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Intro to Genetics: Why Your Cat Looks Like That: Crash Course Biology #31
YouTube: | https://youtube.com/watch?v=YnJPbphsoMY |
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Duration: | 11:48 |
Uploaded: | 2024-02-20 |
Last sync: | 2024-12-21 07:45 |
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MLA Full: | "Intro to Genetics: Why Your Cat Looks Like That: Crash Course Biology #31." YouTube, uploaded by CrashCourse, 20 February 2024, www.youtube.com/watch?v=YnJPbphsoMY. |
MLA Inline: | (CrashCourse, 2024) |
APA Full: | CrashCourse. (2024, February 20). Intro to Genetics: Why Your Cat Looks Like That: Crash Course Biology #31 [Video]. YouTube. https://youtube.com/watch?v=YnJPbphsoMY |
APA Inline: | (CrashCourse, 2024) |
Chicago Full: |
CrashCourse, "Intro to Genetics: Why Your Cat Looks Like That: Crash Course Biology #31.", February 20, 2024, YouTube, 11:48, https://youtube.com/watch?v=YnJPbphsoMY. |
How do traits get passed down in our DNA? And what do genes have to do with cat fur? In this episode of Crash Course Biology, we’ll untangle the simplest patterns of inheritance, and reassure our redheaded friends—you’re not going anywhere.
Chapters:
Are Redheads Going Extinct? 00:00
Alleles & Traits 1:32
Patterns of Inheritance 4:50
Autosomal Dominance 5:56
Incomplete Dominance 7:51
Codominance 8:47
Review & Credits 10:20
This series was produced in collaboration with HHMI BioInteractive, committed to empowering educators and inspiring students with engaging, accessible, and quality classroom resources. Visit https://BioInteractive.org/CrashCourse for more information.
Are you an educator looking for what NGSS Standards are covered in this episode? Check out our Educator Standards Database for Biology here: https://www.thecrashcourse.com/biologystandards
Check out our Biology playlist here: https://www.youtube.com/playlist?list=PL8dPuuaLjXtPW_ofbxdHNciuLoTRLPMgB
Watch this series in Spanish on our Crash Course en Español channel here: https://www.youtube.com/playlist?list=PLkcbA0DkuFjWQZzjwF6w_gUrE_5_d3vd3
Sources: https://docs.google.com/document/d/1GLDtAXE6ekg4Chk2qN3TYbNt0pJbyaHqTqRd6QY8pd4/edit?usp=sharing
Chapters:
Are Redheads Going Extinct? 00:00
Alleles & Traits 1:32
Patterns of Inheritance 4:50
Autosomal Dominance 5:56
Incomplete Dominance 7:51
Codominance 8:47
Review & Credits 10:20
This series was produced in collaboration with HHMI BioInteractive, committed to empowering educators and inspiring students with engaging, accessible, and quality classroom resources. Visit https://BioInteractive.org/CrashCourse for more information.
Are you an educator looking for what NGSS Standards are covered in this episode? Check out our Educator Standards Database for Biology here: https://www.thecrashcourse.com/biologystandards
Check out our Biology playlist here: https://www.youtube.com/playlist?list=PL8dPuuaLjXtPW_ofbxdHNciuLoTRLPMgB
Watch this series in Spanish on our Crash Course en Español channel here: https://www.youtube.com/playlist?list=PLkcbA0DkuFjWQZzjwF6w_gUrE_5_d3vd3
Sources: https://docs.google.com/document/d/1GLDtAXE6ekg4Chk2qN3TYbNt0pJbyaHqTqRd6QY8pd4/edit?usp=sharing
Are we in the middle of a redhead mass extinction?
Headlines like this tend to surface every few years, fretting that the rare ginger genes are getting rarer. But are we really watching the final embers of the fiery-haired flame? Well, hold onto your Ed Sheerans, rumors of their demise have been greatly exaggerated. Sure, if you could pull a hundred random strangers into a room, it’s likely only a few of them will have red hair. And true, red hair mostly happens only when a baby gets two copies of the red-hair gene variant — which, yeah, is pretty rare. But good news: The gene variant also exists in people without red hair. In fact, it can pass on, hidden, for generations, until the stars align, literal ginger syzygy, and it meets up with a second red-hair gene variant.
