireland.[53] Seven Network airs the series in Australia.[54] Wowow, the largest Japanese private satellite and pay-per-view television network in Japan acquired the rights to broadcast the series beginning in April 2018.[55] In the Netherlands, the series began airing on January 29, 2018, on RTL 4 and on video-on-demand service Videoland.[56]

text: Marketing[edit]

text: A full-length trailer was released for ABC's May 2017 Upfront presentation, which /Film's Ethan Anderton described the concept as feeling like "House meets Rain Man, that just might be enough to make it interesting". However, he questioned "how long can audiences be entranced by both the brilliance of [Highmore's] character's savant skills and the difficulties that come from his autism in the workplace."[57] Daniel Fienberg of The Hollywood Reporter felt the trailer was "both kinda progressive and really dated". He added, "Too much felt on-the-nose—especially Hill Harper as the main character's detractor and Richard Schiff as his noble defender", while also commentating that "On-the-nose/premise is how you have to trailer a show like this, and maybe spaced out over 43 minutes it won't grate."[58] Ben Travers and Steve Greene for IndieWire called it "a serious trailer for a serious subject. The first glimpse of Highmore's character hints that they're toeing the line between presenting a thoughtful depiction of his condition and using his perceptive abilities as a kind of secret weapon."[59] The trailer had been viewed over 25.4 million times after a week of its release, including over 22 million views on Facebook.[60]

text: The pilot was screened at ABC's PaleyFest event on September 9, 2017.[61] On March 22, 2018, members of the cast as well as executive producers Shore and Kim attended the 35th annual PaleyFest LA to promote the series, along with a screening of the season finale of the first season.[62]

text: Reception[edit]

text: Ratings[edit]

text:
No.
Title
Air date
Rating/share
(18–49)
Viewers
(millions)
DVR
(18–49)
DVR viewers
(millions)
Total
(18–49)
Total viewers
(millions)

1
"Burnt Food"
September 25, 2017
2.2/9
11.22[19]
2.2
7.86
4.4
19.21[63]

2
"Mount Rushmore"
October 2, 2017
2.2/9
10.93[20]
2.1
7.21
4.3
18.12[64]

3
"Oliver"
October 9, 2017
2.0/7
10.69[21]
2.2
7.53
4.2
18.22[65]

4
"Pipes"
October 16, 2017
2.0/8
10.60[22]
2.1
7.34
4.1
17.96[66]

5
"Point Three Percent"
October 23, 2017
1.8/7
10.39[23]
2.0
7.10
3.8
17.50[67]

6
"Not Fake"
October 30, 2017
1.9/7
10.60[24]
2.0
6.93
3.9
17.51[68]

7
"22 Steps"
November 13, 2017
1.9/7
10.14[25]
1.9
6.92
3.8
17.14[69]

8
"Apple"
November 20, 2017
1.8/7
9.97[26]
1.8
6.98
3.6
16.99[70]

9
"Intangibles"
November 27, 2017
1.7/7
9.25[27]
1.8
6.66
3.5
15.91[71]

10
"Sacrifice"
December 4, 2017
1.6/7
9.03[28]
1.8
6.67
3.4
15.74[72]

11
"Islands Part One"
January 8, 2018
1.6/6
8.30[29]
1.8
7.10
3.4
15.40[73]

12
"Islands Part Two"
January 15, 2018
1.7/6
9.33[30]
1.8
6.66
3.5
16.00[74]

13
"Seven Reasons"
January 22, 2018
1.7/7
9.61[31]
1.9
6.91
3.6
16.53[75]

14
"She"
February 5, 2018
1.7/7
9.63[32]
1.8
7.07
3.5
16.71[76]

15
"Heartfelt"
February 26, 2018
1.3/5
7.82[33]
1.8
6.84
3.1
14.66[77]

16
"Pain"
March 12, 2018
1.8/7
9.88[34]
1.5
6.23
3.3
16.12[78]

17
"Smile"
March 19, 2018
1.6/6
9.03[35]
1.5
6.39
3.1
15.42[79]

