document_title: That's So Raven

question_text: where did the mom go in that's so raven

question_tokens: where did the mom go in that 's so raven

text: That's So Raven

text: Overview[edit]

text: Raven Baxter, a teenage girl, receives short psychic visions of the future events when in deep situations. Attempting to make these visions come true frequently results in trouble and hilarious situations for herself, her family, and her friends.

text: Production[edit]

text: The name for the main character changed several times prior to production, starting with Dawn Baxter in a show named The Future Is on Me. Names changed to Rose Baxter in a show called Absolutely Psychic but finally settling on Raven Baxter when actress Raven-Symoné won the lead part, with the show titled That's So Raven. Symoné originally auditioned for the role of the best friend, Chelsea. Raven-Symoné was credited simply as "Raven" throughout the series.

text: The show filmed a special pilot episode on April 12, 2001, and the first season was filmed from November 9, 2001 – June 2002.[5]

text: That's So Raven was responsible for many firsts for Disney Channel: the series was the highest-rated series in the history of Disney Channel and the first series to garner more than three-million viewers; the third longest-running original series in Disney Channel history, the first Disney Channel series to reach 100 episodes, the first Disney Channel series to produce a spinoff (Cory in the House) and one of the first two live action original series where the lead and most of the supporting main characters are minorities (The Famous Jett Jackson being the other).

text: In addition, it was also the first Disney Channel sitcom to be shot on videotape, to use a multi-camera format, to be shot in front of a studio audience or use a laugh track,[citation needed] and to use the simulated film look created by FilmLook, Inc. (all of which has become standard on all Disney Channel comedies, though a 'filmized' appearance was given to all of the channel's videotaped sitcoms produced from 2009 onward, as the live-action Disney Channel Original Series begin being produced in high definition).

text: The first three seasons were produced by Brookwell McNamara Entertainment. The company later left at the end of season 3, being replaced by Warren & Rinsler Productions. Raven-Symoné then received a producer credit for the show's fourth and final season, with the credit being called "That So Productions". It became the first Disney Channel series to create a spin-off, Cory in the House, which followed her younger brother, Cory, as his dad became the head chef for the President of the United States, causing the two of them to move to Washington, D.C.

text: In the fourth season of That's So Raven and on Cory in the House, Victor states that Tanya (T'Keyah Crystal Keymáh) is in England studying to be a lawyer. The show shot its final few episodes in January 2006, but they weren't all aired until a year later, with the series finale airing in March 2007 and the second-to-last episode shown that November.

text: Opening sequence[edit]

text: The show's title theme song was written by John Coda, who also composed the music cues to signify scene changes and commercial breaks for this series as well as Even Stevens. It was produced by Jeffrey "Def Jef" Fortson and Christopher B. Pearman and was performed by Raven-Symoné, Anneliese van der Pol and Orlando Brown.

text: Each season had opening credits composed of footage from the episodes of that season. Each season also made an exception to the guideline by showing footage from the previous seasons, most of the time when it was needed. For example, if footage being shown was of the characters dancing, then footage of a character or characters would be shown. When originally broadcast, season two followed the guideline, but when season three began airing, the opening credits from season two were inexplicably replaced with the opening credits from season three for daytime network rebroadcasts and subsequent syndication.

text: Each opening sequence, before going to the title card, always ended with the main cast being together (in clips that were not part of any episode). Seasons one, two, and three were of the Baxters sitting on their living room couch, and season four was of the Baxters (with the exception of Tanya), Eddie, and Chelsea coming down the Baxters' living room stairs.

text: At the end of the opening credits, Raven stands next to the title card and says, "Yep, that's me." This remained in season four, except with a new addition. Raven's catchphrase "Oh, Snap!" was dubbed in right before she says, "Yep, that's me."

text: Raven-Symoné performs most of the theme, while Brown performs a rap near the end of the theme and some scattered vocals in the beginning of the theme. Anneliese van der Pol sings the show's title in the chorus. A full-length version of this theme was heard in a music video which aired a few months before the show's U.S. premiere and also can be heard on the show's first soundtrack, released in 2004.

text: In Disney Channel Asia, an Asian version[clarification needed] of the show's theme song was made. The music video debuted on January 17, 2007, back-to-back with the 100th episode of That's So Raven. It also aired in China on CCTV as 那是因此掠夺.[1]

text: Episodes[edit]

text: The series is the third-longest running Disney Channel Original Series, with its popularity extending the show's contract from 65 to 100 episodes. The last episode produced was "The Way We Were", but then "Checkin' Out" was produced. Although it was chronologically the last episode, it did not air last; instead, "Where There's Smoke" aired last.

text: SeasonEpisodesOriginally airedFirst airedLast aired121January 17, 2003 (2003-01-17)March 5, 2004 (2004-03-05)222October 3, 2003 (2003-10-03)September 24, 2004 (2004-09-24)335October 1, 2004 (2004-10-01)January 16, 2006 (2006-01-16)422February 20, 2006 (2006-02-20)November 10, 2007 (2007-11-10)

text: Crossover with The Suite Life of Zack & Cody and Hannah Montana[edit]

text: The episode "Checkin' Out" is the first part of a three-way crossover that continues on The Suite Life of Zack & Cody and concludes on Hannah Montana. Raven Baxter meets Zack and Cody while visiting the Tipton Hotel to do a photo shoot promoting a fashion line for boys. During her stay, Raven upsets Cody with a psychic vision and London Tipton refuses to take interest in one of Raven's clothing designs until Hannah Montana arrives and shows an interest.

text: Cast and characters [edit]

text: Main[edit]

text:
Raven-Symoné (credited as Raven), portrays Raven Lydia Baxter, the main character. Aged 14–17. A precognitive teenager. She has a sassy attitude and a grand personality, and is well known for her style. She also loves fashion, and designs her own clothing. She has friends and a loving family, and she goes to public school. However, on various occasions, she gets "psychic visions" about what may or may not happen later. She is only able to "see" a small segment of some future event, and she frequently errs on what it really means, in which case her attempts to change these events only end up making it happen or making it worse. Her main catchphrases are "Oh Fudge!", "Oh snap!", "Ya nasty!", "How y'all doin'?", and "Oh, no he didn't!" She abruptly says, "I'm okay!" if she falls down in one of her disguises. And, if big guys throw her, she tells them to do it "gently!" In addition, when she disapproves of something, she exclaims "Gotta go!" When she makes an appearance on Cory in the House, her father exclaims, "You didn't get kicked out of design school because they don't give out refunds!", which shows she is attending design school. Raven is also a master of disguise, which fits in with her trouble-making antics and passion for becoming a fashion designer, like her idol, Donna Cabonna, whom she worked for as an intern. Raven Baxter is extremely allergic to mushrooms, and her favorite drink is orange juice. According to Chelsea, her favorite gemstone is diamond, her favorite vegetable is corn, and her favorite animal is stuffed. Often referred to as Rae, Raven does not enjoy nature or camping. She has appeared in every episode of the series, along with her younger brother Cory. In the second spin-off, Raven's Home, Raven eventually married her first love Devon but they got divorced. In between that time, they had two children Nia and Booker - latter of whom, shares Raven's ability to see into the future.
Orlando Brown portrays Edward "Eddie" Thomas. Aged 14–17. He is Raven's male best friend. He is an aspiring rapper, and is a guard on the school basketball team. He is like a "big brother" to Cory Baxter and was commonly portrayed as playful, ambitious, loyal, girl crazy and quick to jump to conclusions. Occasionally, he says "Told ya! Told ya twice!" after he tells Raven not to do something that they both knew she would do. Another common catchphrase of his is "Holla!" after he finishes talking to his friends or girls that he likes. His parents are divorced, which is mentioned several times throughout the series. It is also said that he has a little brother. In one episode, Eddie and Raven not only start to develop romantic feelings for each other but they also kiss on the lips at two separate times; however, by the end of the episode, they decide to remain friends (though its strongly implied they're still interested in one another). Eddie has appeared in every episode except Juicer Consequences.
Kyle Massey portrays Cory Baxter. Aged 10–13. Cory is Raven's younger brother who sometimes acts as the main antagonist of the series. He and Raven often argue, but in the long run, they care deeply for each other. Even as he gets older, he claims that playing pranks on Raven is one of his guilty pleasures. Cory has two best friends, William and Larry. Together, the 3 boys form the band Cory and the Boys, with Cory as the drummer and lead singer, while Larry is the guitarist. William starts out playing the clarinet and then plays the keyboard. The band has one song: "Feelin' the Love". Cory is an aspiring businessman. He is shown to be obsessed with money and often creates "get-rich-quick" schemes behind his parents' backs, in which he always gets into trouble. Cory also has a close relationship with his pet rat, Lionel. Earlier in the series, he had a crush on Chelsea. In the third season starts a relationship with Cindy. His catchphrases are "Cha-ching" and "You Know How I Do!". He and Victor are the main characters in the spin-off series Cory in the House. He has appeared in every episode of the series, along with his older sister Raven.
Anneliese van der Pol portrays Chelsea Daniels. Aged 14–17. Often referred to as Chels, She is Raven's female best friend. She is an environmentalist, vegetarian, and closet artist. She is portrayed as being clumsy and dimwitted (although the first two seasons portray her to be just as smart as Raven, but to extreme limits); at times, her stupidity is so potent that she is frequently oblivious to what should be obvious and unable to discern sarcasm from sincerity. She usually uses the catchphrases "That makes more sense!" or '"This is awkward!" She also likes to make jokes, which only she would laugh at. Despite her apparent lack of common sense and intelligence, she has a few surprises up her sleeve—such as occasionally knowing certain "smart" things, which usually tends to surprise everyone else. In Season 1, it is revealed that Raven and Chelsea's friendship goes all the way back to when they were in pre-school, but she was also shown to be dimwitted back then because she did not notice Raven blowing out the candles on her birthday cake. It should also be noted that Chelsea was just as caring when she was young as she is now because one of her unfulfilled wishes on that same birthday was to stop global warming. She is quite similar to Newt (from Cory in the House) in personality. She is very passionate in saving the environment and caring for the animals, and also much more spiritual compared to Raven who can be materialistic, though it occasionally leads to troubling events like the three friends disputing over a goat and nearly turning herself and Raven into cows. In earlier episodes, Cory has a huge crush on her and unsuccessfully pursues her. Occasionally, Chelsea refers to a specific relative, Cousin Earl, at times. Her parents are Therapists. She also has a dog named Sam. Chelsea is present in every episode except Mother Dearest, Smell of Victory, and Saturday Afternoon Fever. In the second spin-off, Raven's Home, Chelsea is a divorced single mother with a son - Levi, who both live with Raven after the divorce.
T'Keyah Crystal Keymáh portrays Tanya Baxter. (seasons 1–3). Tanya is the mother of Raven and Cory, and wife of Victor. She is a firm, but fun and caring mother who, despite the antics of her children, is always there for them. She halted her studies to raise her family, but decided once the children were older to continue studying law. Before that, she briefly worked as Raven's English teacher at the request of Raven's school principal. Her catchphrase is "Momma like!" She has a very competitive nature to her personality. It's learned that her mother, Viv, is also psychic. In season 4, Tanya is not present; it is said that she has gone off to England to attend law school. On Cory in the House, she is still in England and she does not visit Cory and Victor but is mentioned. In the pilot episode of Raven's Home, it is revealed by Booker that Tanya is still living.
Rondell Sheridan portrays Victor Baxter, the father of Raven and Cory, and husband of Tanya. He starts out as a chef in a restaurant, but he later opens his own restaurant, The Chill Grill. His biggest rival is Leonard Stevenson. In Cory in the House, he gets a job as the President's chef, and it is unknown what became of his restaurant. His catchphrases are "Here comes the pain!" and "I'll go pack!" (Cory in the House)