That’s why, sometimes, two non-redheads can have a baby with a shock of flaming hair. And unless every single person with the gene variant vanishes, the redheads of the world aren’t going anywhere. We know this thanks to the study of how genes get passed down across generations, and a healthy understanding of how this happens can help us avoid these kinds of sensationalized stories—that’s right, today we’re breaking out our Punnett squares and talking about genetics. Hi, I’m Dr. Sammy, your friendly neighborhood entomologist, and this is Crash Course Biology. Ehm, Ed, Reba, Flo, y’all gonna hit us with that funky theme music? [THEME MUSIC]
So, let’s talk about genes – sorry, not those jeans, these genes – individualized sections of DNA on the chromosomes of cells.
Chromosomes are the long strands of genetic material in our cell nuclei—typically, humans have 46 in total, or 23 pairs of two—but genes are the segments along those chromosomes that are used to carry instructions. Humans have over twenty thousand spread across our 46 chromosomes. Every living thing has them, and some way more than others. Like the nearly microscopic freshwater flea, which clocks its gene count at over thirty thousand. Most genes carry specific instructions for making molecules called proteins. When those instructions get read — in a process called gene expression — they shape how an organism looks and functions. You see, each gene comes in different versions, called alleles, which determine an organism's different traits — like, the shape of a seed or a person’s blood type. Whenever we talk about versions, or variants, of genes, we’re talking about alleles; scientists just tend to use the phrases interchangeably. And the reason we don’t all look like clones of each other is that we all have different versions of the same genes, these alleles.
We call an organism’s complete collection of alleles its genotype, which accounts for its entire genetic makeup. Meanwhile, the phenotype describes all the traits that we can observe in an organism. So your genotype might include the alleles for both a long big toe and a short big toe, but you present with a short big toe so that’s the one that’s part of your phenotype. Most traits are determined by more than one gene. Like, there is no single gene out there that determines the shape of your nose structure or your height. Those traits arise from several different alleles interacting with each other, like a bunch of protein-making puppeteers—which I guess sort of makes us all elaborate muppets. Which, I’m cool with by the way. [SINGS] Can you tell me how to get...how to get to Sesame street? So it’s not exactly like that, my desire to meet Elmo aside. But, it is true that not every gene gets expressed in every cell. Cells are always collaborating and communicating, making sure that the right genes turn on in the right place. And while the stuff going on inside is important, factors outside the body, like the environment, can also affect an organism's traits. Take the buckeye butterfly for example.
Buckeyes that hatch during long summer days have light tan wings as part of their phenotype, but those that hatch during shorter fall days have darker red wings. See, the darker wings of autumn buckeyes absorb heat, raising their body temperature so that they can still fly, while lighter wings help the summer babies stay cool. A buckeye’s alleles contain the potential for both shades, but their environment—specifically the temperature and day-length when they’re born—shapes how those genes are expressed.
Now, because humans and a lot of other species reproduce sexually, the offspring’s genetic code ends up a unique mix of their parents’. That’s what happens when an egg and a sperm come together, each containing one set of all of their parents’ genes—one allele for each, so that they end up with two alleles for each gene. Sorry if that ruined any illusions of stork-based delivery for ya. The offspring inherits a unique combination of alleles from both parents. Same genes, but different versions, and different chromosomes of a matching pair. And the interactions of those alleles—and in many cases the organism's environment—affect the traits that ultimately get expressed. We call the way traits pass from generation to generation patterns of inheritance. Most traits come together almost like mosaics — from multiple genes interacting with the environment.
But some are determined by simpler patterns. Take for example the length of a cat’s fur. It’s determined by a single gene called “fibroblast growth factor 5,” or FGF5. There are a number of allele variants of FGF5, including four different long-hair alleles.
But to keep it simple today, we’ll lump them together as one. Think of this big L here as a short-hair allele, and it’s what we call dominant. When the two alleles meet, the dominant allele is the loudest, so it drowns out the little L here, which is the recessive long-hair allele. It only takes one dominant allele for a cat to have short hair. But for long hair, a cat needs two quieter, recessive copies. When one allele completely overrides the other, we call that autosomal dominance.
You might also hear this called Mendelian inheritance — named after Gregor Mendel, a monk who first described this pattern in pea plants over 150 years ago. So, let’s take a look at how this pattern of inheritance actually works. Meet Mortimer. He has short hair, white markings like a tuxedo, and loves long naps in the sun. A real prince, this guy.
And this is Bagel. She’s got long orange fur, razor-sharp claws, and a penchant for spilling coffee on keyboards. You wouldn’t believe how many electronics she’s destroyed, how much blood we’ve lost, or how much we love her. Anyway, opposites attract. And we happen to know Mortimer has one dominant short hair allele, masking one long hair allele. That makes him heterozygous; which means he carries two different alleles for the hair length gene. But fluffy Bagel has two recessive alleles, so she’s homozygous, genetics-speak for samesies: having two matching alleles, either both recessive or both dominant.