18
"More"
March 26, 2018
1.7/6
9.52[36]
1.6
6.32
3.3
15.85[80]

text: The series premiere earned a 2.2/9 rating in the 18- to 49-year-old demographic, with 11.22 million total viewers, making it the most watched Monday drama debut on ABC in 21 years, since Dangerous Minds in September 1996, and the highest rated Monday drama in the 18–49 demographic in 8.5 years, since Castle in March 2009.[81] Factoring live plus seven-day ratings, the pilot was watched by a total of 19.2 million viewers and set a record for DVR viewers with 7.9 million, surpassing the record of 7.67 million set by the pilot of Designated Survivor in 2016.[82] According to TV Guide's November 13-26 issue, the October 9 episode attracted 18.2 million viewers, beating out both NCIS and The Big Bang Theory for the most viewed primetime show that week.[83]

text: Critical response[edit]

text: The review aggregator website Rotten Tomatoes reported a 58% approval rating with an average rating of 5.49/10 based on 38 reviews. The website's consensus reads, "The Good Doctor's heavy-handed bedside manner undermines a solid lead performance, but under all the emotionally manipulative gimmickry, there's still plenty of room to improve."[84] Metacritic, which uses a weighted average, assigned a score of 53 out of 100 based on 15 critics, indicating "mixed or average reviews".[85]

text: Giving his first impression of the series' pilot for TVLine, Matt Webb Mitovich stated, "The Good Doctor boasts great DNA... [and] has the potential to be a refreshingly thought-provoking hospital drama, based on the buttons pushed in the pilot alone." He enjoyed the "warm dynamic" of Schiff and Highmore, while describing Thomas' character as "our emotional 'in' to Shaun's distinct, distant world". He noted that "it takes a while to build up momentum", but concluded that "the very final scene packs quite a punch, as Dr. Murphy unwittingly puts a colleague on notice".[86]

text: The New York Times television critic, James Poniewozik, notes in his Critic's Notebook column, that for the most part the drama is a "hospital melodrama with whiz-bang medical science, a dash of intra-staff romance and shameless sentimentality." Discussing the main characters of Dr. Aaron Glassman (Richard Schiff) and Dr. Shaun Murphy (Freddie Highmore), however, Poniewozik writes that "Mr. Schiff is convincing in the role and Mr. Highmore is striking in his." [87]

text: Speaking of Freddie Highmore's Golden Globe nomination on Monday, December 11, 2017, for his role in The Good Doctor, Laura Bradley, writing for Vanity Fair says: "... Freddie Highmore received the awards recognition that has long and unjustly eluded him..." Bradley feels that Highmore's performance has been "the central key" to the show's enormous success and while the show had lukewarm reviews, most critics have praised Highmore's work. [88]

text: Accolades[edit]

text:
Year
Association
Category
Nominee
Result
Ref.

2018
Golden Globe Awards
Best Actor – Television Series Drama
Freddie Highmore
Nominated
[89][90]

Humanitas Prize
60-Minute Category
David Shore
Won
[91]

Banff Rockie Awards
Scripted Melodrama Series
The Good Doctor
Pending
[92]


document_title: The Graduate

question_text: where did the movie the graduate take place

text: The Graduate

text: Plot[edit]

text: Benjamin Braddock, aged twenty-one, has earned his bachelor's degree from Williams College and has returned home to a party celebrating his graduation at his parents' house in Pasadena, California. Benjamin, visibly uncomfortable as his parents deliver accolades and neighborhood friends ask him about his future plans, evades those who try to congratulate him. Mrs. Robinson, the neglected wife of his father's law partner, insists that he drive her home. Benjamin is coerced inside to have a drink and Mrs. Robinson attempts to seduce him. She invites him up to her daughter Elaine's room to see her portrait and then enters the room naked, making it clear that she is available to him. Benjamin initially rebuffs her but a few days later after his scuba demonstration on his birthday, he clumsily organizes a tryst at the Taft hotel.

text: Benjamin spends the remainder of the summer drifting around in the pool by day, purposefully neglecting to select a graduate school, and seeing Mrs. Robinson at the hotel by night. He discovers that he and Mrs. Robinson have nothing to talk about. However, after Benjamin pesters her one evening, Mrs. Robinson reveals that she entered into a loveless marriage when she accidentally became pregnant with Elaine. Both Mr. Robinson and Benjamin’s parents encourage him to call Elaine, even though Mrs. Robinson makes her disapproval clear.