text: Recurring[edit]

text: Reunion[edit]

text: Eight years after the series ended, there was speculation and rumors that the series would get a second spin-off or revamp. On August 14, 2015, a reunion with Raven and her former co-stars happened on The View, where they discussed all things about the show and past times. Crystal Keymah and Sheridan were not present, but got a special mention from Symoné herself.[6]

text: Merchandise[edit]

text: The That's So Raven franchise has been modeled after fellow Disney Channel hit Lizzie McGuire. Raven has a clothing line, DVD releases, novels, bedroom sets, a perfume, a Girl Talk board game,[7] three video games[8] and two soundtracks, That's So Raven: Songs from and inspired by the hit TV show and That's So Raven Too!.

text: In February 2005, That's So Raven toys were featured in the McDonald's Happy Meal. In April 2005, a doll based on Raven Baxter was released[9] and another was released the following year.

text: In September 2005, the show also spawned a fragrance and an MP3 player. That same month, the clothing line was shipped to Macy's stores. As of 2006, That's So Raven merchandise had made $400 million.[10]

text: Soundtrack albums[edit]

text:
That's So Raven
That's So Raven Too!

text: Series novelizations[edit]

text:
What You See Is What You Get – Smell of Victory & A Dog by Any Other Name
Rescue Me – Driven To Insanity & Mother Dearest
In Raven We Trust – Test of Friendship & Saturday Afternoon Fever
Step Up – Dissin' Cousins & Party Animal
Family Affair – If I Only Had a Job & Teach Your Children Well
2 Good 2 B True – To See or Not to See & Ye Olde Dating Game
Tell It Like It Is – Campaign in the Neck & Separation Anxiety
Dueling Divas' – A Fight at the Opera & The Parties
Showtime! – Wake Up, Victor & A Fish Called Raven
Psyched – Psychics Wanted & Saving Psychic Raven
Boyfriend Blues – Four's a Crowd & Blue in the Face
Be Mine – Hearts And Minds & Close Encounters of the Nerd Kind
The Real Deal – That's So Not Raven & Run, Raven, Run
Over the Top – Out of Control & He's Got the Power
Rebel Raven – Clothes Minded & Spa Day Afternoon
Superstar – Radio Heads & The Road to Audition
House Party – Hizzouse Party & Leave It to Diva
Queen of Hearts – There Goes the Bride & Royal Treatment
Raven Rocks – A Goat's Tale & Boyz 'N Commotion
Extreme Fever – Extreme Cory & When There's Smoke

text: Video games[edit]

text: That's So Raven has spawned three video games:

text:
That's So Raven, Game Boy Advance
That's So Raven 2, Game Boy Advance
That's So Raven: Psychic on the Scene, Nintendo DS

text: Reception[edit]

text: The series premiere was watched by 3.5 million viewers, the first Disney Channel series to garner more than 3 million viewers. The most watched episode of That's So Raven is "Country Cousins", scoring 10.8 million viewers.

text: VHS and DVD releases[edit]

text: Volume releases[edit]

text:
!#
VHS and DVD title
Episodes featured
Release date
Bonus features

1

That's So Raven: Supernaturally Stylish[11]

"If I Only Had a Job"
"He's Got the Power"
"That's So Not Raven"
"Boyz 'N Commotion"

December 7, 2004

"Supernatural" (music video)
"That's So Raven" (music video)

2

That's So Raven: Disguise the Limit[12]

"Art Breaker"
"Country Cousins (Part 1)"
"Country Cousins (Part 2)"
"The Grill Next Door"

August 16, 2005

Master of Disguises (featurette)
Visual commentary by Raven on selected scenes

3

That's So Raven: Raven's House Party[13]

"Opportunity Shocks"
"Double Vision"
"Too Much Pressure"
"Four Aces Club"
"Vision Impossible"

December 6, 2005

Never-before-seen episode
Bloopers and outtakes
That's So Raven Radio Trivia Game

4

That's So Raven: Raven's Makeover Madness (Only on DVD)[14]

"Pin Pals"
"Dues and Don'ts"
"Adventures in Boss-Sitting"
"Hook Up My Space"
"When 6021 Met 4267"

July 18, 2006

Never-before-seen episode
So You Think You Know Raven (Volume 1, trivia game)

text: Other releases[edit]

text:
DVD title
Episode featured
Release date
Bonus features

Disney Channel Holiday (VHS and DVD)

"Escape Clause"

November 1, 2005

N/A

That's So Suite Life of Hannah Montana[15]

"Checkin' Out"

January 16, 2007

So You Think You Know Raven (Volume 2, trivia game)

Hannah Montana Volume 4: One in a Million[16]

"Run, Raven, Run"

January 28, 2008

N/A

text: Name in other countries[edit]

text:
Countries

Name

Australia

That's So Raven

Brazil

As Visões da Raven

Denmark

That's So Raven

Spain

Raven

Greece

Raven

Finland

That's So Raven

France

Phénomène Raven

Germany

Raven Blickt Durch

India

Aisi hai Raven

Italy

Raven

Japan

レイブン 見えちゃってチョー大変! (Reibun Mie Chatte Cho Taihen!)

Mexico

Es Tan Raven

Philippines

That's So Raven

Poland

Świat Raven

Portugal

Raven

United Kingdom

That's So Raven

Taiwan

天才魔女

Turkey

Tam Raven'a Göre

text: Spin-offs[edit]

text: Cory in the House[edit]

text: Cory in the House is the first Disney Channel spin-off and it premiered on January 12, 2007. It was the one chosen out of the many pitched and proposed spin-offs that were to have aired after the completion of That's So Raven, including one about Raven going off to college. Originally Raven-Symoné was offered the spin-off, but she declined it, therefore Disney Channel decided to give it to Kyle Massey.

text: The storyline involves Cory and Victor adjusting to life in Washington, D.C.; Victor has received a job as the Head Chef to the President. The show takes place while Raven is attending fashion college and Tanya is still in London.

text: The series is similar to its sister show, That's So Raven. Cory has two best friends, one a boy, Newton Livingston III (Jason Dolley), and one a girl, Meena Paroom (Maiara Walsh). Note that in That's So Raven, the main character also has two best friends, one a boy and one a girl and Newt and Meena's persona's are similar to Chelsea and Eddie. Cory attends a middle school in Washington, D.C. Also in the series, the president's daughter Sophie (Madison Pettis) constantly pesters Cory, like Cory did to Raven in That's So Raven. Cory also participates in crazy situations in which he learns a moral lesson and will most likely get punished. Candy Smiles plays in Cory's love life multiple times, and Stickler continuously spies on Cory, Newton and especially Meena's.

text: It is implied the episode, "When 6021 Met 4267", that Cory and Victor did move back to San Francisco.

text: In the episode "That's So in the House", Raven came to show designs of new tour guide uniforms to President Martinez (John D'Aquino). Unfortunately, she has a vision of a clock falling on the President, and tackles him, earning the Secret Service a chance to chase her around the grounds. Cory poses as his sister to display the uniforms, modeled by Newton and Meena. Raven is discovered outside the Oval Office window, and chased, until she actually does save Mr. Martinez from the clock. The episode ends with the credits sequence for That's So Pooshnick, a show from Meena's country about a psychic girl who can see the past and always ends up messing up trying to stop the vision from happening again.

text: Stanley and the Juicer have also made special appearances on the show as well.

