document_title: Flash vs. Arrow

question_text: when did the flash first appear on arrow

text: Flash vs. Arrow

text: Plot[edit]

text: Roy Bivolo, a new metahuman with the ability to send people into an uncontrollable rage, uses his ability to rob the Central City bank. Police officer Eddie Thawne proposes to capture the Flash because he was at the crime scene, but is rejected by the captain. The police track Bivolo to a warehouse, where he uses his abilities on a cop to facilitate his escape. Barry Allen arrives in time to save Joe West, but is almost injured himself before Oliver Queen, as the "Arrow", arrives to stop the cop. Later, Oliver informs Barry that he and his team are in Central City tracking a killer who uses lethal boomerangs. Barry suggests that they team-up to catch each other's targets and Oliver reluctantly agrees. Oliver tries to teach Barry to be more mindful of his surroundings, but Barry decides to go after Bivolo by himself. Bivolo uses his abilities on Barry; but because of Barry's powers it makes the effects last longer.

text: Meanwhile, Eddie continues to persuade his superiors to form a task force to hunt down the Flash, expressing his zero tolerance for vigilantes. When an enraged and jealous Barry, as Flash, makes an attempt on Eddie, Oliver tries to stop Barry, and the two engage in a fight. Oliver manages to wrangle Barry long enough for Harrison Wells and Joe to use colored strobe light to reset Barry's emotional state. Afterward, Barry and Oliver capture Bivolo and place him in the prison at S.T.A.R. Labs. Due to the incident, Eddie gets the grounds to form a police task force to arrest the Flash. Barry confirms Oliver's belief that the former has a lot to learn. Oliver advises him to stay away from Iris West, with whom Barry is in love, because men with secret identities never get the girl. Oliver asks Team Flash to keep his alter ego a secret. A new metahuman able to manipulate fire appears in Central City.

text: In a flashback set in Hong Kong, Oliver learns how to torture suspects effectively to obtain information. In the present, Oliver and Roy Harper locate the home of Digger Harkness, the boomerang-wielding murderer, where they find A.R.G.U.S. operatives looking for him as well. Caitlin Snow and Cisco Ramon arrive in Starling City to help Felicity Smoak investigate Sara Lance's death. Digger attempts to kill Lyla Michaels, Roy, and Oliver, but Barry arrives and stops him. Later, Lyla reveals Digger was part of the Suicide Squad. When Oliver uses extreme interrogation methods against a Russian mob member in order to locate Digger, Barry questions how emotionally stable Oliver is. Digger locates Oliver's hideout and wounds Lyla before escaping. In order to leave town, Digger plants five bombs around the city. While Oliver captures Digger, Barry uses both of their teams to defuse the bombs simultaneously. Digger is incarcerated on the island with Slade Wilson. Before Barry and his team's departure, he and Oliver decide to have a friendly duel.

text: Cast and characters[edit]

text: Main[edit]

text:
Actor
Character
Episode

The Flash
Arrow

Grant Gustin[1]
Barry Allen / Flash
Main
Guest

Candice Patton[2]
Iris West
Main
Does not appear

Danielle Panabaker[1]
Caitlin Snow
Main
Guest

Rick Cosnett[2]
Eddie Thawne
Main
Does not appear

Carlos Valdes[1]
Cisco Ramon
Main
Guest

Tom Cavanagh[2]
Harrison Wells
Main
Does not appear

Jesse L. Martin[2]
Joe West
Main
Does not appear

Stephen Amell[1]
Oliver Queen / Arrow
Guest
Main

David Ramsey[1]
John Diggle
Guest
Main

Emily Bett Rickards[1]
Felicity Smoak
Guest
Main

Katie Cassidy[3]
Laurel Lance
Does not appear
Main

Willa Holland[3]
Thea Queen
Does not appear
Main

Colton Haynes[3]
Roy Harper / Arsenal
Does not appear
Main

John Barrowman[3]
Malcolm Merlyn
Does not appear
Main

Paul Blackthorne[3]
Quentin Lance
Does not appear
Main

text: Guest[edit]

text: The Flash[edit]

text:
Paul Anthony as Roy Bivolo / Rainbow Raider[4]
Anna Hopkins as Samantha Clayton[5]
Patrick Sabongui as David Singh[2]
Robbie Amell as Ronnie Raymond / Firestorm[6]

text: Arrow[edit]

text:
Audrey Marie Anderson as Lyla Michaels[3]
Cynthia Addai-Robinson as Amanda Waller[3]
Nick E. Tarabay as Digger Harkness / Captain Boomerang[7]

text: Production[edit]

text: Development[edit]

text: The first indication of potential crossover events in the Arrowverse occurred on The CW during the 2013–14 television season, when Barry Allen was introduced in the eighth episode of Arrow's second season ahead of the debut of The Flash.[8] In July 2014, it was announced that the eighth episodes of the third season of Arrow and the first season of The Flash would be a two-hour crossover event.[9] The crossover was originally planned as the seventh episodes of each series, but was pushed back due to the large amount of work needed to accomplish it.[10] In particular, the schedule coordination of trying to "jam another episode into the 23-episode schedule for each of [the] shows."[11] Marc Guggenheim, creator and executive producer on Arrow, explained that there was "no financially responsible" way of executing the crossover, with budgets being blown, long hours and the actors having to film scenes from both series on the same day.[11]

text: Andrew Kreisberg, creator and executive producer on both series, said, "It's really going to be an adventure with the Arrow and Flash on both episodes. Watching the two teams come together and fight alongside each other, it's one of the most fun parts, ... we just don’t believe in waiting. We really believe in accelerated storytelling."[12] Kreisberg explained that since they are all comic book fans themselves, they have all debated the age-old question of which superhero would win in a fight; "So, the idea that [the Flash and Arrow] would fight each other in one of these episodes was one of our earliest ideas, and that the cast members would have that Comic-Con argument on camera was one of our earliest ideas."[10] Greg Berlanti, creator and executive producer on both series, explained that "crossovers are part of [the characters'] DNA, ... and if we waited ..., then we would be depriving the audience of something we all wanted to see".[11]

text: In October 2014, Kreisberg described the episodes as very important to both Barry and Oliver and what they are going thorough, while also promising "one of the biggest surprises for Arrow of all time in The Flash episode".[13] Guggenheim added, "It's like the bomb underneath the table, and I think part of the fun is waiting to see when Oliver is going to learn what the audience learns on Flash."[14] It was later announced that another secret would be revealed in the final moments of The Flash episode that will help "introduce the next phase of The Flash in a big way".[15] In the episode, Oliver runs into an ex-girlfriend, last seen pregnant with his child in season two of Arrow and had been told by Oliver's mother Moira to tell him that she'd lost the baby and disappear. It is revealed to the viewers that she has a child and it's presumed to be Oliver's. After the airing of the episode, Guggenheim confirmed that indeed it was Oliver's child.[16] At the end of the episode, Robbie Amell, who played Ronnie Raymond—Caitlin's former fiancée presumed dead after the particle accelerator explosion—appears as Firestorm using his powers.[6]

text: Writing[edit]

text: The scripts for the "Flash vs. Arrow" crossover were written in mid-September 2014, with Berlanti and Kreisberg creating the story for the two episodes.[17][18] Berlanti drew inspiration from science fiction action television series The Six Million Dollar Man and The Bionic Woman for the story, while Kreisberg took his cues from the final episode of the fourth series of Doctor Who, titled "Journey's End", a crossover featuring the characters of spin-off shows Torchwood and The Sarah Jane Adventures.[15] The teleplay for The Flash was written by Ben Sokolowski and Brooke Eikmeier,[17] with Arrow's written by executive producers Guggenheim and Grainne Godfree.[18]

text: In late September 2014, Guggenheim revealed that the Arrow episode would be titled "The Brave and The Bold", a reference to a title shared by many comic book series published by DC Comics which feature super-hero team-ups, including the Flash and Green Arrow.[19] Guggenheim said:

text: I've never had so much fun writing a script before[.] ... It was such a blast to work on... I keep telling everyone that we should try for Avengers. It's these two heroes together with a big production value. ... There's the opportunity for inside jokes, and seeing all of the characters together. What happens when Cisco gets his eyes on Thea? There are moments like that, that you just can’t do in a normal episode....It's just so much fun.[20]

text: In October 2014, the title of The Flash episode was announced as "Flash vs. Arrow".[13] Kreisberg revealed that the writers' rooms for both shows were merged while working on the scripts for the episodes, similar to "throwing two casts together".[10]

text: Filming[edit]

text: Filming of the two episodes occurred from September 24, 2014, until October 8, 2014.[18][21] The Flash's episode was directed by Glen Winter,[17] and Arrow's by Jesse Warn.[18] The fight scene between the Flash and Arrow in The Flash episode was shot over three nights. Because this was the first time Stephen Amell's character fought someone with superpowers, he had to change the way he performed stunts to accommodate the special effects.[10] Comparing the filming of both series, Grant Gustin described The Flash shooting as "really tedious," working with "a lot of plate shots that are empty shots of the area we are going to be in" and later added in post-production, as opposed to Arrow where "they shoot it from the perfect angles and what you see is what you get". Gustin also recalled at times it got confusing on set because they were shooting both episodes at the same time.[22]

text: Music[edit]

text:
The Flash vs. Arrow (Music Selections from the Epic 2-Night Event)

Soundtrack album by Blake Neely

Released
December 18, 2014 (2014-12-18)

Recorded
2014

Genre
Soundtrack

Length
49:57

Label
WaterTower Music

Producer
Blake Neely

Arrowverse soundtrack chronology

Arrow:
Season 2
(2014)String Module Error: Match not found2014
The Flash vs. Arrow
(2014)
The Flash: Season 1
(2014)The Flash: Season 12014

text:
Professional ratings

Review scores

Source
Rating

Soundtrack Geek
[23]

text: On December 18, 2014, WaterTower Music released a selection of music from The Flash/Arrow crossover episodes, as well as two bonus tracks from their respective 2014 mid-season finales.[24] Discussing the challenge of merging the themes of both shows into a cohesive score, composer Blake Neely noted that "It wasn’t difficult because I originally designed the two shows to have styles and sounds that could merge and live together when necessary, but also hopefully stand alone as two distinct music worlds." [25]

text: The two bonus tracks were included on the album because "they proved very popular with the fans of the special event". Neely said, "As we were coming to completion and [the album] was about to go, I got all these tweets about these two pieces that people were loving, [and] I just had this idea, let's throw them on as bonus tracks... The fans asked for it and they got it."[26]

text: All music composed by Blake Neely.[27]