text: Benjamin takes Elaine on a date but tries to sabotage it by ignoring her, driving recklessly and taking her to a strip club. After Elaine runs out of the strip club in tears, Benjamin has a change of heart, realizes how rude he was to her, and discovers that Elaine is someone with whom he is comfortable. In search of a late-night drink they visit the Taft hotel but when the staff greet Benjamin as "Mr. Gladstone" (the name he uses during his rendezvous with Mrs. Robinson) Elaine correctly guesses that he has been having an affair with a married woman and accepts his assurances that the affair is now over. To preempt a furious Mrs. Robinson, who threatens to tell Elaine her version of their affair, Benjamin tells Elaine that the married woman was her mother. Elaine is distraught and returns to Berkeley. Benjamin pursues her there and tries to talk to her. She reveals that her mother's story is that he raped her while she was drunk, and refuses to believe that it was in fact her mother who seduced Benjamin. After much discussion over several days, Benjamin begins to make inroads with Elaine. However, Mr. Robinson arrives at Berkeley after learning about the affair, confronts Benjamin at his rooming house, and threatens to put him behind bars if Benjamin sees his daughter again. Mr. Robinson then forces Elaine to drop out of college and takes her away to marry Carl, a classmate with whom she had briefly been involved.

text: Returning to Pasadena in search of Elaine, Benjamin breaks into the Robinson home but encounters Mrs. Robinson. She tells him he will not be able to stop the wedding and then calls the police claiming that her house is being burgled. Benjamin visits Carl’s fraternity brothers who tell him that the wedding is in Santa Barbara, California that very morning. He rushes to the church and arrives just as Elaine is married. He bangs on the glass at the back of the church and screams out "Elaine!" repeatedly. After a brief hesitation, Elaine screams out "Ben!" and starts to run toward him. A brawl ensues as guests try to stop Elaine and Benjamin from leaving together. Elaine manages to break free from her mother, who then slaps her. Benjamin manages to keep the guests at bay by jamming a large cross into the doors of the church. Both he and Elaine then run into the street to flag down a passing bus and take the back seat. Although initially elated at their victory, the pair become increasingly uncomfortable as they journey towards an uncertain future.

text: Cast[edit]

text:
Anne Bancroft as Mrs. Robinson
Dustin Hoffman as Benjamin Braddock
Katharine Ross as Elaine Robinson
William Daniels as Mr. Braddock
Murray Hamilton as Mr. Robinson
Elizabeth Wilson as Mrs. Braddock
Buck Henry as Room clerk
Brian Avery as Carl Smith
Walter Brooke as Mr. McGuire
Norman Fell as Mr. McCleery
Alice Ghostley as Mrs. Singleman
Marion Lorne as Miss DeWitte
Eve McVeagh as Mrs. Carlson

text: Production[edit]

text: Casting[edit]

text: According to TCM host Robert Osborne, "Mike Nichols wanted Doris Day for Mrs. Robinson, Robert Redford for Benjamin Braddock, and Gene Hackman for Mr. Robinson." But there were numerous actors considered or tested for, or who wanted, roles in the film.

text: Day turned down the offer because the nudity required by the role offended her.[5] Nichols' actual first choice for Mrs. Robinson was French actor Jeanne Moreau. The idea behind this was that in the French culture, the "older" women tended to "train" the younger men in sexual matters. Joan Crawford inquired as to play the part, while Lauren Bacall and Audrey Hepburn both wanted the role. Patricia Neal turned down the film as she had recently recovered from a stroke and did not feel ready to accept such a major role. Geraldine Page also turned it down. Other actors considered for the part included Claire Bloom, Angie Dickinson, Sophia Loren, Judy Garland, Rita Hayworth, Susan Hayward, Anouk Aimee, Jennifer Jones, Deborah Kerr, Eva Marie Saint, Rosalind Russell, Simone Signoret, Jean Simmons, Lana Turner, Eleanor Parker, Anne Baxter and Shelley Winters. Angela Lansbury also asked about playing the part. Ava Gardner sought the role of Mrs. Robinson, and reportedly called Nichols saying,"I want to see you! I want to talk about this Graduate thing!" Nichols did not seriously consider her for the role (he wanted a younger woman as Bancroft was 36 and Gardner was 45), but did end up visiting her hotel. He later recounted that "she sat at a little French desk with a telephone, she went through every movie star cliché. She said, 'All right, let's talk about your movie. First of all, I strip for nobody.'" Meanwhile, Natalie Wood turned down not only the role of Mrs. Robinson, but also that of Elaine.

text: For the character of Elaine, casting was also an issue. Patty Duke turned down the part as she did not want to work at the time. Faye Dunaway was also considered for Elaine, but had to turn it down, in favor of Bonnie and Clyde. Sally Field and Shirley MacLaine refused the role as well. Raquel Welch and Joan Collins both wanted the role, but did not succeed in getting it. Carroll Baker tested, but was said to have been too old to portray Anne Bancroft's daughter. Candice Bergen screen-tested as well, as did Goldie Hawn and Jane Fonda. Additionally, Ann-Margret, Elizabeth Ashley, Carol Lynley, Sue Lyon, Yvette Mimieux, Suzanne Pleshette, Lee Remick, Pamela Tiffin, Julie Christie, and Tuesday Weld were all on the director's shortlist before Katharine Ross was cast.