And because we know our cats’ genotypes, we can predict the genotypic and phenotypic ratios of their hypothetical kittens. That’s their probability of inheriting different allele combinations, and therefore having long locks versus sleek fur. We can map out the odds with this chart called a Punnett square. There’s a fifty percent chance that Mortimer and Bagel’s kitten will inherit one copy of each allele, making it heterozygous dominant. The dominant big “L” talks over the recessive little “l,” giving it a short hair phenotype. You wouldn’t even know the kitten has the long-hair allele by looking at it. But there’s also a fifty percent chance a kitten turns out homozygous recessive, inheriting a little “l” from Bagel and a little “l” from Mortimer. Putting a one hundred percent chance of floof in the forecast. But if Mortimer has two copies of the dominant allele, then there’s no way around it: this kitten will be bound for short hair. [CHAPTER 5 - INCOMPLETE DOMINANCE] Sometimes, one allele doesn’t completely overshadow the other, and instead they blend together in what we call incomplete dominance.
This can lead to an expressed trait that’s a mix of the traits associated with each allele. Like, let’s say that the white in Mortimer’s little tuxedo and Bagel’s socks are determined by an incompletely dominant allele for white spots. A cat with big “S” alleles will be mostly covered in white. But in a heterozygous cat with just one copy, the white patches will cover less than half of its body. And since Mortimer and Bagel are both heterozygous for spots, their kitten has a twenty-five percent chance of inheriting two dominant alleles and being mostly white—and the same odds of inheriting two recessive alleles and being spotless. But if I were a gambler, I’d put my bet on it being heterozygous like its parents. There’s a fifty percent chance of that, and a one hundred percent chance of it being adorable.
Sometimes, instead of mixing together, traits linked to two alleles show up separately in what’s called codominance: Kind of like wearing a Hawaiian shirt and a sequined jumpsuit. They’re both jostling for attention. Calico cats — with their blotches of orange and black fur — owe their looks in part to codominance. But they’ve got another pattern of inheritance going on at the same time, called sex-linked inheritance. That’s where a gene is carried on only one of the chromosomes that influences an organism’s sex.
For most mammals, sex chromosomes come in two versions, X or Y. But a cool and important thing to know: XY is /not/ the only system out there. And some organisms don’t have sexes at all. Anyway, in the XY system, an organism with two X chromosomes usually develops as female, while an organism with an X and a Y usually develops as male. So when a gene shows up on the X chromosome and not the Y, its traits will show up at different rates in females and males.
Now back to those calico kitties. A color gene on cats’ X chromosome comes in two alleles: an orange version (XB) and a black version (Xb). If a kitten inherits both alleles (XBXb), each cell only expresses one at a time. So the fur ends up looking like Joseph’s Technicolor Dreamcoat. It’s more straightforward for the XY carrier, who gets only one X chromosome. Inherit one allele, and it’s orange fur; inherit the other, and it’s black. That’s why calico cats are almost always XX. And while codominance isn’t always dependent on sex, it is in the case of calico kitties.
There is so much we can learn by studying genetics. It helps us understand how traits are passed from parent to offspring, why some cats are orange and others are black, and why we don’t have to worry about running out of redheads anytime soon. But it also helps us on a much larger scale, from creating more sustainable agriculture to designing better medicine. Our genes are the first gift our parents ever gave us, instructions that made you, you. And we can trace some basic patterns of inheritance by understanding how dominant and recessive alleles interact. But it goes even deeper than that.
Most traits aren’t just a matter of one allele talking over the other. They’re the result of an ongoing conversation between the stuff in your chromosomes and the stuff around them — multiple alleles, multiple genes, and your whole environment. But we’ll learn more about that next time. Peace!
This series was produced in collaboration with HHMI BioInteractive. If you’re an educator, visit BioInteractive.org/CrashCourse for classroom resources and professional development related to the topics covered in this course. Thanks for watching this episode of Crash Course Biology, which was filmed at our studio in Indianapolis, Indiana, and was made with the help of all these nice people.
If you want to help keep Crash Course free for everyone, forever, you can join our community on Patreon.
Headlines like this tend to surface every few years, fretting that the rare ginger genes are getting rarer. But are we really watching the final embers of the fiery-haired flame? Well, hold onto your Ed Sheerans, rumors of their demise have been greatly exaggerated. Sure, if you could pull a hundred random strangers into a room, it’s likely only a few of them will have red hair. And true, red hair mostly happens only when a baby gets two copies of the red-hair gene variant — which, yeah, is pretty rare. But good news: The gene variant also exists in people without red hair. In fact, it can pass on, hidden, for generations, until the stars align, literal ginger syzygy, and it meets up with a second red-hair gene variant.