text: Failed Movie Attempt[edit]

text: In 2011, to promote her latest film Vampires Suck, Anneliese van der Pol revealed in an interview that a That's So Raven film had been written but failed to go into production. "The storyline saw us going to France. [Raven] was going to start a fashion line in France. Eddie and [Chelsea] were going to fly out and meet her. Of course, something tragic happens. We have to rescue the situation." Van der Pol admitted that Raven's schedule at the time was booked solid for a year and the possibility of the film seemed unlikely. "But no, It's not ever happening. If I hear something, I will be the first to sign on." She also commented on reprising her role of Chelsea Daniels.[17]

text: Raven's Home[edit]

text: On October 27, 2016, it was announced that Raven-Symoné will star in and develop a second spin-off to the original series. Raven departed as a host of The View later in 2016 in order to work on the series full-time.[18] In November 2016, it was announced that Anneliese van der Pol will reprise her role of Chelsea Daniels.[19]

text: In the new series, Raven Baxter is a divorced mother of two pre-teens, Nia and Booker.[20] Booker inherit his mother's psychic abilities during middle school.[20] Chelsea Daniels is also a divorced mother, who is raising a son, Levi, and moves in with Raven.[21]

text: Indian adaptation[edit]

text: Palak Pe Jhalak is the sixth Disney Channel India series to be adapted in Hindi after Art Attack, Good Luck Charlie, The Suite Life of Zack and Cody, Shake It Up and Jessie, and premiered on September 27, 2015. Ayesha Kaduskar is seen playing the role of Nysha Kapoor, a character similar to Raven Baxter played by Raven-Symoné.[22] The original That's So Raven aired on Disney Channel India as well from 2004 to 2010 and Star Plus from 2003 to 2008.

text: Awards and nominations[edit]

text:
Year

Award

Category

Recipient

Result

2003

BAFTA Children's Awards

International

That's So Raven

Nominated[23]

2004

BET Comedy Awards

Outstanding Lead Actress in a Comedy Series

Raven-Symoné

Nominated[24]

Outstanding Comedy Series

That's So Raven

Nominated[24]

Gracie Allen Awards

Outstanding Children/Adolescent Program

That's So Raven

Won[25]

NAACP Image Awards

Outstanding Performance in a Youth/Children's Program

Raven-Symoné

Won[26]

Kids Choice Awards

Favorite Female TV Star

Raven-Symoné

Won[27]

NAMIC Vision Awards

Best Comedic Performance

Raven-Symoné

Nominated[28]

Children's

That's So Raven

Nominated[28]

Teen Choice Awards

Choice TV Actress: Comedy

Raven-Symoné

Nominated[29]

Choice TV Show: Comedy

That's So Raven

Nominated[29]

Young Artist Awards

Best Performance in a TV Series (Comedy or Drama) – Leading Young Actor

Kyle Massey

Nominated[30]

Best Performance in a TV Series (Comedy or Drama) – Leading Young Actress

Raven-Symoné

Nominated[30]

2005

BET Comedy Awards

Outstanding Lead Actress in a Comedy Series

Raven-Symoné

Nominated[31]

Outstanding Comedy Series

That's So Raven

Nominated[31]

Casting Society of America

Best Casting – Children's Programming

Joey Paul Jensen

Won[32]

Genesis Awards

Children's Programming

That's So Raven

Won[33]

Gracie Allen Awards

Outstanding Female Lead in a Comedy

Raven-Symoné

Won[34]

NAACP Image Awards

Outstanding Performance in a Youth/Children's Series/Special

Raven-Symoné

Won[35]

Kids Choice Awards

Favorite TV Actress

Raven-Symoné

Won[36]

NAMIC Vision Awards

Best Comedic Performance

Raven-Symoné

Nominated[28]

Children's

That's So Raven

Nominated[28]

Primetime Emmy Awards

Outstanding Children's Program

That's So Raven

Nominated[37]

Teen Choice Awards

Choice TV Actress: Comedy

Raven-Symoné

Nominated[38]

Choice TV Show: Comedy

That's So Raven

Nominated[38]

Young Artist Awards

Best Performance in a Television Series – Guest Starring Young Actor

Christopher Malpede

Won[39]

Outstanding Young Performers in a TV Series

Orlando BrownKyle MasseyAnneliese van der PolRaven-Symoné

Won[39]

2006

Casting Society of America

Best Casting – Children's TV Programming

Joey Paul Jensen

Nominated[40]

NAACP Image Awards

Outstanding Performance in a Youth/Children's Series or Special

Raven-Symoné

Won[41]

Outstanding Directing in a Comedy Series

Eric Dean Seaton

Nominated[41][42]

Kids Choice Awards

Favorite TV Actress

Raven-Symoné

Nominated[43][44]

Favorite TV Show

That's So Raven

Nominated[43][44]

NAMIC Vision Awards

Best Comedic Performance

Raven-Symoné

Nominated[45][46]

Best Children's

That's So Raven

Won[46]

Teen Choice Awards

TV – Choice Actress: Comedy

Raven-Symoné

Nominated[47]

Young Artist Awards

Best Family Television Series (Comedy)

That's So Raven

Nominated[48]

2007

NAACP Image Awards

Outstanding Actress in a Comedy Series

Raven-Symoné

Nominated[49][50]

Outstanding Performance in a Youth/Children's Program – Series or Special

Kyle Massey

Nominated[49][50]

Raven-Symoné

Won[50]

Outstanding Children's Program

That's So Raven

Won[50]

Kids Choice Awards

Favorite TV Actress

Raven-Symoné

Nominated[51][52]

NAMIC Vision Awards

Children's

That's So Raven

Won[53]

Primetime Emmy Awards

Outstanding Children's Program

That's So Raven

Nominated[54]

Writers Guild of America

Children's Episodic & Specials

Deborah Swisher ("Fur Better or Worse")

Nominated[55][56]

Young Artist Awards

Best Performance in a TV Series (Comedy or Drama) – Leading Young Actor

Kyle Massey

Won[57]

2008

NAACP Image Awards

Outstanding Performance in a Youth/Children's Program (Series or Special)

Raven-Symoné

Won

Outstanding Children's Program

That's So Raven

Won[58]

Kids Choice Awards

Favorite TV Actress

Raven-Symoné

Nominated[59][60]

NAMIC Vision Awards

Best Performance – Comedy

Raven-Symoné

Nominated[61][62]


document_title: The NeverEnding Story (film)

question_text: what is the name called out in the neverending story

root

text: The NeverEnding Story (film)

text: Plot[edit]

text: Bastian Balthazar Bux is a shy and outcast bibliophile ten-year-old raised by his widowed father, teased by bullies from school. On his way to school, he hides from the bullies in a bookstore, interrupting the grumpy bookseller, Mr. Coreander. Bastian asks about one of the books he sees, but Mr. Coreander advises against it. With his curiosity piqued, Bastian seizes the book, leaving a note promising to return it, and hides in the school's attic to read.

tag: p

text: The book describes the fantasy world of Fantasia slowly being devoured by a malevolent force called "The Nothing". Fantasia's ruler, the Childlike Empress, has fallen ill, and Atreyu is tasked to discover the cure, believing that once the Empress is well, the Nothing will no longer be a threat. Atreyu is given a medallion named the AURYN that can guide and protect him in the quest. As Atreyu sets out, the Nothing summons Gmork, a vicious and highly intelligent wolf-like creature, to kill Atreyu.

text: Atreyu's quest directs him to the adviser Morla the Ancient One in the Swamps of Sadness. Though the Auryn protects Atreyu, his beloved horse Artax is lost to the swamp, and he continues alone. Later, Atreyu is surprised by the sudden appearance of Morla, a giant turtle. Bastian, reading, is also surprised and lets out a scream, which Atreyu and Morla appear to hear. Morla does not have the answers Atreyu seeks, but directs him to the Southern Oracle, ten thousand miles distant. Atreyu succumbs to exhaustion trying to escape the Swamps but is saved by the luckdragon Falkor. Falkor takes him to the home of two gnomes that live near the entrance to the Southern Oracle. The gnomes explain that Atreyu will face various trials before reaching the Oracle. Atreyu proceeds to enter the Oracle, and is perplexed when one second trial, a mirror that shows the viewer's true self, reveals a boy which Bastian recognizes as himself. Bastian throws the book aside, but after catching his breath, continues to read. Atreyu eventually meets the Southern Oracle who tells him the only way to save the Empress is to find a human child to give her a new name, beyond the boundaries of Fantasia.

text: Atreyu and Falkor flee before the Nothing consumes the Southern Oracle. In flight, Atreyu is knocked from Falkor's back into the Sea of Possibilities, losing the Auryn in the process. He wakes on the shore of the abandoned ruins, where he meets Rock Biter, who laments the loss of his friends. Atreyu finds a series of paintings depicting his quest. Gmork reveals himself, having been lying in wait and explains that Fantasia represents humanity's imagination, and that the Nothing represents adult apathy and cynicism against it. Atreyu fends off and kills Gmork as the Nothing begins to consume the ruins. Falkor, who had managed to locate the Auryn, rescues Atreyu in time. The two find themselves in a void with only small fragments of Fantasia remaining, and fear they have failed when they spot the Empress's Ivory Tower among the fragments. Inside, Atreyu apologizes for failing the Empress, but she assures him he has succeeded in bringing to her a human child who has been following his quest: Bastian. She further explains that, just as Bastian is following Atreyu's story, "others" are following Bastian's, making this part of the neverending story. As the Nothing begins to consume the Tower, the Empress pleads directly to Bastian to call out her new name, but in amazement that he himself has been incorporated into the story as the child they were looking for, he denies the events as just being a story and Atreyu dies. Bastian runs to the window and calls out the name he had selected into the storm (Moonchild), and loses consciousness.