text:
Track listing

No.
Title
Length

1.
"Rainbow Raider Strikes"
2:24

2.
"Don't Get Involved"
0:41

3.
"Team Arrow in Central City"
2:30

4.
"Training Barry"
1:55

5.
"What's Up, Doc"
2:21

6.
"Barry Gets Whammied"
3:05

7.
"The Flash vs. Arrow"
5:06

8.
"S.T.A.R. Labs Thanks Oliver"
1:51

9.
"Firestorm Appears"
0:52

10.
"Looking for Boomerang"
2:36

11.
"Like a Kid in a Candy Store"
1:26

12.
"Boomerang in A.R.G.U.S."
4:00

13.
"Teaming Up"
1:50

14.
"Torture Tactics"
2:16

15.
"Hope for Saving People Like Us"
1:44

16.
"Light Inside You"
2:28

17.
"Disarming the Bombs"
3:54

18.
"Gift Exchange"
1:30

19.
"The Brave and the Bold"
1:44

20.
"The Man in the Yellow Suit" (Bonus Track)
2:15

21.
"The Climb" (Bonus Track)
3:29

Total length:
49:57

text: Release[edit]

text: Broadcast[edit]

text: The "Flash vs. Arrow" crossover episodes were shown at an exclusive fan screening at the Crest Theatre in Westwood, Los Angeles on November 22, 2014.[28] Afterwards, Amell, Gustin, David Ramsey, Emily Bett Rickards, Danielle Panabaker and Carlos Valdes were joined by executive producers Berlanti, Kreisberg and Guggenheim for a Q&A panel.[29]

text: The first part of the crossover, The Flash, was broadcast on December 2, 2014, followed by part two on Arrow on December 3, both on The CW.[30] The crossover was simulcast with the US broadcast in Canada on CTV.[31] It first aired in the United Kingdom on Channel 5 on December 16 and December 18, 2014.[32] In Australia, the episodes aired back-to-back on January 28, 2015, on Fox8, after Nine Network, which broadcasts Arrow, allowed Fox8 to air the Arrow episode of the crossover.[33]

text: Home media[edit]

text: The episodes, along with the rest of The Flash's first season and Arrow's third season, were released separately on Blu-ray and DVD on September 22, 2015. Bonus features include behind-the-scenes featurettes, audio commentary, deleted scenes, and a blooper reel.[34][35] The episodes became available for streaming on Netflix on October 6 and October 7, 2015, respectively.[36][37]

text: Reception[edit]

text: Ratings[edit]

text:
Series
Episode
Air date
Rating/share
(18–49)
Viewers
(millions)
DVR
(18–49)
DVR viewers
(millions)
Total
(18–49)
Total viewers
(millions)

The Flash
"Flash vs. Arrow"
000000002014-12-02-0000December 2, 2014
1.6/5
4.34[38]
1.0
2.31
2.6
6.65[39]

Arrow
"The Brave and the Bold"
000000002014-12-03-0000December 3, 2014
1.4/4
3.92[40]
N/A
N/A
N/A
N/A

text: The Flash episode had the second-highest number of viewers following the series premiere on October 7, 2014,[41] and the highest 18-49 rating since the second episode. Viewership rose 22% and the 18-49 rating by 14%, over the previous episode, "Power Outage".[42] The Arrow episode was the most viewed of season three, and had the show's largest audience since the series' premiere on October 10, 2012, and a series high 18–49 rating. Its viewership grew by 46% and its 18-49 rating by 56% over the previous episode, "Draw Back Your Bow",[43] and helped contribute to the most watched Wednesday on The CW in more than two years.[44]

text: The Canadian broadcast of The Flash was watched by 2.45 million viewers, earning the highest viewership for the week. The Arrow broadcast had 2.22 million viewers, the second highest for that day, and the fourth highest for the week.[45] In the United Kingdom, the episodes had 1.5 million viewers and 980,000 viewers, respectively. The time shifted versions attracted a total of 1.63 million and 1.26 million viewers, respectively.[32]

text: After the crossover aired, both shows saw increases to their ratings compared to their respective episodes before the crossover. The Flash "surprising[ly]" dipped a mere 6% in the 18–49 rating and rose 4% in total viewers, from the crossover episode, on "a heavily competitive night" for its most watched episode since its series premiere.[46][47] The following Arrow episode dropped by 29% in the 18–49 rating, from the crossover episode.[48] However, compared to its episode before the crossover, Arrow rose in the 18–49 rating, tying its second best rating of the season, behind only the crossover episode with The Flash.[49]

text: Critical response[edit]

text: After the first Arrow/Flash crossover, Brian Lowry of Variety applauded the producers for replicating the success of Arrow, but with "a lighter tone," and "a hero with genuine super powers" in The Flash. He noted while the crossover "does a nifty job of bringing the two series together" it was unlikely "to boost the shared audience between them much more than already exists".[50] Meredith Borders of Birth.Movies.Death called the crossover episodes "fun," noting that..."plenty of show-specific plot stuff was advanced without spelling it out for newbies. New viewers to either show could follow along and have a good time, but veteran viewers were rewarded with major storyline motion."[51]

text: Chancellor Agard, of Entertainment Weekly felt "the 'Flarrow'" crossover event was an overall success. Both episodes "put Team Flash in new situations and it was thrilling to watch how they reacted". Agard felt that while Arrow had "some great and comedic character moments for Team Arrow" none of its stories were advanced so that the episodes "felt like pause buttons" in its action.[52]

text: The Flash[edit]

text: Jesse Schedeen of IGN gave The Flash episode a 7.8 out of 10. He said the "Flash vs. Arrow" episode was "fun" with its focus "on the sheer entertainment value in seeing these two heroes and their allies cross paths"... and "to see the relationship between Barry and Ollie continue to evolve". As "a largely standalone episode" its scope was limited resulting "in yet another underdeveloped villain."[53] Scott Von Doviak writing for The A.V. Club awarded the episode an "A-", calling it "a satisfying showdown" that "actually stands on its own as a mostly self-contained hour of The Flash". Von Doviak complimented writers Greg Berlanti and Andrew Kreisberg, and director Glen Winter, for tackling the "clashing tones of the two shows" and the different personalities of their main characters, and "weaving...[them]... into the fabric of the episode". He also highlighted the fight scene between the Flash and Arrow, saying "It's a well-choreographed battle, with each hero appearing to have the upper hand at various points and clever bits of one-upmanship."[54]

text: Collider.com's Dave Trumbore gave The Flash episode an "A-", saying, it was "fun" seeing the characters together. He noted that the episode pointed out the many challenges Barry Allen "faces as a young up-and-coming crimefighter". He felt that Arrow's "knocks" made the point that "Barry's superpowers are an amazing gift ... he must hone and perfect to become a truly heroic character." Trumbore also "loved how Arrow's attention to detail and commitment to bettering himself through training clashed with Flash's carefree style and almost lazy attitude when it came to beating up baddies".[55] Agard's expectations for the episode were "not disappointed". He felt it delivered "on both the action front" with its impeccable, "epic" fight scene, and "on the character front". While the viewer can enjoy the interaction between the teams everything that happens in the episode pushes "this The Flash's stories forward".[56]

text: Eric Walters of Paste awarded The Flash episode a 9.0 out of 10, stating, ""Flash vs. Arrow" was everything a fan could have wanted from a crossover event," noting it was "tight, well-paced, superbly written and, most importantly, fun...".[57] Caroline Preece of Den of Geek also praised the episode, saying that it "was pretty much everything fans wanted and more". She noted this episode demonstrated how comic book ideas "can translate to the small screen if done with this much care, joy and enthusiasm". Given the "hype" she admired, and was "surprised" by the fact that even "with a little added Oliver, Felicity and Diggle thrown in," the crossover was not the focus of the whole episode.[58]

text: Arrow[edit]

text: Giving the episode a 9.2 out of 10, Schedeen stated it was a "blast to watch" and was "a more cohesive and satisfying episode than the first". Noting that the crossover "wasted some of its potential by delivering two mostly standalone episodes," the Arrow episode was "more consistently entertaining and satisfying than the first". He enjoyed Captain Boomerang suggesting he could be the "most memorable villain to debut this season". Schedeen enjoyed the teams continuing to cross paths, the drama between Barry and Ollie, and "the balance between light and dark [the crossover] needed".[59] Alasdair Wilkins of The A.V. Club gave the episode an "A-", saying it "..can just cut loose and have some ['effortless'] fun for an hour," noting that Barry "is one of the only characters able to call Oliver out on his more mopey strains of bullshit". He felt it was "fitting" the episode "shared the name—"The Brave And The Bold"—with DC Comics' long-running team-up comic". The Flash is "the brave one", who "inspires with his courage" though his "simplistic sense of right and wrong" can lead him to overlook "the darker side of what they do". Oliver is "the bold one", "willing to do whatever it takes to see justice served".[60]

text: Trumbore felt the episode of Arrow closed out the crossover "in spectacular fashion" and gave it an "A". He noted that "both heroes channel their respective cities into their character". Barry Allen's approach to crimefighting is effervescent and "carefree" reflecting "Central City's cutting-edge technology" and "squeaky-clean streets". "Queen's Starling City" with its "ruthless underworld" is "much like the personality of the masked crimefighter himself". He felt the writing was clever in that it allowed the characters to "clash at times, but also ... allow[ed] them to come together in pursuit of a common goal".[61] However, Agard felt Arrow "was a decent enough episode", but not "as good as the first". "'The Brave and the Bold'... felt... like a crossover episode ... servic[ing] Oliver's identity issues and character development." Agrad felt that "Cisco fanboying all over the place" is "fun" and Captain Boomerang is a "most formidable and compelling opponent" because he uses strategy and plans multiple steps ahead".[52]

text: Mark Rozeman at Paste, gave the Arrow episode a 9.3 out of 10, saying, the episode "not only equals its brother episode but, in some ways, manages to surpass it". He saw it as season's "strongest" Arrow episode, and "a great conclusion to the very successful Arrow/The Flash crossover" where in an "emotionally charged hour...all the elements come together with remarkable dexterity". He felt the shows' creative teams should be "applauded" for avoiding a "half-assed bid for ratings" instead turning the crossover "into something that brought out the best of each show". Rozeman argued that if "Flash vs. Arrow" proves that The Flash can stand on its own, then "The Brave and the Bold" is "a great demonstration that Arrow has some fire in it yet."[62] Den of Geek's Mike Cecchini said the episode is "a remarkably self-contained adventure". Noting that both episodes worked well as standalones, "Flash vs. Arrow" was "very clearly an episode" of The Flash and "The Brave and The Bold" is "absolutely an Arrow episode ... handily the best installment of Arrow season three so far". He felt the cinematic scoring was "great" giving the episode 4.5 stars out of 5.[63]

text: Accolades[edit]

text: TVLine named the "Flash vs. Arrow" crossover the 9th biggest television moment of 2014 saying, "There are crossovers. And there are superhero shows. But never in recent TV memory have two live-action costumed crimefighters clashed in super fashion (albeit under extenuating circumstances). The Flash's smooth moves versus Arrow's strength and stratagem made for a thrilling tango that lived up to the hype."[64] IGN ranked the showdown between the Flash and Arrow in The Flash episode as one of the best television fight scenes of 2014.[65] ScreenRant named both "Flash vs. Arrow" and "The Brave and the Bold" as one of the best television episodes of 2014.[66] Blastr and Zap2it also named The Flash episode "Flash vs. Arrow" one of the best television episodes of 2014.[67][68]

text: Additional crossovers[edit]

text: In January 2015, The CW President Mark Pedowitz stated their intention to have an Arrowverse crossover every season.[69] In the 2015–16 television season, a two-part event titled "Heroes Join Forces" between the eighth episodes of the fourth season of Arrow, and the second season of The Flash, was used to set up the new team-up series Legends of Tomorrow.[8] For the 2016–17 television season, The Flash, Arrow and Legends of Tomorrow crossed over in an event titled "Invasion!" that saw the inclusion of the title character of CBS' Supergirl, after that series moved to The CW for its second season.[8][70][71]


document_title: Gene

question_text: the complete collection of dna and genes is called

root

text: Gene

text: History[edit]

text: Discovery of discrete inherited units[edit]

text: The existence of discrete inheritable units was first suggested by Gregor Mendel (1822–1884).[7] From 1857 to 1864, in Brno (Czech Republic), he studied inheritance patterns in 8000 common edible pea plants, tracking distinct traits from parent to offspring. He described these mathematically as 2n combinations where n is the number of differing characteristics in the original peas. Although he did not use the term gene, he explained his results in terms of discrete inherited units that give rise to observable physical characteristics. This description prefigured Wilhelm Johannsen's distinction between genotype (the genetic material of an organism) and phenotype (the visible traits of that organism). Mendel was also the first to demonstrate independent assortment, the distinction between dominant and recessive traits, the distinction between a heterozygote and homozygote, and the phenomenon of discontinuous inheritance.