text: When Dustin Hoffman auditioned for the role of Benjamin, he was asked to perform a love scene with Ross. Hoffman had never done one during his acting classes and believed that, as he said later, "a girl like [Ross] would never go for a guy like me in a million years." Ross agreed, believing that Hoffman "look[ed] about 3 feet tall ... so unkempt. This is going to be a disaster." Producer Joseph E. Levine later admitted that he at first believed that Hoffman "was one of the messenger boys." Despite—or perhaps because of— Hoffman's awkwardness, Nichols chose him for the film.[6] “As far as I’m concerned, Mike Nichols did a very courageous thing casting me in a part that I was not right for, meaning I was Jewish,” said Hoffman. “In fact, many of the reviews were very negative. It was kind of veiled anti-Semitism…. I was called ‘big-nosed’ in the reviews, ‘a nasal voice.’”[7] Before Hoffman was cast, Robert Redford and Warren Beatty were among the top choices. Beatty turned the film down as he was occupied with Bonnie and Clyde. Redford tested for the part of Benjamin (with Candice Bergen as Elaine), but Nichols thought that Redford did not possess the underdog quality that Benjamin needed. When Mike Nichols talked with Redford, Redford asked what he meant. "Well, let's put it this way," said Nichols, "Have you ever struck out with a girl?" "What do you mean?" asked Redford. "That's precisely my point," said Nichols. Charles Grodin turned down the part, as the money was not right. Both Brandon deWilde and Michael Parks auditioned for the role. In addition, Keir Dullea, Robert Duvall, Harrison Ford, George Hamilton, Albert Finney, Gene Wilder, Steve McQueen, Jack Nance, Anthony Perkins, Robert Wagner, and Jack Nicholson were all considered for the part of Benjamin. Burt Ward, who starred as Robin on the Batman television series, had to pass on the role as he was committed to filming the show, and the studio would not lend him anyway.

text: In the role of Mr. Robinson, Gene Hackman was originally cast, but just before filming began, the director decided he was too young and decided to replace him. Marlon Brando, Howard Duff, Brian Keith, George Peppard, Jack Palance, Frank Sinatra, Walter Matthau and Gregory Peck were all other choices for the role that Murray Hamilton eventually played. Susan Hayward was the first choice for Benjamin's mother, Mrs. Braddock, but the role was given to Elizabeth Wilson. And to play Mr. Braddock, Yul Brynner, Kirk Douglas, Jack Lemmon, Robert Mitchum, Karl Malden, Christopher Plummer and Ronald Reagan all came close to getting the role that ended up going to William Daniels.[8]

text: There are considerable age discrepancies between the lead roles and the actors who portrayed them. Benjamin Braddock says, "I will be 21 next week "; at the time of filming, Dustin Hoffman was 29. William Daniels, who plays Hoffman's father, was, at 39, only 10 years older than Hoffman. Mrs. Robinson states, "Benjamin, I am twice your age." Anne Bancroft was 35, only six years older than Hoffman. Mrs. Robinson's daughter Elaine is 19 and was portrayed by Katharine Ross, who was 27 at the time. Elaine May, who portrayed Elaine's college roommate and delivered a note to Benjamin from Elaine, was 35 at the time and only seven months younger than Anne Bancroft. Mrs. Singleman and Miss DeWitte, party guests in one of the Taft Hotel scenes, were said to be sisters, though there was a 38-year age difference between their portrayors, Alice Ghostley (age 44) and Marion Lorne (age 82).

text: Filming locations[edit]

text: Many of the exterior university campus shots of Berkeley were actually filmed on the brick campus of USC in Los Angeles.[9] Other scenes were filmed on Durant Avenue and College Ave. across from the Unit One Dorms in the city of Berkeley, as well as on the Berkeley campus itself (shot remotely from Telegraph Avenue, as the university did not permit commercial filming at the time).

text: The Taft Hotel scenes were filmed at the Ambassador Hotel.