text: When he wakes, he finds himself in blackness with the Empress, with only a grain of sand, the last bit of Fantasia remaining. The Empress tells Bastian that he has the power to bring Fantasia back with his imagination. Bastian re-creates Fantasia, and as he flies on Falkor's back, he sees the land and its inhabitants restored, and that Atreyu has been reunited with Artax. When Falkor asks what his next wish will be, Bastian then brings Falkor back to the real world to chase down the bullies from before. The film ends with the narration that Bastian had many more wishes and adventures, and adds: "but that's another story".

text: Cast[edit]

text:
Barret Oliver as Bastian Balthazar Bux.
Noah Hathaway as Atreyu.
Tami Stronach as The Childlike Empress, to whom Bastian gives the new name of "Moon Child".
Patricia Hayes as Urgl, Engywook's wife and a healer.
Sydney Bromley as Engywook, a gnomish scientist.
Gerald McRaney as Mr. Bux, Bastian's widowed, workaholic father.
Moses Gunn as Cairon, a servant of the Empress.
Alan Oppenheimer as the voices of Falkor, Gmork, Rock Biter, and the Narrator (the latter three are uncredited).
Thomas Hill as Mr. Coreander, a grumpy bookseller.
Deep Roy as Teeny Weeny, a messenger riding on a racing snail.
Tilo Prückner as Nighthob, a messenger riding a narcoleptic bat.
Darryl Cooksey, Drum Garrett, and Nicholas Gilbert as Ethan, Todd, and Lucas, three bullies who torment Bastian.

tag: ul

text: Production[edit]

text: The adaptation only covered the first half of the book. The majority of the film was shot at the Bavaria Studios in Munich, except for the street scenes and the school interior in the real world, which were shot in Vancouver, Canada (the Gastown steam clock can be seen in the bully chase scene near the beginning[4]),[5] and the beach where Atreyu falls, which was filmed at Monsul Beach in Almería (Spain). It was Germany's highest-budgeted film at the time.

text: Music[edit]

text: The film score of The NeverEnding Story was composed by Klaus Doldinger of the German jazz group Passport. The theme song of the North American release of the film was composed by Giorgio Moroder with lyrics by Keith Forsey, and performed by Christopher "Limahl" Hamill, once the lead singer of Kajagoogoo, and Beth Anderson. Released as a single in 1984, it peaked at No. 4 on the UK singles chart, No. 6 on the US Billboard Adult Contemporary chart, and No. 17 on the Billboard Hot 100. The song has been covered by The Birthday Massacre, Creamy, Dragonland, Kenji Haga, and New Found Glory. More recent covers were done by Norwegian synthpop group Echo Image on their 2001 maxi-single Skulk and by German techno group Scooter on their 2007 album Jumping All Over the World. This Limahl song, along with other "techno-pop" treatments to the soundtrack, is not present in the German version of the film, which features Doldinger's orchestral score exclusively.

text: In 1994, Italian house music group Club House released the song "Nowhere Land," featuring Carl, which combines the melody of the tune "Bastian's Happy Flight" with original lyrics.

text: An official soundtrack album was released featuring Doldinger's score and Moroder's theme tune (Moroder also rescored several scenes for the version released outside Germany).[6] The track listing (Doldinger is responsible for everything from track 6 onwards) is as follows:

text: showThe NeverEnding Story (Original Motion Picture Soundtrack)No.TitleLength1."The NeverEnding Story"3:322."Swamps of Sadness"1:573."Ivory Tower"3:104."Ruined Landscape"3:035."Sleepy Dragon"3:596."Bastian's Happy Flight"3:167."Fantasia"0:568."Atreyu's Quest"2:529."Theme of Sadness"2:4310."Atreyu Meets Falkor"2:3111."Mirror Gate - Southern Oracle"3:1012."Gmork"0:2913."Moon Child"1:2414."AURYN"2:2015."Happy Flight"1:21

tag: table

text: In Germany, an album featuring Doldinger's score was released.

text: showDie Unendliche Geschichte — Das AlbumNo.TitleLength1."Flug auf dem Glücksdrachen (Flight of the Luckdragon)"3:122."Die Unendliche Geschichte (Titelmusik) (The NeverEnding Story (Main Title))"2:443."Im Haulewald (In the Howling Forest)"3:014."Der Elfenbeinturm (The Ivory Tower)"1:545."Atréjus Berufung – AURYN Thema (Atreyu's Quest - AURYN Theme)"2:476."Phantásien (Fantasia)"0:527."Artax's Tod (The Death of Artax)"1:138."Die Sümpfe der Traurigkeit (The Swamps of Sadness)"2:399."Atréju's Flug (Atreyu's Flight)"2:2710."Die uralte Morla (Morla, the Ancient One)"2:2711."Das südliche Orakel (The Southern Oracle)"3:1912."Die drei magischen Tore (The Three Magic Gates)"3:2513."Spukstadt (Spook City)"1:3714."Flug zum Elfenbeinturm (Flight to the Ivory Tower)"3:0215."Mondenkind (Moon Child)"1:1916."Die kindliche Kaiserin (The Childlike Empress)"2:1617."Flug auf dem Glücksdrachen (Schlußtitel) (Flight of the Luckdragon (End Title))"1:19

text: Reaction[edit]

text: Release dates[edit]

text: Some international release dates:

text:
6 April 1984 in West Germany (Die unendliche Geschichte)[7]
20 July 1984 in the United States (The NeverEnding Story)[8][9]
6 October 1984 in Brazil (A História Sem Fim)
21 November 1984 in France (L'Histoire sans fin)[10]
6 December 1984 in Spain (La Historia Interminable)[11]
7 December 1984 in Italy (La storia infinita)[12]
4 April 1985 in the United Kingdom (The NeverEnding Story)[13]

text: Critical response[edit]

text: This section needs expansion. You can help by adding to it. (January 2016)

text: The film has a Rotten Tomatoes score of 82% based on reviews from 39 critics. The critical consensus reads: "A magical journey about the power of a young boy's imagination to save a dying fantasy land, The NeverEnding Story remains a much-loved kids' adventure."[14] Metacritic gives the film a score of 46/100 based on reviews from 10 critics.[15]

text: Film critic Roger Ebert gave it three out of four stars and praised its visual effects, saying that "an entirely new world has been created" because of them,[16] a comment echoed by Variety.[2] Joshua Tyler of CinemaBlend referred to it as "One of a scant few true Fantasy masterpieces".[14]

text: Vincent Canby panned the film as a "graceless, humorless fantasy for children" in a 1984 New York Times review. Canby's criticism charged that parts of the film "sounded like 'The Pre-Teenager's Guide to Existentialism'". He further criticized the "tacky" special effects, and that the construction of the dragon looked like "an impractical bathmat".[17]

text: Ende felt that this adaptation's content deviated so far from the spirit of his book that he requested that production either be halted or the film's title be changed; when the producers did neither, he sued them and subsequently lost the case.[18] Ende called the film a "gigantic melodrama of kitsch, commerce, plush and plastic" [Ein "gigantisches Melodram aus Kitsch, Kommerz, Plüsch und Plastik"].[19]

text: Box office[edit]

text: The film performed very well at the box office, grossing US$100 million worldwide against a production budget of DM60 million (approximately US$27 million at the time). Almost five million people went to see it in Germany, a number rarely achieved by German productions, resulting in a gross of about US$20 million domestically. It also grossed a similar amount in the United States; only a modest sum in the American market, which director Wolfgang Petersen ascribed to the film's European sensibilities.[20]

text: Awards[edit]

text:
1984 - Bambi Award for: National film
1984 - Golden Screen Award
1985 - Saturn Award for: Best Performance by a Young Actor (Noah Hathaway)
1985 - Brazilian Film Award for: Best Production
1985 - Film Award in Gold for: Best Production Design

text:
1985 - Saturn Award for: Best Fantasy Film, and Best Music
1985 - International Fantasy Film Award for: Best Film
1985 - Young Artist Award for: Best Family Motion Picture, Best Young Actor, Best Young Supporting Actress.

text: Home media[edit]

text: LaserDisc[edit]

text: The film was released by Warner Bros. on LaserDisc with a digital stereo soundtrack in 1985.

text: A widescreen laserdisc was released on 28 August 1991; no special features were included.

text: DVD[edit]

text: The Region 1 DVD was first released in 2001 by Warner Bros, containing only the North American release of the film. The only audio option is a 2.0 stereo mix in either English or Spanish. The theatrical trailer is the lone extra feature presented.

text: There is also a quite lavish 2003 European version, which is a two-disc special edition with packaging shaped like the book from the film and containing both the North American and German releases of the film. Various extras, such as a 45-minute documentary, music video, and galleries, are presented on the second disc.[21] However, there is no English audio for the German version of the film. This edition is currently[when?] out of print. The standard single-disc edition is also available for the Region 2 market.

text: A Dutch import has also appeared on the Internet in various places, which only contains the North American release of the film but also includes a remastered DTS surround track, which is not found in either the German or the Region 1 release.

text: Also, in 2008, Czech- and Slovak-language DVD versions appeared in Czech Republic and Slovakia.

text: Blu-ray[edit]

text: The first Blu-ray release was a region-free Dutch edition on 24 March 2007.

text: On 2 March 2010, Warner released a Region A Blu-ray edition of the film. The disc includes a lossless DTS-HD Master Audio 5.1 surround track, which marks the first time a 5.1 surround track has been included in a US home video version of the film. No special features or theatrical trailer are included.[22]

text: Recent German releases feature the original Klaus Doldinger soundtrack with the original English audio track.