tag: p

text: Prior to Mendel's work, the dominant theory of heredity was one of blending inheritance, which suggested that each parent contributed fluids to the fertilisation process and that the traits of the parents blended and mixed to produce the offspring. Charles Darwin developed a theory of inheritance he termed pangenesis, from Greek pan ("all, whole") and genesis ("birth") / genos ("origin").[8][9] Darwin used the term gemmule to describe hypothetical particles that would mix during reproduction.

text: Mendel's work went largely unnoticed after its first publication in 1866, but was rediscovered in the late 19th century by Hugo de Vries, Carl Correns, and Erich von Tschermak, who (claimed to have) reached similar conclusions in their own research.[10] Specifically, in 1889, Hugo de Vries published his book Intracellular Pangenesis,[11] in which he postulated that different characters have individual hereditary carriers and that inheritance of specific traits in organisms comes in particles. De Vries called these units "pangenes" (Pangens in German), after Darwin's 1868 pangenesis theory.

text: Sixteen years later, in 1905, Wilhelm Johannsen introduced the term 'gene'[3] and William Bateson that of 'genetics'[12] while Eduard Strasburger, amongst others, still used the term 'pangene' for the fundamental physical and functional unit of heredity.[13]

text: Discovery of DNA[edit]

text: Advances in understanding genes and inheritance continued throughout the 20th century. Deoxyribonucleic acid (DNA) was shown to be the molecular repository of genetic information by experiments in the 1940s to 1950s.[14][15] The structure of DNA was studied by Rosalind Franklin and Maurice Wilkins using X-ray crystallography, which led James D. Watson and Francis Crick to publish a model of the double-stranded DNA molecule whose paired nucleotide bases indicated a compelling hypothesis for the mechanism of genetic replication.[16][17]

text: In the early 1950s the prevailing view was that the genes in a chromosome acted like discrete entities, indivisible by recombination and arranged like beads on a string. The experiments of Benzer using mutants defective in the rII region of bacteriophage T4 (1955-1959) showed that individual genes have a simple linear structure and are likely to be equivalent to a linear section of DNA.[18][19]

text: Collectively, this body of research established the central dogma of molecular biology, which states that proteins are translated from RNA, which is transcribed from DNA. This dogma has since been shown to have exceptions, such as reverse transcription in retroviruses. The modern study of genetics at the level of DNA is known as molecular genetics.

text: In 1972, Walter Fiers and his team at the University of Ghent were the first to determine the sequence of a gene: the gene for Bacteriophage MS2 coat protein.[20] The subsequent development of chain-termination DNA sequencing in 1977 by Frederick Sanger improved the efficiency of sequencing and turned it into a routine laboratory tool.[21] An automated version of the Sanger method was used in early phases of the Human Genome Project.[22]

text: Modern synthesis and its successors[edit]

text: The theories developed in the 1930s and 1940s to integrate Mendelian genetics with Darwinian evolution are called the modern synthesis, a term introduced by Julian Huxley.[23]

text: Evolutionary biologists subsequently refined this concept, such as George C. Williams' gene-centric view of evolution. He proposed an evolutionary concept of the gene as a unit of natural selection with the definition: "that which segregates and recombines with appreciable frequency."[24]:24 In this view, the molecular gene transcribes as a unit, and the evolutionary gene inherits as a unit. Related ideas emphasizing the centrality of genes in evolution were popularized by Richard Dawkins.[25][26]

text: Molecular basis[edit]

text: DNA[edit]

text: The vast majority of living organisms encode their genes in long strands of DNA (deoxyribonucleic acid). DNA consists of a chain made from four types of nucleotide subunits, each composed of: a five-carbon sugar (2'-deoxyribose), a phosphate group, and one of the four bases adenine, cytosine, guanine, and thymine.[2]:2.1

text: Two chains of DNA twist around each other to form a DNA double helix with the phosphate-sugar backbone spiralling around the outside, and the bases pointing inwards with adenine base pairing to thymine and guanine to cytosine. The specificity of base pairing occurs because adenine and thymine align to form two hydrogen bonds, whereas cytosine and guanine form three hydrogen bonds. The two strands in a double helix must therefore be complementary, with their sequence of bases matching such that the adenines of one strand are paired with the thymines of the other strand, and so on.[2]:4.1

text: Due to the chemical composition of the pentose residues of the bases, DNA strands have directionality. One end of a DNA polymer contains an exposed hydroxyl group on the deoxyribose; this is known as the 3' end of the molecule. The other end contains an exposed phosphate group; this is the 5' end. The two strands of a double-helix run in opposite directions. Nucleic acid synthesis, including DNA replication and transcription occurs in the 5'→3' direction, because new nucleotides are added via a dehydration reaction that uses the exposed 3' hydroxyl as a nucleophile.[27]:27.2

text: The expression of genes encoded in DNA begins by transcribing the gene into RNA, a second type of nucleic acid that is very similar to DNA, but whose monomers contain the sugar ribose rather than deoxyribose. RNA also contains the base uracil in place of thymine. RNA molecules are less stable than DNA and are typically single-stranded. Genes that encode proteins are composed of a series of three-nucleotide sequences called codons, which serve as the "words" in the genetic "language". The genetic code specifies the correspondence during protein translation between codons and amino acids. The genetic code is nearly the same for all known organisms.[2]:4.1

text: Chromosomes[edit]

text: The total complement of genes in an organism or cell is known as its genome, which may be stored on one or more chromosomes. A chromosome consists of a single, very long DNA helix on which thousands of genes are encoded.[2]:4.2 The region of the chromosome at which a particular gene is located is called its locus. Each locus contains one allele of a gene; however, members of a population may have different alleles at the locus, each with a slightly different gene sequence.

text: The majority of eukaryotic genes are stored on a set of large, linear chromosomes. The chromosomes are packed within the nucleus in complex with storage proteins called histones to form a unit called a nucleosome. DNA packaged and condensed in this way is called chromatin.[2]:4.2 The manner in which DNA is stored on the histones, as well as chemical modifications of the histone itself, regulate whether a particular region of DNA is accessible for gene expression. In addition to genes, eukaryotic chromosomes contain sequences involved in ensuring that the DNA is copied without degradation of end regions and sorted into daughter cells during cell division: replication origins, telomeres and the centromere.[2]:4.2 Replication origins are the sequence regions where DNA replication is initiated to make two copies of the chromosome. Telomeres are long stretches of repetitive sequence that cap the ends of the linear chromosomes and prevent degradation of coding and regulatory regions during DNA replication. The length of the telomeres decreases each time the genome is replicated and has been implicated in the aging process.[29] The centromere is required for binding spindle fibres to separate sister chromatids into daughter cells during cell division.[2]:18.2

text: Prokaryotes (bacteria and archaea) typically store their genomes on a single large, circular chromosome. Similarly, some eukaryotic organelles contain a remnant circular chromosome with a small number of genes.[2]:14.4 Prokaryotes sometimes supplement their chromosome with additional small circles of DNA called plasmids, which usually encode only a few genes and are transferable between individuals. For example, the genes for antibiotic resistance are usually encoded on bacterial plasmids and can be passed between individual cells, even those of different species, via horizontal gene transfer.[30]

text: Whereas the chromosomes of prokaryotes are relatively gene-dense, those of eukaryotes often contain regions of DNA that serve no obvious function. Simple single-celled eukaryotes have relatively small amounts of such DNA, whereas the genomes of complex multicellular organisms, including humans, contain an absolute majority of DNA without an identified function.[31] This DNA has often been referred to as "junk DNA". However, more recent analyses suggest that, although protein-coding DNA makes up barely 2% of the human genome, about 80% of the bases in the genome may be expressed, so the term "junk DNA" may be a misnomer.[6]

text: Structure and function[edit]

text:
Regulatory sequence
Regulatory sequence
Enhancer
/silencer
Promoter
5'UTR
Open reading frame
3'UTR
Enhancer
/silencer
Proximal
Core
Start
Stop
Terminator
Transcription
DNA
Exon
Exon
Exon
Intron
Intron
Post-transcriptional
modification
Pre-
mRNA
Protein coding region
5'cap
Poly-A tail
Translation
Mature
mRNA
Protein

The structure of a eukaryotic protein-coding gene. Regulatory sequence controls when and where expression occurs for the protein coding region (red). Promoter and enhancer regions (yellow) regulate the transcription of the gene into a pre-mRNA which is modified to remove introns (light grey) and add a 5' cap and poly-A tail (dark grey). The mRNA 5' and 3' untranslated regions (blue) regulate translation into the final protein product.[32]

Polycistronic operon
Regulatory sequence
Regulatory sequence
Enhancer
Enhancer
/silencer
/silencer
Operator
Promoter
5'UTR
ORF
ORF
UTR
3'UTR
Start
Start
Stop
Stop
Terminator
Transcription
DNA
RBS
RBS
Protein coding region
Protein coding region
mRNA
Translation
Protein

The structure of a prokaryotic operon of protein-coding genes. Regulatory sequence controls when expression occurs for the multiple protein coding regions (red). Promoter, operator and enhancer regions (yellow) regulate the transcription of the gene into an mRNA. The mRNA untranslated regions (blue) regulate translation into the final protein products.[32]

tag: table

text: The structure of a gene consists of many elements of which the actual protein coding sequence is often only a small part. These include DNA regions that are not transcribed as well as untranslated regions of the RNA.