That’s why, sometimes, two non-redheads can have a baby with a shock of flaming hair. And unless every single person with the gene variant vanishes, the redheads of the world aren’t going anywhere. We know this thanks to the study of how genes get passed down across generations, and a healthy understanding of how this happens can help us avoid these kinds of sensationalized stories—that’s right, today we’re breaking out our Punnett squares and talking about genetics. Hi, I’m Dr. Sammy, your friendly neighborhood entomologist, and this is Crash Course Biology. Ehm, Ed, Reba, Flo, y’all gonna hit us with that funky theme music? [THEME MUSIC]
So, let’s talk about genes – sorry, not those jeans, these genes – individualized sections of DNA on the chromosomes of cells.
Chromosomes are the long strands of genetic material in our cell nuclei—typically, humans have 46 in total, or 23 pairs of two—but genes are the segments along those chromosomes that are used to carry instructions. Humans have over twenty thousand spread across our 46 chromosomes. Every living thing has them, and some way more than others. Like the nearly microscopic freshwater flea, which clocks its gene count at over thirty thousand. Most genes carry specific instructions for making molecules called proteins. When those instructions get read — in a process called gene expression — they shape how an organism looks and functions. You see, each gene comes in different versions, called alleles, which determine an organism's different traits — like, the shape of a seed or a person’s blood type. Whenever we talk about versions, or variants, of genes, we’re talking about alleles; scientists just tend to use the phrases interchangeably. And the reason we don’t all look like clones of each other is that we all have different versions of the same genes, these alleles.
We call an organism’s complete collection of alleles its genotype, which accounts for its entire genetic makeup. Meanwhile, the phenotype describes all the traits that we can observe in an organism. So your genotype might include the alleles for both a long big toe and a short big toe, but you present with a short big toe so that’s the one that’s part of your phenotype. Most traits are determined by more than one gene. Like, there is no single gene out there that determines the shape of your nose structure or your height. Those traits arise from several different alleles interacting with each other, like a bunch of protein-making puppeteers—which I guess sort of makes us all elaborate muppets. Which, I’m cool with by the way. [SINGS] Can you tell me how to get...how to get to Sesame street? So it’s not exactly like that, my desire to meet Elmo aside. But, it is true that not every gene gets expressed in every cell. Cells are always collaborating and communicating, making sure that the right genes turn on in the right place. And while the stuff going on inside is important, factors outside the body, like the environment, can also affect an organism's traits. Take the buckeye butterfly for example.
Buckeyes that hatch during long summer days have light tan wings as part of their phenotype, but those that hatch during shorter fall days have darker red wings. See, the darker wings of autumn buckeyes absorb heat, raising their body temperature so that they can still fly, while lighter wings help the summer babies stay cool. A buckeye’s alleles contain the potential for both shades, but their environment—specifically the temperature and day-length when they’re born—shapes how those genes are expressed.
Now, because humans and a lot of other species reproduce sexually, the offspring’s genetic code ends up a unique mix of their parents’. That’s what happens when an egg and a sperm come together, each containing one set of all of their parents’ genes—one allele for each, so that they end up with two alleles for each gene. Sorry if that ruined any illusions of stork-based delivery for ya. The offspring inherits a unique combination of alleles from both parents. Same genes, but different versions, and different chromosomes of a matching pair. And the interactions of those alleles—and in many cases the organism's environment—affect the traits that ultimately get expressed. We call the way traits pass from generation to generation patterns of inheritance. Most traits come together almost like mosaics — from multiple genes interacting with the environment.
But some are determined by simpler patterns. Take for example the length of a cat’s fur. It’s determined by a single gene called “fibroblast growth factor 5,” or FGF5. There are a number of allele variants of FGF5, including four different long-hair alleles.
But to keep it simple today, we’ll lump them together as one. Think of this big L here as a short-hair allele, and it’s what we call dominant. When the two alleles meet, the dominant allele is the loudest, so it drowns out the little L here, which is the recessive long-hair allele. It only takes one dominant allele for a cat to have short hair. But for long hair, a cat needs two quieter, recessive copies. When one allele completely overrides the other, we call that autosomal dominance.
You might also hear this called Mendelian inheritance — named after Gregor Mendel, a monk who first described this pattern in pea plants over 150 years ago. So, let’s take a look at how this pattern of inheritance actually works. Meet Mortimer. He has short hair, white markings like a tuxedo, and loves long naps in the sun. A real prince, this guy.