text: On 7 October 2014, a 30th Anniversary Edition Blu-ray was released, which duplicates the DTS surround track of its predecessor. Originally described as a "newly" remastered version of the film, Warner released a statement indicating that "the only remastered version is The NeverEnding Story II", while not elaborating further on this current US release.[23] The 30th Anniversary Edition contains the original theatrical trailer, a commentary track by director Wolfgang Petersen, documentaries and interviews from both 1984 and 2014, and a German-language/English-subtitled feature detailing the digital restoration process of the film.

text: Legacy[edit]

text: The film has since been an inspiration in popular culture.

text: Music[edit]

text:
The American metal band Atreyu derived their name from the character of Atreyu.
The Mexican pop punk band Fälkor derived their name from the character of Falkor, changing the styling of the middle a for ä.
The American rock band Bayside have used quotes from the film as titles of their songs. Examples include "They look like strong hands" and "They're not horses, they're unicorns".
The American rock band Rooney made reference to the film in the song "I'm Shakin'" ("I tossed and turned all night 'cause I was looking for an ending / This was so because I watched all day The NeverEnding Story with Atreyu")
The American pop punk band, New Found Glory, covered the film's theme song on their album, From the Screen to Your Stereo.
The Spanish indie-rock band Vetusta Morla derived their name from the character of Morla the Ancient One ("vetusta" means "ancient" in spanish).
The American rock band The Aquabats describe Falkor's potential romantic life in their song "Luck Dragon Lady!" on the album Hi-Five Soup!.

text: Warner Bros. planned adaptation of the novel[edit]

text: In 2009, it was reported that Warner Bros., The Kennedy/Marshall Company and Leonardo DiCaprio's Appian Way were in the early stages of creating another adaptation of Ende's novel. They intend to "examine the more nuanced details of the book" rather than remake the original film by Petersen.[24]

text: In 2011, producer Kathleen Kennedy said that problems securing the rights to the story may mean a second adaptation is "not meant to be."[25]


document_title: Alcohol laws of Wisconsin

question_text: how old do you need to be to serve alcohol in wisconsin

text: Alcohol laws of Wisconsin

text: History[edit]

text: When Wisconsin became a state, settlers from the eastern United States (known as Yankees) took issue with the consumption of alcohol by German immigrants on Sunday, as well as the prevalence of alcoholism. The Wisconsin legislature passed a law in 1849 that made liquor sellers liable for the costs incurred by local governments in supporting alcoholics. Ten years later, the state prohibited liquor sales on Sundays.[1]

text: In 1872, alcohol regulation reached new heights in the state with the passage of the Graham Law. This legislation prohibited drunkenness and the sale of alcohol to minors, and required all liquor sellers to post a $2,000 bond (more than $30,000 in 2007 U.S. dollars).[2] German-Americans fought the new law in the courts and at the ballot box. Although they lost challenges in the courts, they were able to elect a legislature friendlier to alcohol consumption. In 1874, the new lawmakers passed less restrictive laws that lowered the bond to $500, allowed Sunday liquor sales, and created certain safe havens for liquor sellers to escape liability for alcoholics.[1]

text: Alcohol consumption was banned in Wisconsin during Prohibition (1920-1933). But even before Prohibition ended, Wisconsin created work-arounds. In 1926, voters approved a referendum allowing the manufacture of beer, if not its consumption. The state repealed its law enforcing Prohibition in 1929.[3] Wisconsin Senator John J. Blaine sponsored the Act that later became the Twenty-first Amendment to the United States Constitution, ending Prohibition.[4] The state was the second to ratify the amendment on April 25, 1933.[5]

text: Retail sale of alcohol[edit]

text: State law prohibits retail sale of liquor and wine between 9:00 p.m. and 6:00 a.m., and beer between midnight and 6:00 a.m.[6] State law allows local municipalities to further restrict retail sales of alcohol, or ban the issuance of retail liquor licenses altogether.[7] Local ordinances often prohibit retail beer sale after 9:00 p.m.

text: At least two municipalities in Wisconsin prohibited the retail sale of alcohol until recently: the city of Sparta,[8][9] and the village of Ephraim.[10][11] In the April 1, 2014 Wisconsin spring election, voters in Sparta narrowly passed a referendum to allow the sale of beer and wine in groceries and convenience stores. The ban on the sale of liquor within the city remains in effect.[12] In the April 5, 2016, voters in Ephraim passed a referendum to allow the sale of beer and wine in restaurants and businesses.[13]

text: Beverage sale of alcohol[edit]

text: State law requires that bars be closed between 2:00 a.m. and 6:00 a.m. Monday through Friday and between 2:30 a.m. and 6:00 a.m. on Saturday and Sunday. Exceptions are made on New Year's Eve, when no closing is required, and for changes in Daylight Saving Time. State law does not permit municipalities to further restrict when bars must be closed.[6] Municipalities may elect, however, to prohibit the issuance of liquor licenses, making the municipality effectively dry.[7]

text: Drinking age[edit]

text: The drinking age in Wisconsin is 21. Those under the legal drinking age may be served, possess, or consume alcohol if they are with a parent, legal guardian, or spouse who is of legal drinking age.[14] Those age 18 to 20 may also possess (but not consume) alcohol as part of their employment.[6]

text: The 1983 Wisconsin Act 74, effective July 1, 1984, created a drinking age of 19. Meeting in special session at the call of the governor, the legislature enacted 1985 Wisconsin Act 337, which raised the drinking age to 21 and brought the state into compliance with the NMDA (National Minimum Drinking Age) on September 1, 1986.[15]

text: The NMDA law was amended to permit an exception for those persons who were between ages 18 and 21 on the effective date of the law. Wisconsin 19- and 20-year-olds were “grandfathered in” by this exception after enactment of Act 337. In effect, the state did not have a uniform age of 21 until September 1, 1988.[15]


document_title: Mutation

question_text: when do genetic changes to a population due to mutations become more common

text: Mutation

text: Description[edit]

text: Mutations can involve the duplication of large sections of DNA, usually through genetic recombination.[8] These duplications are a major source of raw material for evolving new genes, with tens to hundreds of genes duplicated in animal genomes every million years.[9] Most genes belong to larger gene families of shared ancestry, known as homology.[10] Novel genes are produced by several methods, commonly through the duplication and mutation of an ancestral gene, or by recombining parts of different genes to form new combinations with new functions.[11][12]

text: Here, protein domains act as modules, each with a particular and independent function, that can be mixed together to produce genes encoding new proteins with novel properties.[13] For example, the human eye uses four genes to make structures that sense light: three for cone cell or color vision and one for rod cell or night vision; all four arose from a single ancestral gene.[14] Another advantage of duplicating a gene (or even an entire genome) is that this increases engineering redundancy; this allows one gene in the pair to acquire a new function while the other copy performs the original function.[15][16] Other types of mutation occasionally create new genes from previously noncoding DNA.[17][18]

text: Changes in chromosome number may involve even larger mutations, where segments of the DNA within chromosomes break and then rearrange. For example, in the Homininae, two chromosomes fused to produce human chromosome 2; this fusion did not occur in the lineage of the other apes, and they retain these separate chromosomes.[19] In evolution, the most important role of such chromosomal rearrangements may be to accelerate the divergence of a population into new species by making populations less likely to interbreed, thereby preserving genetic differences between these populations.[20]

text: Sequences of DNA that can move about the genome, such as transposons, make up a major fraction of the genetic material of plants and animals, and may have been important in the evolution of genomes.[21] For example, more than a million copies of the Alu sequence are present in the human genome, and these sequences have now been recruited to perform functions such as regulating gene expression.[22] Another effect of these mobile DNA sequences is that when they move within a genome, they can mutate or delete existing genes and thereby produce genetic diversity.[5]

text: Nonlethal mutations accumulate within the gene pool and increase the amount of genetic variation.[23] The abundance of some genetic changes within the gene pool can be reduced by natural selection, while other "more favorable" mutations may accumulate and result in adaptive changes.

text: For example, a butterfly may produce offspring with new mutations. The majority of these mutations will have no effect; but one might change the color of one of the butterfly's offspring, making it harder (or easier) for predators to see. If this color change is advantageous, the chance of this butterfly's surviving and producing its own offspring are a little better, and over time the number of butterflies with this mutation may form a larger percentage of the population.

text: Neutral mutations are defined as mutations whose effects do not influence the fitness of an individual. These can accumulate over time due to genetic drift. It is believed that the overwhelming majority of mutations have no significant effect on an organism's fitness.[24][better source needed] Also, DNA repair mechanisms are able to mend most changes before they become permanent mutations, and many organisms have mechanisms for eliminating otherwise-permanently mutated somatic cells.

text: Beneficial mutations can improve reproductive success.[25][26]

text: History[edit]

text: Mutationism is one of several alternatives to evolution by natural selection that have existed both before and after the publication of Charles Darwin's 1859 book, On the Origin of Species. In the theory, mutation was the source of novelty, creating new forms and new species, potentially instantaneously,[27] in a sudden jump.[28] This was envisaged as driving evolution, which was limited by the supply of mutations.