text: The church used for the wedding scene is actually the United Methodist Church in La Verne. In a commentary audio released with the 40th anniversary DVD, Hoffman revealed that he was uneasy about the scene in which he pounds on the church window, as the minister of the church had been watching the filming disapprovingly. The wedding scene was highly influenced by the ending of the 1924 comedy film Girl Shy starring Harold Lloyd, who also served as an advisor for the scene in The Graduate.[10][11] The residences used for the Braddocks' house and the Robinsons' house were located on North Palm Drive in Beverly Hills. The scene with Benjamin and Elaine at night in his car at the drive-in restaurant was filmed in Westwood Village, Los Angeles.

text: The scenes of Benjamin driving to Berkeley on the San Francisco–Oakland Bay Bridge were filmed on the top level of the bridge—leading into San Francisco—the opposite direction of Berkeley. In another scene as he drives south to Santa Barbara, his Alfa Romeo Spider is shown heading north through the Gaviota Tunnel, also the wrong direction.

text: Music[edit]

text: The film boosted the profile of folk-rock duo Simon & Garfunkel. Originally, Nichols and O'Steen used their existing songs like "The Sound of Silence" merely as a pacing device for the editing until Nichols decided that substituting original music would not be effective and decided to include them on the soundtrack, an unusual move at that time.[12]

text: According to a Variety article by Peter Bart in the May 15, 2005, issue, Lawrence Turman, his producer, then made a deal for Simon to write three new songs for the movie. By the time they had nearly finished editing the film, Simon had only written one new song. Nichols begged him for more, but Simon, who was touring constantly, told him he did not have the time. He did play him a few notes of a new song he had been working on; "It's not for the movie... it's a song about times past—about Mrs. Roosevelt and Joe DiMaggio and stuff." Nichols advised Simon, "It's now about Mrs. Robinson, not Mrs. Roosevelt."[13]

text: On the strength of the hit single "Mrs. Robinson", the soundtrack album rose to the top of the charts in 1968. However, the version that appears in the film is markedly different from the hit single version, which would not be issued until Simon & Garfunkel's next album, Bookends. The actual film version of "Mrs. Robinson" does appear on The Graduate soundtrack LP.

text: In addition to the Simon & Garfunkel songs, the film features an instrumental score by Dave Grusin.

text: Reception[edit]

text: Critical response[edit]

text: The Graduate was met with positive reviews from critics upon its release. A.D. Murphy of Variety and Roger Ebert of the Chicago Sun-Times praised the film, with Murphy describing it as a "delightful satirical comedy-drama"[14] and Ebert claiming it was the "funniest American comedy of the year".[15]

text: Modern critics continue to praise the film, if not always with the same ardor. For the film's thirtieth anniversary reissue, Ebert retracted some of his previous praise for the film, noting that he felt its time had passed and that he now had more sympathy for Mrs. Robinson than Benjamin (whom he considered "an insufferable creep"), viewing one's sympathy for Mrs. Robinson and disdainful attitude toward Ben as a function of aging and wisdom.[16] He, along with Gene Siskel, gave the film a positive if unenthusiastic review on the television program Siskel & Ebert.[17] Furthermore, the film's rating in the AFI list of the greatest American films fell from 7th in 1997 to 17th in the 2007 update. Lang Thompson, however, argued that "it really hasn't dated much".[18]

text: Review aggregator Rotten Tomatoes gives the film an approval rating of 91% based on 74 reviews, with an average rating of 8.8/10. The site's consensus reads, "The music, the performances, the precision in capturing the post-college malaise—The Graduate's coming-of-age story is indeed one for the ages."[19] On the similar website Metacritic, the film holds a score of 77 out of 100, based on 10 critics, indicating "generally favorable reviews".[20]

text: Awards and honors[edit]

text: The film received Academy Award nominations for Best Picture (Lawrence Turman), Best Actor (Dustin Hoffman), Best Actress (Anne Bancroft), Best Supporting Actress (Katharine Ross), Best Adapted Screenplay (Buck Henry and Calder Willingham), and Best Cinematography (Robert L. Surtees). Mike Nichols won the Academy Award for Best Director.

text: The film also received Golden Globe Award nominations for Best Actor – Motion Picture Musical or Comedy (Hoffman), and Best Screenplay (Henry and Willingham). Bancroft won the Golden Globe Award for Best Actress – Motion Picture Musical or Comedy, Nichols won the Golden Globe Award for Best Director, Turman and Joseph E. Levin won the Golden Globe Award for Best Motion Picture – Musical or Comedy, Hoffman won the Golden Globe Award for New Star of the Year – Actor, and Ross won the Golden Globe Award for New Star of the Year – Actress.