text: Flanking the open reading frame, genes contain a regulatory sequence that is required for their expression. First, genes require a promoter sequence. The promoter is recognized and bound by transcription factors and RNA polymerase to initiate transcription.[2]:7.1 The recognition typically occurs as a consensus sequence like the TATA box. A gene can have more than one promoter, resulting in messenger RNAs (mRNA) that differ in how far they extend in the 5' end.[33] Highly transcribed genes have "strong" promoter sequences that form strong associations with transcription factors, thereby initiating transcription at a high rate. Others genes have "weak" promoters that form weak associations with transcription factors and initiate transcription less frequently.[2]:7.2 Eukaryotic promoter regions are much more complex and difficult to identify than prokaryotic promoters.[2]:7.3

text: Additionally, genes can have regulatory regions many kilobases upstream or downstream of the open reading frame that alter expression. These act by binding to transcription factors which then cause the DNA to loop so that the regulatory sequence (and bound transcription factor) become close to the RNA polymerase binding site.[34] For example, enhancers increase transcription by binding an activator protein which then helps to recruit the RNA polymerase to the promoter; conversely silencers bind repressor proteins and make the DNA less available for RNA polymerase.[35]

text: The transcribed pre-mRNA contains untranslated regions at both ends which contain a ribosome binding site, terminator and start and stop codons.[36] In addition, most eukaryotic open reading frames contain untranslated introns which are removed before the exons are translated. The sequences at the ends of the introns, dictate the splice sites to generate the final mature mRNA which encodes the protein or RNA product.[37]

text: Many prokaryotic genes are organized into operons, with multiple protein-coding sequences that are transcribed as a unit.[38][39] The genes in an operon are transcribed as a continuous messenger RNA, referred to as a polycistronic mRNA. The term cistron in this context is equivalent to gene. The transcription of an operon’s mRNA is often controlled by a repressor that can occur in an active or inactive state depending on the presence of certain specific metabolites.[40] When active, the repressor binds to a DNA sequence at the beginning of the operon, called the operator region, and represses transcription of the operon; when the repressor is inactive transcription of the operon can occur (see e.g. Lac operon). The products of operon genes typically have related functions and are involved in the same regulatory network.[2]:7.3

text: Functional definitions[edit]

text: Defining exactly what section of a DNA sequence comprises a gene is difficult.[4] Regulatory regions of a gene such as enhancers do not necessarily have to be close to the coding sequence on the linear molecule because the intervening DNA can be looped out to bring the gene and its regulatory region into proximity. Similarly, a gene's introns can be much larger than its exons. Regulatory regions can even be on entirely different chromosomes and operate in trans to allow regulatory regions on one chromosome to come in contact with target genes on another chromosome.[41][42]

text: Early work in molecular genetics suggested the concept that one gene makes one protein. This concept (originally called the one gene-one enzyme hypothesis) emerged from an influential 1941 paper by George Beadle and Edward Tatum on experiments with mutants of the fungus Neurospora crassa.[43] Norman Horowitz, an early colleague on the Neurospora research, reminisced in 2004 that “these experiments founded the science of what Beadle and Tatum called biochemical genetics. In actuality they proved to be the opening gun in what became molecular genetics and all the developments that have followed from that.”[44] The one gene-one protein concept has been refined since the discovery of genes that can encode multiple proteins by alternative splicing and coding sequences split in short section across the genome whose mRNAs are concatenated by trans-splicing.[6][45][46]

text: A broad operational definition is sometimes used to encompass the complexity of these diverse phenomena, where a gene is defined as a union of genomic sequences encoding a coherent set of potentially overlapping functional products.[12] This definition categorizes genes by their functional products (proteins or RNA) rather than their specific DNA loci, with regulatory elements classified as gene-associated regions.[12]

text: Gene expression[edit]

text: In all organisms, two steps are required to read the information encoded in a gene's DNA and produce the protein it specifies. First, the gene's DNA is transcribed to messenger RNA (mRNA).[2]:6.1 Second, that mRNA is translated to protein.[2]:6.2 RNA-coding genes must still go through the first step, but are not translated into protein.[47] The process of producing a biologically functional molecule of either RNA or protein is called gene expression, and the resulting molecule is called a gene product.

text: Genetic code[edit]

text: The nucleotide sequence of a gene's DNA specifies the amino acid sequence of a protein through the genetic code. Sets of three nucleotides, known as codons, each correspond to a specific amino acid.[2]:6 The principle that three sequential bases of DNA code for each amino acid was demonstrated in 1961 using frameshift mutations in the rIIB gene of bacteriophage T4[48] (see Crick, Brenner et al. experiment).

text: Additionally, a "start codon", and three "stop codons" indicate the beginning and end of the protein coding region. There are 64 possible codons (four possible nucleotides at each of three positions, hence 43 possible codons) and only 20 standard amino acids; hence the code is redundant and multiple codons can specify the same amino acid. The correspondence between codons and amino acids is nearly universal among all known living organisms.[49]

text: Transcription[edit]

text: Transcription produces a single-stranded RNA molecule known as messenger RNA, whose nucleotide sequence is complementary to the DNA from which it was transcribed.[2]:6.1 The mRNA acts as an intermediate between the DNA gene and its final protein product. The gene's DNA is used as a template to generate a complementary mRNA. The mRNA matches the sequence of the gene's DNA coding strand because it is synthesised as the complement of the template strand. Transcription is performed by an enzyme called an RNA polymerase, which reads the template strand in the 3' to 5' direction and synthesizes the RNA from 5' to 3'. To initiate transcription, the polymerase first recognizes and binds a promoter region of the gene. Thus, a major mechanism of gene regulation is the blocking or sequestering the promoter region, either by tight binding by repressor molecules that physically block the polymerase, or by organizing the DNA so that the promoter region is not accessible.[2]:7

text: In prokaryotes, transcription occurs in the cytoplasm; for very long transcripts, translation may begin at the 5' end of the RNA while the 3' end is still being transcribed. In eukaryotes, transcription occurs in the nucleus, where the cell's DNA is stored. The RNA molecule produced by the polymerase is known as the primary transcript and undergoes post-transcriptional modifications before being exported to the cytoplasm for translation. One of the modifications performed is the splicing of introns which are sequences in the transcribed region that do not encode protein. Alternative splicing mechanisms can result in mature transcripts from the same gene having different sequences and thus coding for different proteins. This is a major form of regulation in eukaryotic cells and also occurs in some prokaryotes.[2]:7.5[50]

text: Translation[edit]

text: Translation is the process by which a mature mRNA molecule is used as a template for synthesizing a new protein.[2]:6.2 Translation is carried out by ribosomes, large complexes of RNA and protein responsible for carrying out the chemical reactions to add new amino acids to a growing polypeptide chain by the formation of peptide bonds. The genetic code is read three nucleotides at a time, in units called codons, via interactions with specialized RNA molecules called transfer RNA (tRNA). Each tRNA has three unpaired bases known as the anticodon that are complementary to the codon it reads on the mRNA. The tRNA is also covalently attached to the amino acid specified by the complementary codon. When the tRNA binds to its complementary codon in an mRNA strand, the ribosome attaches its amino acid cargo to the new polypeptide chain, which is synthesized from amino terminus to carboxyl terminus. During and after synthesis, most new proteins must fold to their active three-dimensional structure before they can carry out their cellular functions.[2]:3

text: Regulation[edit]

text: Genes are regulated so that they are expressed only when the product is needed, since expression draws on limited resources.[2]:7 A cell regulates its gene expression depending on its external environment (e.g. available nutrients, temperature and other stresses), its internal environment (e.g. cell division cycle, metabolism, infection status), and its specific role if in a multicellular organism. Gene expression can be regulated at any step: from transcriptional initiation, to RNA processing, to post-translational modification of the protein. The regulation of lactose metabolism genes in E. coli (lac operon) was the first such mechanism to be described in 1961.[51]

text: RNA genes[edit]

text: A typical protein-coding gene is first copied into RNA as an intermediate in the manufacture of the final protein product.[2]:6.1 In other cases, the RNA molecules are the actual functional products, as in the synthesis of ribosomal RNA and transfer RNA. Some RNAs known as ribozymes are capable of enzymatic function, and microRNA has a regulatory role. The DNA sequences from which such RNAs are transcribed are known as non-coding RNA genes.[47]

text: Some viruses store their entire genomes in the form of RNA, and contain no DNA at all.[52][53] Because they use RNA to store genes, their cellular hosts may synthesize their proteins as soon as they are infected and without the delay in waiting for transcription.[54] On the other hand, RNA retroviruses, such as HIV, require the reverse transcription of their genome from RNA into DNA before their proteins can be synthesized. RNA-mediated epigenetic inheritance has also been observed in plants and very rarely in animals.[55]

text: Inheritance[edit]

text: Organisms inherit their genes from their parents. Asexual organisms simply inherit a complete copy of their parent's genome. Sexual organisms have two copies of each chromosome because they inherit one complete set from each parent.[2]:1

text: Mendelian inheritance[edit]

text: According to Mendelian inheritance, variations in an organism's phenotype (observable physical and behavioral characteristics) are due in part to variations in its genotype (particular set of genes). Each gene specifies a particular trait with different sequence of a gene (alleles) giving rise to different phenotypes. Most eukaryotic organisms (such as the pea plants Mendel worked on) have two alleles for each trait, one inherited from each parent.[2]:20

text: Alleles at a locus may be dominant or recessive; dominant alleles give rise to their corresponding phenotypes when paired with any other allele for the same trait, whereas recessive alleles give rise to their corresponding phenotype only when paired with another copy of the same allele. If you know the genotypes of the organisms, you can determine which alleles are dominant and which are recessive. For example, if the allele specifying tall stems in pea plants is dominant over the allele specifying short stems, then pea plants that inherit one tall allele from one parent and one short allele from the other parent will also have tall stems. Mendel's work demonstrated that alleles assort independently in the production of gametes, or germ cells, ensuring variation in the next generation. Although Mendelian inheritance remains a good model for many traits determined by single genes (including a number of well-known genetic disorders) it does not include the physical processes of DNA replication and cell division.[56][57]

text: DNA replication and cell division[edit]

text: The growth, development, and reproduction of organisms relies on cell division; the process by which a single cell divides into two usually identical daughter cells. This requires first making a duplicate copy of every gene in the genome in a process called DNA replication.[2]:5.2 The copies are made by specialized enzymes known as DNA polymerases, which "read" one strand of the double-helical DNA, known as the template strand, and synthesize a new complementary strand. Because the DNA double helix is held together by base pairing, the sequence of one strand completely specifies the sequence of its complement; hence only one strand needs to be read by the enzyme to produce a faithful copy. The process of DNA replication is semiconservative; that is, the copy of the genome inherited by each daughter cell contains one original and one newly synthesized strand of DNA.[2]:5.2

text: The rate of DNA replication in living cells was first measured as the rate of phage T4 DNA elongation in phage-infected E. coli and found to be impressively rapid.[58] During the period of exponential DNA increase at 37 °C, the rate of elongation was 749 nucleotides per second.