And this is Bagel. She’s got long orange fur, razor-sharp claws, and a penchant for spilling coffee on keyboards. You wouldn’t believe how many electronics she’s destroyed, how much blood we’ve lost, or how much we love her. Anyway, opposites attract. And we happen to know Mortimer has one dominant short hair allele, masking one long hair allele. That makes him heterozygous; which means he carries two different alleles for the hair length gene. But fluffy Bagel has two recessive alleles, so she’s homozygous, genetics-speak for samesies: having two matching alleles, either both recessive or both dominant.
And because we know our cats’ genotypes, we can predict the genotypic and phenotypic ratios of their hypothetical kittens. That’s their probability of inheriting different allele combinations, and therefore having long locks versus sleek fur. We can map out the odds with this chart called a Punnett square. There’s a fifty percent chance that Mortimer and Bagel’s kitten will inherit one copy of each allele, making it heterozygous dominant. The dominant big “L” talks over the recessive little “l,” giving it a short hair phenotype. You wouldn’t even know the kitten has the long-hair allele by looking at it. But there’s also a fifty percent chance a kitten turns out homozygous recessive, inheriting a little “l” from Bagel and a little “l” from Mortimer. Putting a one hundred percent chance of floof in the forecast. But if Mortimer has two copies of the dominant allele, then there’s no way around it: this kitten will be bound for short hair. [CHAPTER 5 - INCOMPLETE DOMINANCE] Sometimes, one allele doesn’t completely overshadow the other, and instead they blend together in what we call incomplete dominance.
This can lead to an expressed trait that’s a mix of the traits associated with each allele. Like, let’s say that the white in Mortimer’s little tuxedo and Bagel’s socks are determined by an incompletely dominant allele for white spots. A cat with big “S” alleles will be mostly covered in white. But in a heterozygous cat with just one copy, the white patches will cover less than half of its body. And since Mortimer and Bagel are both heterozygous for spots, their kitten has a twenty-five percent chance of inheriting two dominant alleles and being mostly white—and the same odds of inheriting two recessive alleles and being spotless. But if I were a gambler, I’d put my bet on it being heterozygous like its parents. There’s a fifty percent chance of that, and a one hundred percent chance of it being adorable.
Sometimes, instead of mixing together, traits linked to two alleles show up separately in what’s called codominance: Kind of like wearing a Hawaiian shirt and a sequined jumpsuit. They’re both jostling for attention. Calico cats — with their blotches of orange and black fur — owe their looks in part to codominance. But they’ve got another pattern of inheritance going on at the same time, called sex-linked inheritance. That’s where a gene is carried on only one of the chromosomes that influences an organism’s sex.
For most mammals, sex chromosomes come in two versions, X or Y. But a cool and important thing to know: XY is /not/ the only system out there. And some organisms don’t have sexes at all. Anyway, in the XY system, an organism with two X chromosomes usually develops as female, while an organism with an X and a Y usually develops as male. So when a gene shows up on the X chromosome and not the Y, its traits will show up at different rates in females and males.
Now back to those calico kitties. A color gene on cats’ X chromosome comes in two alleles: an orange version (XB) and a black version (Xb). If a kitten inherits both alleles (XBXb), each cell only expresses one at a time. So the fur ends up looking like Joseph’s Technicolor Dreamcoat. It’s more straightforward for the XY carrier, who gets only one X chromosome. Inherit one allele, and it’s orange fur; inherit the other, and it’s black. That’s why calico cats are almost always XX. And while codominance isn’t always dependent on sex, it is in the case of calico kitties.
There is so much we can learn by studying genetics. It helps us understand how traits are passed from parent to offspring, why some cats are orange and others are black, and why we don’t have to worry about running out of redheads anytime soon. But it also helps us on a much larger scale, from creating more sustainable agriculture to designing better medicine. Our genes are the first gift our parents ever gave us, instructions that made you, you. And we can trace some basic patterns of inheritance by understanding how dominant and recessive alleles interact. But it goes even deeper than that.
Most traits aren’t just a matter of one allele talking over the other. They’re the result of an ongoing conversation between the stuff in your chromosomes and the stuff around them — multiple alleles, multiple genes, and your whole environment. But we’ll learn more about that next time. Peace!
This series was produced in collaboration with HHMI BioInteractive. If you’re an educator, visit BioInteractive.org/CrashCourse for classroom resources and professional development related to the topics covered in this course. Thanks for watching this episode of Crash Course Biology, which was filmed at our studio in Indianapolis, Indiana, and was made with the help of all these nice people.
If you want to help keep Crash Course free for everyone, forever, you can join our community on Patreon.