text: Before Darwin, biologists commonly believed in saltationism, the possibility of large evolutionary jumps, including immediate speciation. For example, in 1822 Étienne Geoffroy Saint-Hilaire argued that species could be formed by sudden transformations, or what would later be called macromutation.[29] Darwin opposed saltation, insisting on gradualism in evolution as in geology. In 1864, Albert von Kölliker revived Geoffroy's theory.[30] In 1901 the geneticist Hugo de Vries gave the name "mutation" to seemingly new forms that suddenly arose in his experiments on the evening primrose Oenothera lamarckiana, and in the first decade of the 20th century, mutationism, or as de Vries named it mutationstheorie,[31][27] became a rival to Darwinism supported for a while by geneticists including William Bateson,[32] Thomas Hunt Morgan, and Reginald Punnett.[33][27]

text: Understanding of mutationism is clouded by the mid-20th century portrayal of the early mutationists by supporters of the modern synthesis as opponents of Darwinian evolution and rivals of the biometrics school who argued that selection operated on continuous variation. In this portrayal, mutationism was defeated by a synthesis of genetics and natural selection that supposedly started later, around 1918, with work by the mathematician Ronald Fisher.[34][35][36][37] However, the alignment of Mendelian genetics and natural selection began as early as 1902 with a paper by Udny Yule,[38] and built up with theoretical and experimental work in Europe and America. Despite the controversy, the early mutationists had by 1918 already accepted natural selection and explained continuous variation as the result of multiple genes acting on the same characteristic, such as height.[35][36]

text: Mutationism, along with other alternatives to Darwinism like Lamarckism and orthogenesis, was discarded by most biologists as they came to see that Mendelian genetics and natural selection could readily work together; mutation took its place as a source of the genetic variation essential for natural selection to work on. However, mutationism did not entirely vanish. In 1940, Richard Goldschmidt again argued for single-step speciation by macromutation, describing the organisms thus produced as "hopeful monsters", earning widespread ridicule.[39][40] In 1987, Masatoshi Nei argued controversially that evolution was often mutation-limited.[41] Modern biologists such as Douglas J. Futuyma conclude that essentially all claims of evolution driven by large mutations can be explained by Darwinian evolution.[42]

text: Causes[edit]

text: Four classes of mutations are (1) spontaneous mutations (molecular decay), (2) mutations due to error-prone replication bypass of naturally occurring DNA damage (also called error-prone translesion synthesis), (3) errors introduced during DNA repair, and (4) induced mutations caused by mutagens. Scientists may also deliberately introduce mutant sequences through DNA manipulation for the sake of scientific experimentation.

text: One 2017 study claimed that 66% of cancer-causing mutations are random, 29% are due to the environment (the studied population spanned 69 countries), and 5% are inherited.[43]

text: Spontaneous mutation[edit]

text: Spontaneous mutations occur with non-zero probability even given a healthy, uncontaminated cell. They can be characterized by the specific change:[44]

text:
Tautomerism — A base is changed by the repositioning of a hydrogen atom, altering the hydrogen bonding pattern of that base, resulting in incorrect base pairing during replication.
Depurination — Loss of a purine base (A or G) to form an apurinic site (AP site).
Deamination — Hydrolysis changes a normal base to an atypical base containing a keto group in place of the original amine group. Examples include C → U and A → HX (hypoxanthine), which can be corrected by DNA repair mechanisms; and 5MeC (5-methylcytosine) → T, which is less likely to be detected as a mutation because thymine is a normal DNA base.
Slipped strand mispairing — Denaturation of the new strand from the template during replication, followed by renaturation in a different spot ("slipping"). This can lead to insertions or deletions.

text: Error-prone replication bypass[edit]

text: There is increasing evidence that the majority of spontaneously arising mutations are due to error-prone replication (translesion synthesis) past DNA damage in the template strand. Naturally occurring oxidative DNA damages arise at least 10,000 times per cell per day in humans and 50,000 times or more per cell per day in rats.[45] In mice, the majority of mutations are caused by translesion synthesis.[46] Likewise, in yeast, Kunz et al.[47] found that more than 60% of the spontaneous single base pair substitutions and deletions were caused by translesion synthesis.

text: Errors introduced during DNA repair[edit]

text: Although naturally occurring double-strand breaks occur at a relatively low frequency in DNA, their repair often causes mutation. Non-homologous end joining (NHEJ) is a major pathway for repairing double-strand breaks. NHEJ involves removal of a few nucleotides to allow somewhat inaccurate alignment of the two ends for rejoining followed by addition of nucleotides to fill in gaps. As a consequence, NHEJ often introduces mutations.[48]

text: Induced mutation[edit]

text: Induced mutations are alterations in the gene after it has come in contact with mutagens and environmental causes.

text: Induced mutations on the molecular level can be caused by:

text:
Chemicals

Hydroxylamine
Base analogs (e.g., Bromodeoxyuridine (BrdU))
Alkylating agents (e.g., N-ethyl-N-nitrosourea (ENU)). These agents can mutate both replicating and non-replicating DNA. In contrast, a base analog can mutate the DNA only when the analog is incorporated in replicating the DNA. Each of these classes of chemical mutagens has certain effects that then lead to transitions, transversions, or deletions.
Agents that form DNA adducts (e.g., ochratoxin A)[50]
DNA intercalating agents (e.g., ethidium bromide)
DNA crosslinkers

This figure depicts the following processes of transcription, splicing, and translation of a eukaryotic gene.

Oxidative damage
Nitrous acid converts amine groups on A and C to diazo groups, altering their hydrogen bonding patterns, which leads to incorrect base pairing during replication.

Radiation

Ultraviolet light (UV) (non-ionizing radiation). Two nucleotide bases in DNA—cytosine and thymine—are most vulnerable to radiation that can change their properties. UV light can induce adjacent pyrimidine bases in a DNA strand to become covalently joined as a pyrimidine dimer. UV radiation, in particular longer-wave UVA, can also cause oxidative damage to DNA.[51]
Ionizing radiation. Exposure to ionizing radiation, such as gamma radiation, can result in mutation, possibly resulting in cancer or death.

text: Classification of types[edit]

text: By effect on structure[edit]

text: The sequence of a gene can be altered in a number of ways.[53] Gene mutations have varying effects on health depending on where they occur and whether they alter the function of essential proteins. Mutations in the structure of genes can be classified into several types.

text: Small-scale mutations[edit]

text: Small-scale mutations, affecting a gene in one or a few nucleotides, include:

text: Substitution mutations, often caused by chemicals or malfunction of DNA replication, exchange a single nucleotide for another.[54] These changes are classified as transitions or transversions.[55] Most common is the transition that exchanges a purine for a purine (A ↔ G) or a pyrimidine for a pyrimidine, (C ↔ T). A transition can be caused by nitrous acid, base mis-pairing, or mutagenic base analogs such as BrdU. Less common is a transversion, which exchanges a purine for a pyrimidine or a pyrimidine for a purine (C/T ↔ A/G). An example of a transversion is the conversion of adenine (A) into a cytosine (C). A point mutation are modifications of single base pairs of DNA or other small base pairs within a gene. A point mutation can be reversed by another point mutation, in which the nucleotide is changed back to its original state (true reversion) or by second-site reversion (a complementary mutation elsewhere that results in regained gene functionality).

text: Point mutations that occur within the protein coding region of a gene may be classified into three kinds, depending upon what the erroneous codon codes for:

text:
Silent mutations, which code for the same (or a sufficiently similar) amino acid.
Missense mutations, which code for a different amino acid.
Nonsense mutations, which code for a stop codon and can truncate the protein.

text:
Insertions add one or more extra nucleotides into the DNA. They are usually caused by transposable elements, or errors during replication of repeating elements. Insertions in the coding region of a gene may alter splicing of the mRNA (splice site mutation), or cause a shift in the reading frame (frameshift), both of which can significantly alter the gene product. Insertions can be reversed by excision of the transposable element.
(Point) deletions remove one or more nucleotides from the DNA. Like insertions, these mutations can alter the reading frame of the gene. In general, they are irreversible: Though exactly the same sequence might in theory be restored by an insertion, transposable elements able to revert a very short deletion (say 1–2 bases) in any location either are highly unlikely to exist or do not exist at all.

text: Large-scale mutations[edit]

text: Large-scale mutations in chromosomal structure include:

text:
Amplifications (or gene duplications) leading to multiple copies of all chromosomal regions, increasing the dosage of the genes located within them.
Deletions of large chromosomal regions, leading to loss of the genes within those regions.
Mutations whose effect is to juxtapose previously separate pieces of DNA, potentially bringing together separate genes to form functionally distinct fusion genes (e.g., bcr-abl). These include:

Chromosomal translocations: interchange of genetic parts from nonhomologous chromosomes.
Interstitial deletions: an intra-chromosomal deletion that removes a segment of DNA from a single chromosome, thereby apposing previously distant genes. For example, cells isolated from a human astrocytoma, a type of brain tumor, were found to have a chromosomal deletion removing sequences between the Fused in Glioblastoma (FIG) gene and the receptor tyrosine kinase (ROS), producing a fusion protein (FIG-ROS). The abnormal FIG-ROS fusion protein has constitutively active kinase activity that causes oncogenic transformation (a transformation from normal cells to cancer cells).
Chromosomal inversions: reversing the orientation of a chromosomal segment.