text: After DNA replication is complete, the cell must physically separate the two copies of the genome and divide into two distinct membrane-bound cells.[2]:18.2 In prokaryotes (bacteria and archaea) this usually occurs via a relatively simple process called binary fission, in which each circular genome attaches to the cell membrane and is separated into the daughter cells as the membrane invaginates to split the cytoplasm into two membrane-bound portions. Binary fission is extremely fast compared to the rates of cell division in eukaryotes. Eukaryotic cell division is a more complex process known as the cell cycle; DNA replication occurs during a phase of this cycle known as S phase, whereas the process of segregating chromosomes and splitting the cytoplasm occurs during M phase.[2]:18.1

text: Molecular inheritance[edit]

text: The duplication and transmission of genetic material from one generation of cells to the next is the basis for molecular inheritance, and the link between the classical and molecular pictures of genes. Organisms inherit the characteristics of their parents because the cells of the offspring contain copies of the genes in their parents' cells. In asexually reproducing organisms, the offspring will be a genetic copy or clone of the parent organism. In sexually reproducing organisms, a specialized form of cell division called meiosis produces cells called gametes or germ cells that are haploid, or contain only one copy of each gene.[2]:20.2 The gametes produced by females are called eggs or ova, and those produced by males are called sperm. Two gametes fuse to form a diploid fertilized egg, a single cell that has two sets of genes, with one copy of each gene from the mother and one from the father.[2]:20

text: During the process of meiotic cell division, an event called genetic recombination or crossing-over can sometimes occur, in which a length of DNA on one chromatid is swapped with a length of DNA on the corresponding homologous non-sister chromatid. This can result in reassortment of otherwise linked alleles.[2]:5.5 The Mendelian principle of independent assortment asserts that each of a parent's two genes for each trait will sort independently into gametes; which allele an organism inherits for one trait is unrelated to which allele it inherits for another trait. This is in fact only true for genes that do not reside on the same chromosome, or are located very far from one another on the same chromosome. The closer two genes lie on the same chromosome, the more closely they will be associated in gametes and the more often they will appear together; genes that are very close are essentially never separated because it is extremely unlikely that a crossover point will occur between them. This is known as genetic linkage.[59]

text: Molecular evolution[edit]

text: Mutation[edit]

text: DNA replication is for the most part extremely accurate, however errors (mutations) do occur.[2]:7.6 The error rate in eukaryotic cells can be as low as 10−8 per nucleotide per replication,[60][61] whereas for some RNA viruses it can be as high as 10−3.[62] This means that each generation, each human genome accumulates 1–2 new mutations.[62] Small mutations can be caused by DNA replication and the aftermath of DNA damage and include point mutations in which a single base is altered and frameshift mutations in which a single base is inserted or deleted. Either of these mutations can change the gene by missense (change a codon to encode a different amino acid) or nonsense (a premature stop codon).[63] Larger mutations can be caused by errors in recombination to cause chromosomal abnormalities including the duplication, deletion, rearrangement or inversion of large sections of a chromosome. Additionally, DNA repair mechanisms can introduce mutational errors when repairing physical damage to the molecule. The repair, even with mutation, is more important to survival than restoring an exact copy, for example when repairing double-strand breaks.[2]:5.4

text: When multiple different alleles for a gene are present in a species's population it is called polymorphic. Most different alleles are functionally equivalent, however some alleles can give rise to different phenotypic traits. A gene's most common allele is called the wild type, and rare alleles are called mutants. The genetic variation in relative frequencies of different alleles in a population is due to both natural selection and genetic drift.[64] The wild-type allele is not necessarily the ancestor of less common alleles, nor is it necessarily fitter.

text: Most mutations within genes are neutral, having no effect on the organism's phenotype (silent mutations). Some mutations do not change the amino acid sequence because multiple codons encode the same amino acid (synonymous mutations). Other mutations can be neutral if they lead to amino acid sequence changes, but the protein still functions similarly with the new amino acid (e.g. conservative mutations). Many mutations, however, are deleterious or even lethal, and are removed from populations by natural selection. Genetic disorders are the result of deleterious mutations and can be due to spontaneous mutation in the affected individual, or can be inherited. Finally, a small fraction of mutations are beneficial, improving the organism's fitness and are extremely important for evolution, since their directional selection leads to adaptive evolution.[2]:7.6

text: Sequence homology[edit]

text: Genes with a most recent common ancestor, and thus a shared evolutionary ancestry, are known as homologs.[65] These genes appear either from gene duplication within an organism's genome, where they are known as paralogous genes, or are the result of divergence of the genes after a speciation event, where they are known as orthologous genes,[2]:7.6 and often perform the same or similar functions in related organisms. It is often assumed that the functions of orthologous genes are more similar than those of paralogous genes, although the difference is minimal.[66][67]

text: The relationship between genes can be measured by comparing the sequence alignment of their DNA.[2]:7.6 The degree of sequence similarity between homologous genes is called conserved sequence. Most changes to a gene's sequence do not affect its function and so genes accumulate mutations over time by neutral molecular evolution. Additionally, any selection on a gene will cause its sequence to diverge at a different rate. Genes under stabilizing selection are constrained and so change more slowly whereas genes under directional selection change sequence more rapidly.[68] The sequence differences between genes can be used for phylogenetic analyses to study how those genes have evolved and how the organisms they come from are related.[69][70]

text: Origins of new genes[edit]

text: The most common source of new genes in eukaryotic lineages is gene duplication, which creates copy number variation of an existing gene in the genome.[71][72] The resulting genes (paralogs) may then diverge in sequence and in function. Sets of genes formed in this way comprise a gene family. Gene duplications and losses within a family are common and represent a major source of evolutionary biodiversity.[73] Sometimes, gene duplication may result in a nonfunctional copy of a gene, or a functional copy may be subject to mutations that result in loss of function; such nonfunctional genes are called pseudogenes.[2]:7.6

text: "Orphan" genes, whose sequence shows no similarity to existing genes, are less common than gene duplicates. Estimates of the number of genes with no homologs outside humans range from 18[74] to 60.[75] Two primary sources of orphan protein-coding genes are gene duplication followed by extremely rapid sequence change, such that the original relationship is undetectable by sequence comparisons, and de novo conversion of a previously non-coding sequence into a protein-coding gene.[76] De novo genes are typically shorter and simpler in structure than most eukaryotic genes, with few if any introns.[71] Over long evolutionary time periods, de novo gene birth may be responsible for a significant fraction of taxonomically-restricted gene families.[77]

text: Horizontal gene transfer refers to the transfer of genetic material through a mechanism other than reproduction. This mechanism is a common source of new genes in prokaryotes, sometimes thought to contribute more to genetic variation than gene duplication.[78] It is a common means of spreading antibiotic resistance, virulence, and adaptive metabolic functions.[30][79] Although horizontal gene transfer is rare in eukaryotes, likely examples have been identified of protist and alga genomes containing genes of bacterial origin.[80][81]

text: Genome[edit]

text: The genome is the total genetic material of an organism and includes both the genes and non-coding sequences.[82]

text: Number of genes[edit]

text: The genome size, and the number of genes it encodes varies widely between organisms. The smallest genomes occur in viruses (which can have as few as 2 protein-coding genes),[91] and viroids (which act as a single non-coding RNA gene).[92] Conversely, plants can have extremely large genomes,[93] with rice containing >46,000 protein-coding genes.[94] The total number of protein-coding genes (the Earth's proteome) is estimated to be 5 million sequences.[95]

text: Although the number of base-pairs of DNA in the human genome has been known since the 1960s, the estimated number of genes has changed over time as definitions of genes, and methods of detecting them have been refined. Initial theoretical predictions of the number of human genes were as high as 2,000,000.[96] Early experimental measures indicated there to be 50,000–100,000 transcribed genes (expressed sequence tags).[97] Subsequently, the sequencing in the Human Genome Project indicated that many of these transcripts were alternative variants of the same genes, and the total number of protein-coding genes was revised down to ~20,000[90] with 13 genes encoded on the mitochondrial genome.[88] Of the human genome, only 1–2% consists of protein-coding genes,[98] with the remainder being 'noncoding' DNA such as introns, retrotransposons, and noncoding RNAs.[98][99] Every multicellular organism has all its genes in each cell of its body but not every gene functions in every cell .

text: Essential genes[edit]

text: Essential genes are the set of genes thought to be critical for an organism's survival.[101] This definition assumes the abundant availability of all relevant nutrients and the absence of environmental stress. Only a small portion of an organism's genes are essential. In bacteria, an estimated 250–400 genes are essential for Escherichia coli and Bacillus subtilis, which is less than 10% of their genes.[102][103][104] Half of these genes are orthologs in both organisms and are largely involved in protein synthesis.[104] In the budding yeast Saccharomyces cerevisiae the number of essential genes is slightly higher, at 1000 genes (~20% of their genes).[105] Although the number is more difficult to measure in higher eukaryotes, mice and humans are estimated to have around 2000 essential genes (~10% of their genes).[106] The synthetic organism, Syn 3, has a minimal genome of 473 essential genes and quasi-essential genes (necessary for fast growth), although 149 have unknown function.[100]

text: Essential genes include Housekeeping genes (critical for basic cell functions)[107] as well as genes that are expressed at different times in the organisms development or life cycle.[108] Housekeeping genes are used as experimental controls when analysing gene expression, since they are constitutively expressed at a relatively constant level.

text: Genetic and genomic nomenclature[edit]

text: Gene nomenclature has been established by the HUGO Gene Nomenclature Committee (HGNC) for each known human gene in the form of an approved gene name and symbol (short-form abbreviation), which can be accessed through a database maintained by HGNC. Symbols are chosen to be unique, and each gene has only one symbol (although approved symbols sometimes change). Symbols are preferably kept consistent with other members of a gene family and with homologs in other species, particularly the mouse due to its role as a common model organism.[109]

text: Genetic engineering[edit]

text: Genetic engineering is the modification of an organism's genome through biotechnology. Since the 1970s, a variety of techniques have been developed to specifically add, remove and edit genes in an organism.[110] Recently developed genome engineering techniques use engineered nuclease enzymes to create targeted DNA repair in a chromosome to either disrupt or edit a gene when the break is repaired.[111][112][113][114] The related term synthetic biology is sometimes used to refer to extensive genetic engineering of an organism.[115]

text: Genetic engineering is now a routine research tool with model organisms. For example, genes are easily added to bacteria[116] and lineages of knockout mice with a specific gene's function disrupted are used to investigate that gene's function.[117][118] Many organisms have been genetically modified for applications in agriculture, industrial biotechnology, and medicine.

text: For multicellular organisms, typically the embryo is engineered which grows into the adult genetically modified organism.[119] However, the genomes of cells in an adult organism can be edited using gene therapy techniques to treat genetic diseases.


document_title: Many happy returns (greeting)

question_text: many many happy returns of the day meaning

text: Many happy returns (greeting)

text: "Many happy returns" is a greeting which is used by some on birthdays, and by others in response to "Merry Christmas" and "Happy New Year". Since the 18th century this has been used as a salutation to offer the hope that a happy day being marked would recur many more times. It is now primarily used, by some, on birthdays. Prior to the mid-19th century, it was used at any celebratory or festive event. The phrase is more common in British English, Indian English, Hiberno English and to some degree in Canadian English than in American English.

text: Current usage is often as a more formal option than "Happy Birthday". It is also often found on greetings cards.

text: Its earliest attributable use was by Lady Newdigate in a letter written in 1789 (and published in Newdigate-Newdegate Cheverels in 1898)[1]

text: Many happy returns of þe day to us my Dr Love

text: The letter was written in London on 31 May 1789 by Hester Margaretta, Lady Newdigate, to her husband, Sir Roger Newdigate, 5th Baronet, and refers to a wish for their wedding day.