text: In addition, the film won the BAFTA Award for Best Film, BAFTA Award for Best Direction (Nichols), BAFTA Award for Most Promising Newcomer to Leading Film Roles (Hoffman), the BAFTA Award for Best Editing (Sam O'Steen). Bancroft was nominated for the BAFTA Award for Best Actress in a Leading Role.

text: In 1996, The Graduate was selected for preservation in the U.S. National Film Registry by the Library of Congress as being "culturally, historically, or aesthetically significant", and placed #21 on the list of highest-grossing films in the United States and Canada, adjusted for inflation.[4]

text: Years later in interviews, Bancroft conceded that, much to her surprise, Mrs. Robinson was the role with which she was most identified, and added "Men still come up to me and tell me 'You were my first sexual fantasy.'"

text: The film is listed in 1001 Movies You Must See Before You Die.[21]

text: In 1985 Alfa Romeo introduced the Graduate, a version of the Alfa Romeo Spider which recalled the car used in the movie. This version of the car was produced until 1990.

text: American Film Institute

text: The film is recognized by American Film Institute in these lists:

text:
1998: AFI's 100 Years...100 Movies – #7[22]
2000: AFI's 100 Years...100 Laughs – #9[23]
2002: AFI's 100 Years...100 Passions – #52[24]
2004: AFI's 100 Years...100 Songs:

"Mrs. Robinson" – #6[25]

2005: AFI's 100 Years...100 Movie Quotes:

Mr. Maguire: "Plastics." – #42[26]
Benjamin Braddock: "Mrs. Robinson, you're trying to seduce me. Aren't you?" – #63[27]

2007: AFI's 100 Years...100 Movies (10th Anniversary Edition) – #17[28]

text: Stage adaptation[edit]

text: Terry Johnson's adaptation of the original novel and the film ran both on London's West End and on Broadway, and has toured the United States. There is a Brazilian version adapted by Miguel Falabella. Several actresses have starred as Mrs. Robinson, including Kathleen Turner, Lorraine Bracco, Jerry Hall, Amanda Donohoe, Morgan Fairchild, Anne Archer, Vera Fischer, Patricia Richardson and Linda Gray.

text: The stage production adds several scenes that are not in the novel or the film, as well as using material from both film and novel. [29] It also uses songs by Simon & Garfunkel not used in the film, such as "Bridge Over Troubled Water" as well as music from other popular musicians from the era such as The Byrds and The Beach Boys.[30]

text: The West End production opened at the Gielgud Theatre on April 5, 2000, after previews from March 24, with Kathleen Turner starring as Mrs. Robinson.[31][32] The production closed in January 2002. Jerry Hall replaced Turner on July 31, 2000, followed by Amanda Donohoe from February 2001, Anne Archer from June 2001, and Linda Gray from October 2001.[33][34] The 2003 UK touring production starred Glynis Barber as Mrs. Robinson.[35]

text: The Broadway production opened at the Plymouth Theatre on April 4, 2002, and closed on March 2, 2003, after 380 performances. Directed by Terry Johnson, the play featured the cast of Jason Biggs as Benjamin Braddock, Alicia Silverstone as Elaine Robinson, and Kathleen Turner as Mrs. Robinson. The play received no award nominations.[36] Linda Gray briefly filled-in for Turner in September 2002. Lorraine Bracco replaced Turner from November 19, 2002.[37]

text: The Graduate ran at the Cape Playhouse (Dennis, Massachusetts) in July 2011, and starred Patricia Richardson.[38]

text: Possibility of sequel[edit]

text: Charles Webb has written a sequel to his original novel titled Home School, but initially refused to publish it in its entirety because of a contract he signed in the 1960s. When he sold film rights to The Graduate, he surrendered the rights to any sequels. If he were to publish Home School, Canal+, the French media company that owns the rights to The Graduate, would be able to adapt it for the screen without his permission.[39] Extracts of Home School were printed in The Times on May 2, 2006.[40] Webb also told the newspaper that there was a possibility he would find a publisher for the full text, provided he could retrieve the film rights using French copyright law.[41] On May 30, 2006, The Times reported that Webb had signed a publishing deal for Home School with Random House which he hoped would enable him to instruct French lawyers to attempt to retrieve his rights. The novel was published in Britain in 2007.[42]

text: While not technically a sequel, the 2005 film Rumor Has It revolves around characters who live in Pasadena and are rumored to have inspired their counterparts in The Graduate.