Loss of heterozygosity: loss of one allele, either by a deletion or a genetic recombination event, in an organism that previously had two different alleles.

text: By effect on function[edit]

text:
Loss-of-function mutations, also called inactivating mutations, result in the gene product having less or no function (being partially or wholly inactivated). When the allele has a complete loss of function (null allele), it is often called an amorph or amorphic mutation in the Muller's morphs schema. Phenotypes associated with such mutations are most often recessive. Exceptions are when the organism is haploid, or when the reduced dosage of a normal gene product is not enough for a normal phenotype (this is called haploinsufficiency).
Gain-of-function mutations, also called activating mutations, change the gene product such that its effect gets stronger (enhanced activation) or even is superseded by a different and abnormal function. When the new allele is created, a heterozygote containing the newly created allele as well as the original will express the new allele; genetically this defines the mutations as dominant phenotypes. Several of Muller's morphs correspond to gain of function, including hypermorph and neomorph. In December 2017, the U.S. government lifted a temporary ban implemented in 2014 that banned federal funding for any new "gain-of-function" experiments that enhance pathogens "such as Avian influenza, SARS and the Middle East Respiratory Syndrome or MERS viruses."[56]
Dominant negative mutations (also called antimorphic mutations) have an altered gene product that acts antagonistically to the wild-type allele. These mutations usually result in an altered molecular function (often inactive) and are characterized by a dominant or semi-dominant phenotype. In humans, dominant negative mutations have been implicated in cancer (e.g., mutations in genes p53,[57] ATM,[58] CEBPA[59] and PPARgamma[60]). Marfan syndrome is caused by mutations in the FBN1 gene, located on chromosome 15, which encodes fibrillin-1, a glycoprotein component of the extracellular matrix.[61] Marfan syndrome is also an example of dominant negative mutation and haploinsufficiency.[62][63]
Hypomorphs, after Mullerian classification, are characterized by altered gene products that acts with decreased gene expression compared to the wild type allele.
Neomorphs are characterized by the control of new protein product synthesis.
Lethal mutations are mutations that lead to the death of the organisms that carry the mutations.
A back mutation or reversion is a point mutation that restores the original sequence and hence the original phenotype.[64]

text: By effect on fitness[edit]

text: In applied genetics, it is usual to speak of mutations as either harmful or beneficial.

text:
A harmful, or deleterious, mutation decreases the fitness of the organism.
A beneficial, or advantageous mutation increases the fitness of the organism. Mutations that promotes traits that are desirable, are also called beneficial. In theoretical population genetics, it is more usual to speak of mutations as deleterious or advantageous than harmful or beneficial.
A neutral mutation has no harmful or beneficial effect on the organism. Such mutations occur at a steady rate, forming the basis for the molecular clock. In the neutral theory of molecular evolution, neutral mutations provide genetic drift as the basis for most variation at the molecular level.
A nearly neutral mutation is a mutation that may be slightly deleterious or advantageous, although most nearly neutral mutations are slightly deleterious.

text: Distribution of fitness effects[edit]

text: Attempts have been made to infer the distribution of fitness effects (DFE) using mutagenesis experiments and theoretical models applied to molecular sequence data. DFE, as used to determine the relative abundance of different types of mutations (i.e., strongly deleterious, nearly neutral or advantageous), is relevant to many evolutionary questions, such as the maintenance of genetic variation,[65] the rate of genomic decay,[66] the maintenance of outcrossing sexual reproduction as opposed to inbreeding[67] and the evolution of sex and genetic recombination.[68] In summary, the DFE plays an important role in predicting evolutionary dynamics.[69][70] A variety of approaches have been used to study the DFE, including theoretical, experimental and analytical methods.

text: Mutagenesis experiment: The direct method to investigate the DFE is to induce mutations and then measure the mutational fitness effects, which has already been done in viruses, bacteria, yeast, and Drosophila. For example, most studies of the DFE in viruses used site-directed mutagenesis to create point mutations and measure relative fitness of each mutant.[71][72][73][74] In Escherichia coli, one study used transposon mutagenesis to directly measure the fitness of a random insertion of a derivative of Tn10.[75] In yeast, a combined mutagenesis and deep sequencing approach has been developed to generate high-quality systematic mutant libraries and measure fitness in high throughput.[76] However, given that many mutations have effects too small to be detected[77] and that mutagenesis experiments can detect only mutations of moderately large effect; DNA sequence data analysis can provide valuable information about these mutations.

text: Molecular sequence analysis: With rapid development of DNA sequencing technology, an enormous amount of DNA sequence data is available and even more is forthcoming in the future. Various methods have been developed to infer the DFE from DNA sequence data.[78][79][80][81] By examining DNA sequence differences within and between species, we are able to infer various characteristics of the DFE for neutral, deleterious and advantageous mutations.[23] To be specific, the DNA sequence analysis approach allows us to estimate the effects of mutations with very small effects, which are hardly detectable through mutagenesis experiments.

text: One of the earliest theoretical studies of the distribution of fitness effects was done by Motoo Kimura, an influential theoretical population geneticist. His neutral theory of molecular evolution proposes that most novel mutations will be highly deleterious, with a small fraction being neutral.[82][83] Hiroshi Akashi more recently proposed a bimodal model for the DFE, with modes centered around highly deleterious and neutral mutations.[84] Both theories agree that the vast majority of novel mutations are neutral or deleterious and that advantageous mutations are rare, which has been supported by experimental results. One example is a study done on the DFE of random mutations in vesicular stomatitis virus.[71] Out of all mutations, 39.6% were lethal, 31.2% were non-lethal deleterious, and 27.1% were neutral. Another example comes from a high throughput mutagenesis experiment with yeast.[76] In this experiment it was shown that the overall DFE is bimodal, with a cluster of neutral mutations, and a broad distribution of deleterious mutations.

text: Though relatively few mutations are advantageous, those that are play an important role in evolutionary changes.[85] Like neutral mutations, weakly selected advantageous mutations can be lost due to random genetic drift, but strongly selected advantageous mutations are more likely to be fixed. Knowing the DFE of advantageous mutations may lead to increased ability to predict the evolutionary dynamics. Theoretical work on the DFE for advantageous mutations has been done by John H. Gillespie[86] and H. Allen Orr.[87] They proposed that the distribution for advantageous mutations should be exponential under a wide range of conditions, which, in general, has been supported by experimental studies, at least for strongly selected advantageous mutations.[88][89][90]

text: In general, it is accepted that the majority of mutations are neutral or deleterious, with rare mutations being advantageous; however, the proportion of types of mutations varies between species. This indicates two important points: first, the proportion of effectively neutral mutations is likely to vary between species, resulting from dependence on effective population size; second, the average effect of deleterious mutations varies dramatically between species.[23] In addition, the DFE also differs between coding regions and noncoding regions, with the DFE of noncoding DNA containing more weakly selected mutations.[23]

text: By impact on protein sequence[edit]

text:
A frameshift mutation is a mutation caused by insertion or deletion of a number of nucleotides that is not evenly divisible by three from a DNA sequence. Due to the triplet nature of gene expression by codons, the insertion or deletion can disrupt the reading frame, or the grouping of the codons, resulting in a completely different translation from the original.[91] The earlier in the sequence the deletion or insertion occurs, the more altered the protein produced is.

For example, the code CCU GAC UAC CUA codes for the amino acids proline, aspartic acid, tyrosine, and leucine. If the U in CCU was deleted, the resulting sequence would be CCG ACU ACC UAx, which would instead code for proline, threonine, threonine, and part of another amino acid or perhaps a stop codon (where the x stands for the following nucleotide).

text:
A nonsense mutation is a point mutation in a sequence of DNA that results in a premature stop codon, or a nonsense codon in the transcribed mRNA, and possibly a truncated, and often nonfunctional protein product. This sort of mutation has been linked to different mutations, such as congenital adrenal hyperplasia. (See Stop codon.)
Missense mutations or nonsynonymous mutations are types of point mutations where a single nucleotide is changed to cause substitution of a different amino acid. This in turn can render the resulting protein nonfunctional. Such mutations are responsible for diseases such as Epidermolysis bullosa, sickle-cell disease, and SOD1-mediated ALS.[92]
A neutral mutation is a mutation that occurs in an amino acid codon that results in the use of a different, but chemically similar, amino acid. The similarity between the two is enough that little or no change is often rendered in the protein. For example, a change from AAA to AGA will encode arginine, a chemically similar molecule to the intended lysine.
Silent mutations are mutations that do not result in a change to the amino acid sequence of a protein but do change the nucleotide sequence, unless the changed amino acid is sufficiently similar to the original. They may occur in a region that does not code for a protein, or they may occur within a codon in a manner that does not alter the final amino acid sequence. Silent mutations are also called silent substitutions, since they are not palpable changes as the changes in phenotype. The phrase silent mutation is often used interchangeably with the phrase synonymous mutation; however, synonymous mutations are a subcategory of the former, occurring only within exons (and necessarily exactly preserving the amino acid sequence of the protein). Synonymous mutations occur due to the degenerate nature of the genetic code. There can also be silent mutations in nucleotides outside of the coding regions, such as the introns, because the exact nucleotide sequence is not as crucial as it is in the coding regions.

text: By inheritance[edit]

text: In multicellular organisms with dedicated reproductive cells, mutations can be subdivided into germline mutations, which can be passed on to descendants through their reproductive cells, and somatic mutations (also called acquired mutations),[93] which involve cells outside the dedicated reproductive group and which are not usually transmitted to descendants.

text: A germline mutation gives rise to a constitutional mutation in the offspring, that is, a mutation that is present in every cell. A constitutional mutation can also occur very soon after fertilisation, or continue from a previous constitutional mutation in a parent.[94]

text: The distinction between germline and somatic mutations is important in animals that have a dedicated germline to produce reproductive cells. However, it is of little value in understanding the effects of mutations in plants, which lack dedicated germline. The distinction is also blurred in those animals that reproduce asexually through mechanisms such as budding, because the cells that give rise to the daughter organisms also give rise to that organism's germline. A new germline mutation not inherited from either parent is called a de novo mutation.

text: Diploid organisms (e.g., humans) contain two copies of each gene—a paternal and a maternal allele. Based on the occurrence of mutation on each chromosome, we may classify mutations into three types.

text:
A heterozygous mutation is a mutation of only one allele.
A homozygous mutation is an identical mutation of both the paternal and maternal alleles.
Compound heterozygous mutations or a genetic compound consists of two different mutations in the paternal and maternal alleles.[95]

text: A wild type or homozygous non-mutated organism is one in which neither allele is mutated.