text: A much earlier reference is found in Joseph Addison's newspaper The Freeholder:[2]

text: The usual Salutation to a Man upon his Birth-day among the ancient Romans was Multos & foelices; in which they wished him many happy Returns of it.

text: An alternative explanation is that "returns" here is used in the sense of "yield" or "profit" that it is still found in "investment returns". Therefore, "many happy returns of the day" would be a wishing a person a rewarding day, full of happiness. This use has been traced back to Joseph Addison in 1716. [3][4]

text: "Many happy returns" is Winnie-the-Pooh's preferred method of wishing people a happy birthday, as seen throughout the story "In Which Eeyore has a Birthday and Gets Two Presents" in the 1926 collection Winnie-the-Pooh.


document_title: Mark Sloan (Grey's Anatomy)

question_text: when does sloan come into grey's anatomy

question_tokens: when does sloan come into grey 's anatomy

text: Mark Sloan (Grey's Anatomy)

text: Storylines[edit]

text: Mark first appears in season two, introduced as a highly respected otolaryngologist sub-specialized in plastic surgery and the childhood best friend of neurosurgeon Derek Shepherd (Patrick Dempsey). In his first appearance, he flirts with Meredith Grey, and Derek punches him in the face. Derek explains that Mark had an affair with his wife, Addison (Kate Walsh) while they were living in New York. Mark travels to Seattle, intent on convincing Addison to return with him, but his offer is rejected and Derek declines to renew their friendship. Mark returns during season three at Addison's drunken behest, but she again rejects him once sober. Undeterred, Mark sells his successful private practice (which he previously shared with Derek) and takes over the plastics program at Seattle Grace Hospital. During Meredith's morphine rampage, Mark finds out about his nickname McSteamy which was given to him by her during his first trip to Seattle back when he attempted to get Addison back and earn Derek's friendship back. It is later revealed that Mark has at some point slept with all of Derek's sisters. Mark has a brief fling with Addison's friend, orthopedic surgeon Callie Torres (Sara Ramirez), and develops a friendship with Derek's girlfriend, intern Meredith Grey (Ellen Pompeo). It is revealed that after Derek left New York, Mark and Addison continued their relationship for two months, during which she conceived and aborted his child. Just weeks after moving to Seattle he quickly observes that Derek's true love was Meredith and tries to convince Addison that her marriage with Derek was over. Mark enters into a sixty-day abstinence pact with Addison, agreeing that if they can remain celibate for that time, Addison will give their relationship another chance. Addison ultimately breaks the pact by having sex with intern Alex Karev (Justin Chambers), and soon thereafter departs from Seattle to work in Los Angeles.

text: Mark supports Derek when Meredith comes close to dying after drowning, and the two are able to rekindle their friendship. It is eventually revealed that he and Derek grew up together and that he, having lost his mother as a child and emotionally neglected by his father, considered Derek's mother as his maternal figure. As he was an only child and Derek was the only son, they became close friends and he was Derek's best man at the latter's wedding to Addison. He also forms a friendship with Callie, and develops an attraction to cardiothoracic surgeon Erica Hahn (Brooke Smith). Erica does not reciprocate his feelings, and he is supportive of Callie when she and Erica have a brief relationship. When Addison shows up at Seattle Grace for a case, Mark attempts to sleep with Addison again but she refuses. The nurses later start a club against him called Nurses United Against Mark Sloan. After a string of unresolved sexual tension on his part, Mark then finds himself seduced by Lexie Grey (Chyler Leigh), despite Derek's request that he keep their relationship platonic even before their relationship had begun. They begin a sexual relationship, which Lexie halts until he is willing to publicly admit to being her partner. Mark eventually agrees and tells Derek, who attacks him. Animosity exists between them for several episodes, before they once more repair their friendship. Mark and Lexie's relationship becomes increasingly serious. He meets her father, Thatcher (Jeff Perry); and at the end of season five, asks her to move in with him. Though Lexie initially declines, he remains committed to their relationship, and she agrees early in season six.

text: Mark discovers that he has an 18-year-old daughter, Sloan Riley (Leven Rambin), who arrives seeking his support after becoming pregnant and being evicted by her mother. Mark permits her to move in with him, which angers Lexie. When Lexie makes it clear that she knew that Mark would choose his own daughter over her, she puts an end to their relationship. Sloan experiences difficulties in her pregnancy, so Mark takes her to LA to be treated. He and Addison once again sleep together, but when he comes back he tells Lexie because he doesn't want to lie to her and wants them to get back together, but when she tells him she slept with Alex it puts an end to their relationship. When Sloan decides to give her baby up for adoption, Mark and Callie offer to raise it together. Sloan declines his offer and leaves Seattle, leaving Mark distraught. He enters into a relationship with cardiothoracic surgeon Teddy Altman (Kim Raver), despite the fact she is in love with their trauma colleague, Owen Hunt (Kevin McKidd). Sloan returns unexpectedly and gives birth to a son. She reconsiders having the baby adopted, but when Mark reassures her that he will support her no matter what, gives the baby to an adoptive couple from Washington.

text: In the sixth-season finale, a gunman commits mass murder at the hospital. Mark helps Lexie save Alex, her new boyfriend. In the aftermath of the shooting, Lexie has a nervous breakdown and Mark has her committed to the psychiatric unit. Their friendship is strained, however Lexie softens towards him when she learns that he is still in love with her. As Lexie goes to talk to Mark about him still being in love with her, she sees Mark entering his apartment with Derek's sister Amelia kissing her and ultimately having sex with her. When Callie's girlfriend, pediatric surgeon Arizona Robbins (Jessica Capshaw), breaks up with her, she and Mark have a drunken one-night stand. Shortly thereafter, he reconciles with Lexie, but is delighted when Callie discovers she is pregnant with his child. Lexie, however, is dismayed by the news and leaves Mark.

text: Mark asks Dr. Jackson Avery to find out how Lexie's doing, but Jackson lies to Mark that he wasn't able to find it out, and he (Jackson) starts dating Lexie shortly after that. In the meanwhile, Callie and Mark's daughter is born. Mark later gives Jackson and Lexie his blessing, and tells Lexie he will let her go; Lexie replies that she is still in love with him, but right now she needs Jackson to be happy. After giving Jackson a hard time, Mark finally acknowledges his surgery skills and decides to teach him, although he still evidences feelings towards Lexie, while he shows his own parenting skills with Sofia. He also starts getting along better with Arizona. After a long time without dating, Mark finally embarks on a relationship with Julia. This makes Lexie jealous, which leads to her and Jackson breaking up. Lexie struggles to tell Mark how she feels but finally admits it leaving him torn between her and Julia. In the season 8 finale, Mark, Lexie, Derek, Meredith, Cristina, and Arizona are involved in an aviation accident while on the way to Boise, Idaho to perform surgery on conjoined twins, crushing Lexie under debris. After trying and failing to save her, Mark holds a dying Lexie by the hand, telling her that he has and will always love her. He and the remaining surviving crash victims are left stranded in the woods, mourning Lexie and fighting to stay alive.

text: In the ninth-season premiere, it is discovered that Mark is on life support due to the extensive injuries he sustained in the plane crash and, as determined by his will, the machines would be turned off if he showed no signs of waking within 30 days. Flashbacks of some moments in Mark's life showcased him being videotaped as he was extending his congratulations to newlyweds Callie and Arizona. At the end of the speech, he declares that Lexie was the one he wanted to grow old and dance with in their granddaughter's wedding. At 5:00 that day, with Derek and Callie keeping vigil at his bedside, the machines were turned off, and Mark Sloan died shortly thereafter. The following episode reveals that he had a surge of good health upon his return to Seattle Grace before ultimately succumbing to his injuries. His 'surge' allowed him enough energy to advise his protégé Jackson, 'when you love someone, tell them', which is believed to be a reflection on the major obstacle of his failed relationship with Lexie. During this momentary energy, Mark also took the opportunity to make a clean break with his girlfriend, Julia, stating that the situation was not fair to her as he had always loved only Lexie. Following his death, Shonda Rhimes muses regarding Mark and Lexie's relationship: '...he and Lexie get to be together in a way. Their love remains true.”[1] Seattle Grace Mercy West Hospital is later renamed Grey Sloan Memorial Hospital in tribute to Lexie and Mark.

text: Development[edit]

text: Casting and creation[edit]

text: This section needs expansion. You can help by adding to it. (July 2011)

text: Dane auditioned for the role during the casting of the pilot and ultimately received the role, which was only later introduced in the show.[3] He initially appeared as a guest-star in the episode "Yesterday" of the second season, becoming a series regular from the third season episode "Sometimes a Fantasy", first broadcast in October 2006.[4] Casting director Linda Lowy gave the insight: "You can't forget about McSteamy. We cast (Dane) for one episode, and I think the women across the nation went kind of crazy. Everyone was talking about him, so we decided to make him a regular."[5] In July 2012, TVLine announced Dane would leave the show after the first two episodes of the ninth season. Rhimes said she and Dane decided to end Mark's storyline after much discussion. She added: "It was a thing that Eric had been thinking about for a while, but it felt like the right time to him."[6][7] However, E! Online reported that Rhimes had been forced by the network to reduce the cast for budget reasons and that Dane had not asked to leave the series.[8]

text: Characterization[edit]

text: This section needs expansion. You can help by adding to it. (June 2013)

text: The American Broadcasting Company (ABC) characterized Sloan as "charming", "confident", "smug", "smarmy", and "great with his hands".[9] Shonda Rhimes said of the character: "Mark, the original bad boy, is struggling with his own demons. He brings a healthy serving of mystery and potential conflict to Seattle Grace."[10] Actress Kate Walsh said: "He's the guy you shouldn't go out with but you can't help yourself."[10] Carolina Paiz, one of the writers of the series, wrote: "he can be impertinent and evil and demeaning."[11]

text: Reception[edit]

text: His role in the episode "In the Midnight Hour" from the fifth season was well received by Debbie Chang of BuddyTV who wrote, "Mark (Eric Dane) is pretty freaking awesome in this episode. He's lascivious as all heck, but he's showing some compassion." His scenes with Shepherd were described as "fun."[12] Victor Balta of Today listed their friendship in its "TV's best bromances". He called them "the most exciting couple on Grey’s," explaining "they’ve demonstrated an easy chemistry that makes for some of the great comic relief around Seattle Grace Hospital with their banter, sage wisdom on each other’s lives, and locker room-style teasing."[13] Their bromance was furthermore included in lists by About.com, BuddyTV, Cosmopolitan, Wetpaint.[14][15][16][17] However, following the announcement of Dane's upcoming departure from the show, Mark Perigard of the Boston Herald felt he and Derek "never clicked like you’d expect friends would. Any scene they had together ranged from uncomfortable to forced."[18]

text: His bromance with Jackson Avery was also well received. Janalen Samson of BuddyTV wrote: "Eric Dane has always shown a facility for sly, deft comedy and these scenes with Jesse Williams are proving to be gems. I do love a good Bromance and these two actors are bringing the love and the funny in spades.[19] Writing for TV Fanatic, Courtney Morrison commented: "Sloan has brought the GA comedy scale up a bit with his bromances and mentoring Jackson.[20] The pairing was listed in Zap2it's 25 Top Bromances of 2012.[21] Los Angeles Times TV columnist, Carina Mackenzie, described his scenes with Torres as "always perfectly sharp."[22]

text: At the 13th Screen Actors Guild Awards, Dane was part of the Grey's Anatomy cast awarded the "Outstanding Performance by an Ensemble in a Drama Series" accolade, for which they were also nominated the following year.[23][24]


document_title: List of earthquakes in New Zealand

question_text: when was the last time new zealand had an earthquake

text: List of earthquakes in New Zealand

text: Pre-19th century[edit]

text:
Date
Location
Region
Magnitude (ML)
Magnitude (MW)
Depth
Latitude
Longitude
Fatalities
Further information