document_title: Linebacker

question_text: where does the strong side linebacker line up

text: Linebacker

text: History[edit]

text: Before the advent of the two-platoon system with separate units for offense and defense, the player who was the team's center on offense was often, though not always, the team's linebacker on defense. Hence today one usually sees four defensive linemen to the offense's five or more. Most sources claim coach Fielding H. Yost and center Germany Schulz of the University of Michigan invented the position.[1][2][3][4][5] Schulz was Yost's first linebacker in 1904 when he stood up from his usual position on the line. Yost was horrified at first, but came to see the wisdom in Schulz's innovation.[6] William Dunn of Penn St. was another Western linebacker soon after Schulz.

text: However, there are various historical claims tied to the linebacker position, including some before 1904. For example, Percy Given of Georgetown is another center with a claim to the title "first linebacker," supposedly standing up behind the line well before Schulz in a game against Navy in 1902.[7] Despite Given, most sources have the first linebacker in the South as Frank Juhan of Sewanee.[8] In the East, Ernest Cozens of Penn was "one of the first of the roving centers,"[9] another, archaic term for the position, supposedly coined by Hank Ketcham of Yale.[10] Walter E. Bachman of Lafayette was said to be "the developer of the "roving center" concept."[11] Edgar Garbisch of Army was credited with developing the "roving center method" of playing defensive football in 1921.[12]

text: In professional football, Cal Hubbard is credited with pioneering the linebacker position. He starred as a tackle and end, playing off the line in a style similar to that of a modern linebacker.[13]

text: Types[edit]

text: Middle linebacker[edit]

text: The middle or inside linebacker (MLB or ILB), sometimes called "Mike" or "Mohr",[14] is often referred to as the "quarterback of the defense."[15] Often it is the middle linebacker who receives the defensive play calls from the sideline and relays that play to the rest of the team–and in the NFL he is usually the defensive player with the electronic sideline communicator. A jack-of-all-trades, the middle linebacker can be asked to blitz (though they often blitz less than the outside linebacker), cover, spy the quarterback, or even have a deep middle-of-the-field responsibility in the Tampa 2 defense. In standard defenses, middle linebackers commonly lead the team in tackles. The terms middle and inside linebacker are often used interchangeably;[16] they are also used to distinguish between a single middle linebacker playing in a 4–3 defense, and two inside linebackers playing in a 3–4 defense.[17] In a 3–4 defense that has these two inside linebackers, the larger, more run-stopping-oriented linebacker is usually still called "Mike", while the smaller, more pass protection/route coverage-oriented player is called "Will". "Mikes" usually line up towards the strong side or on the side the offense is more likely to run on (based on personnel matchups) while Wills may line up on the other side or even a little farther back between the defensive line and the secondary.

text: Outside linebacker[edit]

text: The outside linebacker (OLB), sometimes called the "Buck, Sam, and Rebel" is usually responsible for outside containment. This includes the strongside and weakside designations below. They are also responsible for blitzing the quarterback.

text: Strongside linebacker[edit]

text: The strongside linebacker (SLB) is often nicknamed "Sam" or striker[14] for purposes of calling a blitz. Since the strong side of the offensive team is the side on which the tight end lines up, or whichever side contains the most personnel, the strongside linebacker usually lines up across from the tight end. Often the strongside linebacker will be called upon to tackle the running back on a play, because the back will be following the tight end's block. He is most often the strongest linebacker; at the least he possesses the ability to withstand, shed, and fight off blocks from a tight end or fullback blocking the backside of a pass play. The linebacker should also have strong safety abilities in pass situation to cover the tight end in man on man situations. He should also have considerable quickness to read and get into coverage in zone situations. The strongside linebacker is also commonly known as the left outside linebacker (LOLB).

text: Weakside linebacker[edit]

text: The weakside linebacker (WLB), or the "Will" in 4–3 Defense, sometimes called the backside linebacker, or "Buck", as well as other names like Jack or Bandit[14] must be the fastest of the three, because he is often the one called into pass coverage. He is also usually chasing the play from the backside, so the ability to maneuver through traffic is a necessity for the Will. The Will usually aligns off the line of scrimmage at the same depth as Mike. Because of his position on the weakside, the Will does not often have to face large interior linemen one on one unless one is pulling. In coverage, the Will often covers the back that attacks his side of the field first in man coverage, while covering the weak flat in Texas Loop or hook/curl areas in zone coverage. The weakside linebacker is also commonly known as the right outside linebacker (ROLB). The ROLB needs to be strong in all areas of the physical realm.