text: Special classes[edit]

text:
Conditional mutation is a mutation that has wild-type (or less severe) phenotype under certain "permissive" environmental conditions and a mutant phenotype under certain "restrictive" conditions. For example, a temperature-sensitive mutation can cause cell death at high temperature (restrictive condition), but might have no deleterious consequences at a lower temperature (permissive condition).[96] These mutations are non-autonomous, as their manifestation depends upon presence of certain conditions, as opposed to other mutations which appear autonomously.[97] The permissive conditions may be temperature,[98] certain chemicals,[99] light[99] or mutations in other parts of the genome.[97] In vivo mechanisms like transcriptional switches can create conditional mutations. For instance, association of Steroid Binding Domain can create a transcriptional switch that can change the expression of a gene based on the presence of a steroid ligand.[100] Conditional mutations have applications in research as they allow control over gene expression. This is especially useful studying diseases in adults by allowing expression after a certain period of growth, thus eliminating the deleterious effect of gene expression seen during stages of development in model organisms.[99] DNA Recombinase systems like Cre-Lox Recombination used in association with promoters that are activated under certain conditions can generate conditional mutations. Dual Recombinase technology can be used to induce multiple conditional mutations to study the diseases which manifest as a result of simultaneous mutations in multiple genes.[99] Certain inteins have been identified which splice only at certain permissive temperatures, leading to improper protein synthesis and thus, loss of function mutations at other temperatures.[101] Conditional mutations may also be used in genetic studies associated with ageing, as the expression can be changed after a certain time period in the organism's lifespan.[98]
Replication timing quantitative trait loci affects DNA replication.

text: Nomenclature[edit]

text: In order to categorize a mutation as such, the "normal" sequence must be obtained from the DNA of a "normal" or "healthy" organism (as opposed to a "mutant" or "sick" one), it should be identified and reported; ideally, it should be made publicly available for a straightforward nucleotide-by-nucleotide comparison, and agreed upon by the scientific community or by a group of expert geneticists and biologists, who have the responsibility of establishing the standard or so-called "consensus" sequence. This step requires a tremendous scientific effort. Once the consensus sequence is known, the mutations in a genome can be pinpointed, described, and classified. The committee of the Human Genome Variation Society (HGVS) has developed the standard human sequence variant nomenclature,[102] which should be used by researchers and DNA diagnostic centers to generate unambiguous mutation descriptions. In principle, this nomenclature can also be used to describe mutations in other organisms. The nomenclature specifies the type of mutation and base or amino acid changes.

text:
Nucleotide substitution (e.g., 76A>T) — The number is the position of the nucleotide from the 5' end; the first letter represents the wild-type nucleotide, and the second letter represents the nucleotide that replaced the wild type. In the given example, the adenine at the 76th position was replaced by a thymine.

If it becomes necessary to differentiate between mutations in genomic DNA, mitochondrial DNA, and RNA, a simple convention is used. For example, if the 100th base of a nucleotide sequence mutated from G to C, then it would be written as g.100G>C if the mutation occurred in genomic DNA, m.100G>C if the mutation occurred in mitochondrial DNA, or r.100g>c if the mutation occurred in RNA. Note that, for mutations in RNA, the nucleotide code is written in lower case.

Amino acid substitution (e.g., D111E) — The first letter is the one letter code of the wild-type amino acid, the number is the position of the amino acid from the N-terminus, and the second letter is the one letter code of the amino acid present in the mutation. Nonsense mutations are represented with an X for the second amino acid (e.g. D111X).
Amino acid deletion (e.g., ΔF508) — The Greek letter Δ (delta) indicates a deletion. The letter refers to the amino acid present in the wild type and the number is the position from the N terminus of the amino acid were it to be present as in the wild type.

text: Mutation rates[edit]

text: Mutation rates vary substantially across species, and the evolutionary forces that generally determine mutation are the subject of ongoing investigation.

text: Harmful mutations[edit]

text: Changes in DNA caused by mutation can cause errors in protein sequence, creating partially or completely non-functional proteins. Each cell, in order to function correctly, depends on thousands of proteins to function in the right places at the right times. When a mutation alters a protein that plays a critical role in the body, a medical condition can result. Some mutations alter a gene's DNA base sequence but do not change the function of the protein made by the gene. One study on the comparison of genes between different species of Drosophila suggests that if a mutation does change a protein, this will probably be harmful, with an estimated 70 percent of amino acid polymorphisms having damaging effects, and the remainder being either neutral or weakly beneficial.[7] Studies have shown that only 7% of point mutations in noncoding DNA of yeast are deleterious and 12% in coding DNA are deleterious. The rest of the mutations are either neutral or slightly beneficial.[103]

text: If a mutation is present in a germ cell, it can give rise to offspring that carries the mutation in all of its cells. This is the case in hereditary diseases. In particular, if there is a mutation in a DNA repair gene within a germ cell, humans carrying such germline mutations may have an increased risk of cancer. A list of 34 such germline mutations is given in the article DNA repair-deficiency disorder. An example of one is albinism, a mutation that occurs in the OCA1 or OCA2 gene. Individuals with this disorder are more prone to many types of cancers, other disorders and have impaired vision. On the other hand, a mutation may occur in a somatic cell of an organism. Such mutations will be present in all descendants of this cell within the same organism, and certain mutations can cause the cell to become malignant, and, thus, cause cancer.[104]

text: A DNA damage can cause an error when the DNA is replicated, and this error of replication can cause a gene mutation that, in turn, could cause a genetic disorder. DNA damages are repaired by the DNA repair system of the cell. Each cell has a number of pathways through which enzymes recognize and repair damages in DNA. Because DNA can be damaged in many ways, the process of DNA repair is an important way in which the body protects itself from disease. Once DNA damage has given rise to a mutation, the mutation cannot be repaired. DNA repair pathways can only recognize and act on "abnormal" structures in the DNA. Once a mutation occurs in a gene sequence it then has normal DNA structure and cannot be repaired.

text: Beneficial mutations[edit]

text: Although mutations that cause changes in protein sequences can be harmful to an organism, on occasions the effect may be positive in a given environment. In this case, the mutation may enable the mutant organism to withstand particular environmental stresses better than wild-type organisms, or reproduce more quickly. In these cases a mutation will tend to become more common in a population through natural selection.

text: For example, a specific 32 base pair deletion in human CCR5 (CCR5-Δ32) confers HIV resistance to homozygotes and delays AIDS onset in heterozygotes.[105] One possible explanation of the etiology of the relatively high frequency of CCR5-Δ32 in the European population is that it conferred resistance to the bubonic plague in mid-14th century Europe. People with this mutation were more likely to survive infection; thus its frequency in the population increased.[106] This theory could explain why this mutation is not found in Southern Africa, which remained untouched by bubonic plague. A newer theory suggests that the selective pressure on the CCR5 Delta 32 mutation was caused by smallpox instead of the bubonic plague.[107]

text: An example of a harmful mutation is sickle-cell disease, a blood disorder in which the body produces an abnormal type of the oxygen-carrying substance hemoglobin in the red blood cells. One-third of all indigenous inhabitants of Sub-Saharan Africa carry the gene, because, in areas where malaria is common, there is a survival value in carrying only a single sickle-cell gene (sickle cell trait).[108] Those with only one of the two alleles of the sickle-cell disease are more resistant to malaria, since the infestation of the malaria Plasmodium is halted by the sickling of the cells that it infests.

text: Prion mutations[edit]

text: Prions are proteins and do not contain genetic material. However, prion replication has been shown to be subject to mutation and natural selection just like other forms of replication.[109] The human gene PRNP codes for the major prion protein, PrP, and is subject to mutations that can give rise to disease-causing prions.

text: Somatic mutations[edit]

text: A change in the genetic structure that is not inherited from a parent, and also not passed to offspring, is called a somatic mutation.[93] Somatic mutations are not inherited because they do not affect the germline. These types of mutations are usually prompted by environmental causes, such as ultraviolet radiation or any exposure to certain harmful chemicals, and can cause diseases including cancer.[110]

text: With plants, some somatic mutations can be bred without the need for seed production, for example, by grafting and stem cuttings. These type of mutation have led to new types of fruits, such as the "Delicious" apple and the "Washington" navel orange.[111]

text: Human and mouse somatic cells have a mutation rate more than ten times higher than the germline mutation rate for both species; mice have a higher rate of both somatic and germline mutations per cell division than humans. The disparity in mutation rate between the germline and somatic tissues likely reflects the greater importance of genome maintenance in the germline than in the soma.[112]

text: Amorphic mutations[edit]

text: An amorph, a term utilized by Muller in 1932, is a mutated allele, which has lost the ability of the parent (whether wild type or any other type) allele to encode any functional protein. An amorphic mutation may be caused by the replacement of an amino acid that deactivates an enzyme or by the deletion of part of a gene that produces the enzyme.

text: Cells with heterozygous mutations (one good copy of gene and one mutated copy) may function normally with the unmutated copy until the good copy has been spontaneously somatically mutated. This kind of mutation happens all the time in living organisms, but it is difficult to measure the rate. Measuring this rate is important in predicting the rate at which people may develop cancer.[113]

text: Point mutations may arise from spontaneous mutations that occur during DNA replication. The rate of mutation may be increased by mutagens. Mutagens can be physical, such as radiation from UV rays, X-rays or extreme heat, or chemical (molecules that misplace base pairs or disrupt the helical shape of DNA). Mutagens associated with cancers are often studied to learn about cancer and its prevention.

text: Hypomorphic and hypermorphic mutations[edit]

text: A hypomorphic mutation is a replacement of amino acids that would hinder enzyme activity, which would reduce the enzyme level but not to the point of complete loss. Usually, hypomorphic mutations are recessive, but haploinsufficiency causes some alleles to be dominant.

text: A hypermorphic mutation changes the regulation of the gene and causes it to overproduce the gene produce causing a greater than normal enzyme levels. These type of alleles are dominant gain of function type of alleles.