1100
Alpine Fault
South Island
7.6–8.3

[4]

1460
Wellington Region
Wellington
8.0
8.0
25 km
41.39°S
174.80°E

[5]

1610-20
Alpine Fault
South Island
7.6–8.3

[4][6]

1717
Alpine Fault
South Island
8.1

[4][6]

text: 19th century[edit]

text: Information for earthquakes before 1840 are later estimates.

text:
Date
Location
Region
Magnitude (ML)
Magnitude (MW)
Depth
Latitude
Longitude
Fatalities
Further information

1815
New Plymouth
Taranaki
7.0 [7]

25 km
38.99°S
174.00°E

1817
Fiordland
South Island
7.0 [8]

25 km
45.99°S
167.00°E

1826
Fiordland
South Island
8.0 [9]
8.0
25 km
44.99°S
167.00°E

1835
South Auckland
Auckland
7.0 [10]

25 km
36.99°S
175.00°E

Apparently a large shallow earthquake followed by aftershocks. Evidence rests on a single report that has so far not been verified[11]

1838
Waitotara Forest
Manawatu
7.0 [12]

25 km
39.39°S
176.10°E

26 May 1840
Paraparaumu
Wellington
6.0 [13]

25 km
41.00°S
175.00°E

8 Jul 1843
Near Taihape
Manawatu
7.6 [14]
7.6
12 km
39.59°S
176.20°E
2
1843 Wanganui earthquake

13 Jul 1846
Snares Islands
Southland
6.3 [15]

25 km
47.00°S
166.00°E

19 Nov 1846
Karamea
West Coast
6.5 [16]

25 km
41.00°S
172.00°E

4 Dec 1846
Wellington
Wellington
6.0 [17]

25 km
41.00°S
174.50°E

16 Oct 1848
Blenheim
Marlborough
7.4 [18]
7.8
12 km
41.89°S
173.60°E
3
1848 Marlborough earthquake

27 Jul 1851
Motueka
Tasman
6.0 [19]

25 km
41.00°S
173.00°E

23 Jan 1855
Lake Wairarapa
Wairarapa
8.2[20]
8.2
33 km
41.198°S
175.20°E
9
1855 Wairarapa earthquake[21][22][23][24]

23 Feb 1863
Waipukurau
Hawke's Bay
7.5[25]

25 km
40.00°S
176.50°E

1863 Hawke's Bay earthquake[26][27]

19 Oct 1868
Cape Farewell
Tasman
7.2 [28]

12 km[29]
40.20°S
173.00°E

Felt throughout Central New Zealand

5 Jun 1869
Christchurch
Canterbury
4.7[30]–5.7[31]

5 km
43.55°S
172.60°E

1869 Christchurch earthquake

18 Jul 1876
Palmerston North
Manawatu
6.8 [32]

50 km
40.19°S
175.80°E

Felt strongly in Palmerston North

25 Jun 1881
Palmerston North
Manawatu
6.7 [33]

33 km
40.39°S
175.60°E

Felt strongly in Palmerston North

5 Dec 1881
Castle Hill[34]
Canterbury
6.0 [35]

12 km
43.13°S
171.77°E

Damaged stone buildings in Christchurch, including ChristChurch Cathedral[36]

1 Sep 1888
Lewis Pass
Canterbury
7.0 [37]
7.1
12 km
42.59°S
172.55°E

1888 North Canterbury earthquake

23 Jun 1891
Port Waikato
Auckland
6.2 [38]

12 km
37.43°S
174.43°E

Felt in Auckland/Waikato

12 Feb 1893
Nelson
Tasman Bay
6.7 [39]

70 km
40.99°S
173.80°E

Felt throughout Central New Zealand

18 Aug 1895
Taupo
Bay of Plenty
6.0 [40]

12 km
38.80°S
176.80°E

Felt throughout Central New Zealand

8 Dec 1897
Wanganui
Manawatu
6.5 [41]

40 km
39.99°S,
175.00°E

Felt throughout North Island, Strong in Wanganui

text:
Date
Location
Region
Magnitude (ML)
Magnitude (MW)
Depth
Latitude
Longitude
Fatalities
Further information

16 Nov 1901
Cheviot
North Canterbury
6.8 [42]

12 km
42.74°S
173.35°E
1
1901 Cheviot earthquake

9 Aug 1904
Cape Turnagain
Hawke's Bay
7.0 [43]
7.2
16 km
40.40°S
176.40°E

1904 Cape Turnagain earthquake

7 Oct 1914
East Cape
Gisborne
6.6 [44]

12 km
37.80°S
178.20°E

Felt throughout eastern North Island

22 Nov 1914
Tauranga
Bay of Plenty
7.3 [45]

300 km
37.49°S
176.50°E

Felt throughout North Island

1 May 1917
Raoul Island
Kermadec Islands

8.0
50 km
29.00°S
177.00°W

Felt throughout New Zealand[46]

6 Aug 1917
Castlepoint
Manawatu
6.8 [47]

12 km
40.80°S
176.00°E

Felt throughout North Island

3 Nov 1918
Puysegur Trench
South of New Zealand
6.8 [48]

50 km
47.00°S
165.40°E

Felt throughout Southland

29 Jun 1921
Kaweka Forest
Hawke's Bay
7.0 [49]

80 km
39.29°S
176.40°E

Felt throughout North Island

25 Dec 1922
Motunau
North Canterbury
6.4

20 km
42.99°S
173.00°E

Felt throughout Upper half of South Island

9 Mar 1929
Arthur's Pass
Canterbury
7.0 [50]

12 km
42.83°S
171.83°E

1929 Arthur's Pass earthquake

17 Jun 1929
Murchison
West Coast
7.3 [51]
7.8
20 km
41.69°S
172.20°E
17
1929 Murchison earthquake

23 Jun 1929
Murchison
West Coast
6.5 [52]

12 km
41.78°S
172.32°E

12 Feb 1930
Porangahau
Hawke's Bay
6.2

33 km
40.39°S
176.55°E

Felt throughout lower half of North Island

3 Feb 1931
North of Napier
Hawke's Bay
7.4 [53]
7.8
20 km
39.29°S
177.00°E
256
1931 Hawke's Bay earthquake

13 Feb 1931
East of Napier
Hawke's Bay
7.3 [54]

30 km
39.55°S
177.31°E

Aftershock to M 7.4 event

16 Sep 1932
Wairoa
Hawke's Bay
6.9 [55]

12 km
38.95°S
177.59°E

Caused further damage to the already devastated Hawke's Bay.

5 Mar 1934
Pahiatua
Manawatu
7.2 [56]

12 km
40.54°S
176.29°E
2
1934 Pahiatua earthquake

15 Mar 1934
Wairoa
Hawke's Bay
6.3

25 km
39.31°S
177.23°E

Felt strongly in Hawke's Bay and Gisborne

24 May 1936
Whakatane
Bay of Plenty
6.5 [57]

150 km
37.99°S
177.00°E

Felt in North Island

16 Dec 1938
Fiordland
Southland
7.0

60 km
44.99°S
167.00°E

Felt throughout South Island

11 Feb 1939
Fiordland
Southland
7.0 [58]

25 km
45.00°S
167.50°E

Felt throughout South Island

26 Feb 1940
Hastings
Hawke's Bay
6.0

25 km
39.50°S
176.50°E

Felt throughout North Island

24 Jun 1942
Masterton
Wairarapa
6.9 [59]

12 km
40.96°S
175.69°E
1[60]
June 1942 Wairarapa earthquake

1 Aug 1942
Masterton
Wairarapa
6.8 [61]

40 km
41.01°S
175.52°E
1
August 1942 Wairarapa earthquake

17 Feb 1943
Te Anau
Southland
6.5

123 km
45.29°S
168.00°E

Felt throughout South Island

2 Aug 1943
Te Anau
Southland
6.1 [62]

33 km
45.64°S
166.67°E

Felt throughout South Island

2 Sep 1945
Stewart Island
Southland
6.5 [63]

12 km
47.47°S,
166.12°E

Felt throughout Southland and Otago

26 Jun 1946
Lake Coleridge
Canterbury
6.5[64]

12 km
43.30°S
171.47°E

Mainshock

26 Mar 1947
Offshore Poverty Bay
Gisborne
7.1

38.55°S
178.42°E

1947 Gisborne earthquakes and tsunami

17 May 1947
Offshore Tolaga Bay
Gisborne
7.1

38.21°S
178.60°E

1947 Gisborne earthquakes and tsunami

22 May 1948
Hanmer Springs
North Canterbury
6.4

12 km
42.49°S
173.00°E

Mainshock

22 May 1948
Cheviot
North Canterbury
6.2

12 km
42.83°S
173.05°E

Separate event triggered by the M 6.4 earthquake 5 minutes prior

9 Feb 1949
Hawera
Taranaki
6.4

199 km
39.67°S
174.35°E

Felt throughout North Island

text:
Date
Location
Region
Magnitude (ML)
Magnitude (MW)
Depth
Latitude
Longitude
Fatalities
Further information

10 Feb 1951
Porangahau
Hawke's Bay
6.1

33 km
40.21°S
177.04°E

Felt throughout North Island [65]