text: Formations[edit]

text: The number of linebackers is dependent upon the formation called for in the play; formations can call for as few as none, or as many as seven. Most defensive schemes call for three or four, and they are generally named for the number of linemen, followed by the number of linebackers (with the 46 defense being an exception). For example, the 4–3 defense has four defensive linemen and three linebackers; conversely, the 3–4 defense has three linemen and four linebackers.

text: 4–3 defense[edit]

text: In the 4–3 defense there are four down linemen and three linebackers. The middle linebacker is designated "Mike" (or "Mac") and two outside linebackers are designated "Sam" and "Will" according to how they line up against the offensive formation. If there is a strong call, the linebacker on the strongside is called "Sam", while the linebacker on the weakside is called "Will". The outside linebacker's job is to cover the end to make sure a run doesn't escape, and to watch the pass and protect from it. The middle linebacker's job is to stop runs between the tackles and watch the entire field to see the play develop. On pass plays, the linebackers' responsibilities vary based upon whether a man or zone coverage is called. In a zone coverage, the linebackers will generally drop into hook zones across the middle of the field. However, some zones will send the outside linebackers into the flats (area directly to the left and right of the hash marks, extending 4–5 yards downfield). In a man-to-man call, the "Sam" will often cover the tight end with help from a safety over the top, while at other times, the "Sam" and "Will" will be responsible for the first man out of the backfield on their side of the center, with the "Mike" covering if a second man exits on that side of the field.

text: In the "Tampa 2" zone defense the middle linebacker is required to drop quickly into a deep middle zone pass coverage thus requiring a quick player at this position.

text: 3–4 defense[edit]

text: In the 3–4 defense there are three linemen playing the line of scrimmage with four linebackers backing them up, typically two outside linebackers and two inside linebackers. The weak side inside linebacker is typically called the "Will," while the strong side or middle inside linebacker is called the "Mike". "Sam" is a common designation for strong outside linebacker, while the other position is usually called "Jack" and is often a hybrid DE/LB. Usually, teams that run a 3–4 defense look for college defensive ends that are too small to play the position in the pros and not quite fluid enough to play outside linebacker in a 4–3 defense as their "Jack" linebacker.

text: The idea behind the 3–4 defense is to disguise where the fourth rusher will come from. Instead of the standard four down-linemen in the 4–3, only three players are clearly attacking on nearly every play. A key for running this defense successfully is having a defensive front of three large defensive linemen who command constant double teams. In particular, the nose tackle, who plays over the offensive center, must be able to hold ground and to occupy several offensive blockers to allow the linebackers to make plays. The focus of the 3–4 defensive line is to occupy offensive linemen thus freeing the linebackers to tackle the running back or to rush the passer or otherwise drop into pass coverage.

text: Generally, the primary responsibilities for both outside linebackers are to stop the run and rush the quarterback in passing situations, in which they line in front of the tackles like true defensive ends. The outside linebackers in a 3–4 defense are players who are very skilled at rushing the quarterback and they would be playing defensive end in a 4–3 defense. When it comes to the inside linebackers, one is generally a run-stuffing player who is better able to handle offensive linemen and stop running backs when the offense features a running play, while the other is often a smaller, faster player who excels in pass coverage. However, the smaller or cover LB should also be able to scrape and plug running lanes decently.

text: The design concept of the 3–4 defense is to confuse the offensive line in their blocking assignments, particularly in pass blocking, and to create a more complex read for the quarterback. Many 3–4 defenses have the ability to quickly hybrid into a 4–3 on the field.

text: 46 defense[edit]

text: In the 46 defense there are four linemen, three linebackers and a safety who is moved up behind the line of scrimmage. Thus, it appears as if there are 4 linebackers, but it is really 3 linebackers with one safety playing up with the other linebackers.

text: Three of the defensive linemen are over both of the offensive guards and the center, thereby making it difficult to double team any one of the three interior defensive linemen. This can also take away the ability of the offense to pull the guards on a running play, because this would leave one of the defenders unblocked, or, at best, give another lineman a very difficult block to make on one of the defenders. The safety, like the linebacker, can blitz, play man-on-man, play zone, or drop back into deep coverage like a normal safety would do. The 46 is used in heavy run situations to stop the run, when a team wants to bring lots of pressure, or merely to confuse the quarterback and offensive line.

text: 4–4 defense[edit]

text: This defense is effective at run-stopping but is weaker than a 4–3 defense at pass coverage because it uses only three defensive backs. One of the outside linebackers is usually called into either blitz or pass coverage to make up for the missing DB. In the NFL and college football, this alignment is used mainly in short yardage situations or near the goal line. It is commonly used in high school football.