24 Jun 1951
Toaroa Junction
Manawatu
6.3

33 km
39.45°S
176.20°E

Felt throughout North Island

29 Sep 1953
Tauranga
Bay of Plenty
7.2 [66]

273 km
37.59°S
176.48°E

Felt throughout North Island

27 Feb 1955
Raoul Island
Kermadec Islands
7.8

18 km
28.40°S
175.37°W

Felt in the East half of North Island

29 Dec 1956
Matawai
Gisborne
6.1
6.1
33 km
39.72°S
176.87°E

Felt strongly along the East Coast of the North Island

31 Jan 1958
Waipawa
Hawke's Bay
6.1

12 km
30.30°S
177.50°E

14 Sep 1959
Raoul Island
Kermadec Islands

7.8
35 km
28.82°S
177.07°W

Felt in the East half of North Island

28 Mar 1960
Mokau
Taranaki
6.6 [67]

237 km
39.04°S
174.81°E

Doublet earthquake to 6.5 event

28 Mar 1960
Mokau
Taranaki
6.5 [68]

209 km
39.04°S
174.77°E

Doublet earthquake to 6.6 event

25 May 1960
Milford Sound
Southland
6.3

12 km
44.17°S
167.72°E

27 Dec 1961
Martinborough
Wellington
6.2

12 km
41.51°S
176.11°E

Struck offshore, 65 km east of Martinborough

18 Dec 1963
Raoul Islands
Kermadec Islands

7.7
35 km
24.77°S
176.52°W

Felt in the East half of North Island

11 April 1965
Kaikoura
North Canterbury
6.1

12 km
42.76°S
173.87°E

Felt in Kaikoura/North Canterbury

21 May 1965
George Sound
Southland
6.4

101 km
44.94°S
167.36°E

4 Mar 1966
Gisborne
East Cape
6.0

33 km
38.73°S
178.11°E

Felt in Gisborne

23 April 1966
Cook Strait
Marlborough
5.8
5.8
12 km
41.64°S
174.54°E

Caused damage in Wellington

24 May 1968
Inangahua Junction
West Coast
6.7[69]
7.1[69]
12 km
41.75°S
172.04°E
2
1968 Inangahua earthquake

6 Jan 1973
Taupo
Waikato
7.0

163 km
39.03°S
175.26°E

Felt throughout New Zealand

5 May 1976
Milford Sound
Southland
6.6

12 km
44.67°S
167.38°E

15 Jan 1976
Raoul Island
Kermadec Islands

7.8
43 km
29.21°S
177.63°W

Foreshock to M 8.2 event

15 Jan 1976
Raoul Island
Kermadec Islands

8.2
31 km
29.17°S
177.31°W

Main shock

18 Jan 1977
Cook Strait
Marlborough
6.0

33 km
41.84°S
174.58°E

12 Oct 1979
Puysegur Trench
South of New Zealand
6.5

12 km
46.70°S
166.03°E

31 Dec 1984
White Island
Bay of Plenty
6.3

12 km
36.59°S
177.55°E

Felt around the Bay of Plenty

21 Oct 1986
Raoul Island
Kermadec Islands

8.3
33 km
28.15°S
176.29°W

Felt throughout New Zealand[70]

2 Mar 1987
Edgecumbe
Bay of Plenty
6.1
6.5
10 km
37.88°S
176.80°E

1987 Edgecumbe earthquake

4 Jun 1988
Te Anau
Southland
6.1

73 km
45.12°S
167.29°E

24 May 1989
Puysegur Trench
South of New Zealand

8.2

Felt in the South Island

31 May 1989
Doubtful Sound
Southland
6.1

23 km
45.33°S
166.87°E

13 May 1990
Weber
Manawatu
6.2[71]
6.4[71]
29 km
40.42S
176.47°E

Mainshock

28 Jan 1991
Buller Ranges
West Coast
6.1

9.9 km
41.90°S
171.65°E

Foreshock to M 6.3 event

29 Jan 1991
Buller Ranges
West Coast
6.3

17.3 km
41.90°S
171.72°E

Mainshock

8 Sep 1991
South Taranaki Bight
Manawatu
6.3

86 km
40.24°S
175.16°E

Felt throughout North Island

27 May 1992
Wairau Valley
Marlborough
6.8

79 km
41.60°S
173.66°E

Felt in Central New Zealand

21 June 1992
White Island
Bay of Plenty
6.1

5 km
37.57°S
176.82°E

Felt in Bay of Plenty

10 Aug 1993
Secretary Island
Southland
6.7
7.0
5 km
45.21°S
166.70°E

Felt as far away as Australia

10 Aug 1993
Gisborne
East Cape
6.3

45 km
38.52°S
177.90°E

Felt strongly in Gisborne.

11 Apr 1993
Hastings
Hawke's Bay
6.1

37 km
39.72°S
176.71°E

Felt strongly throughout Hawke's Bay

18 Jun 1994
Arthur's Pass
Canterbury
6.7 [72]
6.7
4 km
43.00°S
171.47°E

Mainshock

19 Jun 1994
Lake Coleridge
Canterbury
6.1

5 km
43.16°S,
171.47°E

Triggered from the M 6.7 Arthur's Pass event

24 Nov 1995
Arthur's Pass
Canterbury
6.3

7 km
42.95°S,
171.81°E

Felt strongly in the South Island

6 Feb 1995
NE of New Zealand
East Cape
7.0

12 km
37.7°7S
179.68°E

Mainshock

10 Feb 1995
NE of New Zealand
East Cape
6.6

12 km
37.92°7S
179.51°E

25 May 1997
Raoul Island
Kermadec Islands

7.9
339 km
33.61°S
177.80°E

Felt throughout North Island and upper half of South Island

20 Apr 1998
Taumaranui
Manawatu
6.7 [73]

232 km
39,02S
174.92°E

Felt throughout the North Island

25 Oct 1999
Taupo
Waikato
7.0

160 km
38.56S
175.91°E

Felt throughout New Zealand

text:
Date
Location
Region
Magnitude (ML)
Magnitude (MW)
Depth
Latitude
Longitude
Fatalities
Further information

15 Aug 2000
L'Esperance Rock
Kermadec Islands
7.6 [74]

436 km
31.94°S
178.55°E

Felt in Christchurch

1 Nov 2000
Fiordland
Southland
6.2 [75]

9 km
45.12°S
166.95°E

21 Aug 2001
NE of New Zealand
East Cape
7.1 [76]
7.1
33 km
36.98°S
179.16°E

Felt in the Gisborne area

21 Oct 2001
NE of New Zealand
East Cape
6.3

12 km
36.89°S
179.86°E

Felt in the Gisborne area

8 Dec 2001
Haast
West Coast
6.2

5 km
44.11°S
168.60°E

Mainshock

22 Aug 2003
Fiordland
Southland
7.0 [77]
7.2
24 km
45.19°S,
166.83°E

Felt throughout South Island

22 Nov 2004
Puysegur Trench
South of New Zealand
7.1 [78]
7.0
12 km
46.57°S
165.08°E

Reportedly felt as far north as Hamilton.

14 Mar 2005
Opunake
Manawatu-Wanganui
6.4

154 km
40.17°S
173.63°E

Felt strongly throughout central New Zealand

16 May 2006
L'Esperance Rock
Kermadec Islands
7.5 [79]
7.4
150 km
31.56°S,
179.30°W

Felt in East half of New Zealand

16 May 2006
Raoul Island
Kermadec Islands
7.1

33 km
31.98°S,
177.21°W

Felt in East half on North Island

16 Oct 2007
Fiordland
Southland
6.7 [80]
6.7
5 km
44.72°S
167.39°E

Felt lower half of South Island

9 Dec 2007
Raoul Island
Kermadec Islands

7.8
152 km
25.99°S
177.51°W

Felt in East half of New Zealand

20 Dec 2007
Gisborne
East Cape
6.7 [81]
6.6
44 km
38.89°S
178.44°E

2007 Gisborne earthquake

25 Aug 2008
Hastings
Hawke's Bay
5.9

31 km
39.71°S
176.85°E

2008 Hastings earthquake

15 Jul 2009
Puysegur Trench
South of New Zealand
6.1 [82]

33 km
46.07°S
165.75°E

Felt throughout Southland and Otago

15 Jul 2009
Dusky Sound
Southland

7.8 [83]
12 km
45.76°S
166.58°E

2009 Fiordland earthquake

text:
Date
Location
Region
Magnitude (ML)
Magnitude (MW)
Magnitude (Mb)
Depth
Latitude
Longitude
Fatalities
Further information

4 Sep 2010
Darfield
Canterbury
7.1
7.0
6.4
11 km
43.52°S
172.16°E

2010 Canterbury earthquake[84][85]

22 Feb 2011
Christchurch
Canterbury
6.3
6.1
6.1
6 km
43.58S
172.67E
185 [86]
2011 Christchurch earthquake[87][88]

13 Jun 2011
Christchurch
Canterbury
6.4
5.9
6.0
7 km
43.56°S
172.73°E
1
June 2011 Christchurch earthquake[89][90]

5 Jul 2011
Taupo
Waikato
6.5
5.5
5.4
153 km
38.65°S
175.70°E

Felt throughout New Zealand.[91][92]

7 Jul 2011
Raoul Island
Kermadec Islands
7.6
7.6
7.0
20 km
29.31°S
176.20°W

Felt as far away as Christchurch.[93][94]

22 Oct 2011
Raoul Island
Kermadec Islands
7.3
7.4
6.5
33 km
28.99°S
176.18°W

Felt in eastern half of the North Island.[95][96]

23 Dec 2011
Christchurch
Canterbury
6.0
5.9
5.7
7 km
43.52°S
172.74°E

Caused damage in the Christchurch region.[97][98]

3 Jul 2012
South Taranaki Bight
Taranaki
6.5
6.3
5.9
254 km
40.00°S
173.75°E

2012 Opunake earthquake[99][100]

21 Jul 2013
Cook Strait
Marlborough
6.5
6.5
6.1
17 km
41.61°S
174.33°E

2013 Seddon earthquake[101][102]

16 Aug 2013
Lake Grassmere
Marlborough
6.6
6.5
6.0
8 km
41.73°S
174.15°E

2013 Lake Grassmere earthquake[103][104]

16 Aug 2013
Lake Grassmere
Marlborough
6.0
5.9
5.8
8 km
41.67°S
174.26°E

Largest aftershock to 2013 Lake Grassmere earthquake[105][106]

20 Jan 2014
Eketahuna
Wairarapa
6.2
6.1
5.8
34 km
40.62°S
175.85°E

2014 Eketahuna earthquake[107][108]

13 Oct 2014
Fiordland
Southland
6.2
5.8
5.4
9 km
46.29°S
165.87°E

[109][110]

14 Oct 2014
NE of Whakatane
Bay of Plenty
6.5

5.7
82 km
34.90°S
179.65°E

[111][112]

17 Nov 2014
NE of Gisborne
Gisborne
6.5
6.7
6.2
22 km
37.68°S
179.68°E

Felt strongly across the North Island[113][114]

6 Jan 2015
W of Arthur's Pass
Canterbury
6.0
5.6
5.5
5 km
43.06°S
171.25°E

Felt throughout the South Island[115][116]

24 Apr 2015
SE of St Arnaud
Marlborough
6.2
6.1
6.0
52 km
42.09°S
173.07°E

Felt throughout New Zealand[117][118]

2 Feb 2016
E of Macauley Island
Kermadec Islands
6.6
6.2
6.3
366 km
31.65°S
177.74°E

Felt widely in the North Island.[119]

14 Feb 2016
Christchurch
Canterbury
5.7
5.8

15 km
43.5°S
172.83°E

2016 Christchurch earthquake[120][121]

2 Sep 2016
NE of East Cape
East Cape
7.1
7.1

55 km
37.01°S
179.63°E

2016 Te Araroa earthquake[122][123]

14 Nov 2016
Culverden
North Canterbury
7.8
7.8[124][125]

15 km
42.757°S
173.077°E
2[126]
2016 Kaikoura earthquake[127]

11 Jul 2017
NW of Auckland Island
South Tasman Sea
6.6
6.6
6.3
10 km
49.546°S
164.031°E

[128]