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Meiosis: Why Are All Humans Unique?: Crash Course Biology #30
YouTube: | https://youtube.com/watch?v=pj1oFx42d48 |
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Duration: | 12:50 |
Uploaded: | 2024-02-13 |
Last sync: | 2024-09-27 07:00 |
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MLA Full: | "Meiosis: Why Are All Humans Unique?: Crash Course Biology #30." YouTube, uploaded by CrashCourse, 13 February 2024, www.youtube.com/watch?v=pj1oFx42d48. |
MLA Inline: | (CrashCourse, 2024) |
APA Full: | CrashCourse. (2024, February 13). Meiosis: Why Are All Humans Unique?: Crash Course Biology #30 [Video]. YouTube. https://youtube.com/watch?v=pj1oFx42d48 |
APA Inline: | (CrashCourse, 2024) |
Chicago Full: |
CrashCourse, "Meiosis: Why Are All Humans Unique?: Crash Course Biology #30.", February 13, 2024, YouTube, 12:50, https://youtube.com/watch?v=pj1oFx42d48. |
Ever wonder why we aren’t exact clones of our parents, or why siblings aren’t exactly alike? The reason traces back to meiosis. In this episode of Crash Course Biology, we’ll discover how egg and sperm cells get made and learn why you’re a totally unique remix of your parents’ DNA.
Introduction: Why Are We All Unique? 0:00
Gametes 1:33
Meiosis 4:09
The Phases of Meiosis 4:44
Nondisjunction 7:14
Why We Aren't Clones 8:18
Meiosis & Genetic Diversity 9:49
Review & Credits 11:32
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.
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
***
Crash Course is on Patreon! You can support us directly by signing up at http://www.patreon.com/crashcourse
Thanks to the following patrons for their generous monthly contributions that help keep Crash Course free for everyone forever:
David Fanska, Andrew Woods, Sean Saunders, DL Singfield, Ken Davidian, Stephen Akuffo, Toni Miles, Steve Segreto, Kyle & Katherine Callahan, Laurel Stevens, Burt Humburg, Aziz Y, Perry Joyce, Scott Harrison, Mark & Susan Billian, Alan Bridgeman, Breanna Bosso, Matt Curls, Jennifer Killen, Starstuff42, Jon Allen, Sarah & Nathan Catchings, team dorsey, Bernardo Garza, Trevin Beattie, Eric Koslow, Indija-ka Siriwardena, Jason Rostoker, Siobhán, Ken Penttinen, Nathan Taylor, Barrett & Laura Nuzum, Les Aker, William McGraw, Vaso, ClareG, Rizwan Kassim, Constance Urist, Alex Hackman, pinapples of solidarity, Katie Dean, Stephen McCandless, Thomas Greinert, Wai Jack Sin, Ian Dundore, Caleb Weeks
__
Want to find Crash Course elsewhere on the internet?
Instagram - https://www.instagram.com/thecrashcourse/
Facebook - http://www.facebook.com/YouTubeCrashCourse
Twitter - http://www.twitter.com/TheCrashCourse
CC Kids: http://www.youtube.com/crashcoursekids
Introduction: Why Are We All Unique? 0:00
Gametes 1:33
Meiosis 4:09
The Phases of Meiosis 4:44
Nondisjunction 7:14
Why We Aren't Clones 8:18
Meiosis & Genetic Diversity 9:49
Review & Credits 11:32
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.
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
***
Crash Course is on Patreon! You can support us directly by signing up at http://www.patreon.com/crashcourse
Thanks to the following patrons for their generous monthly contributions that help keep Crash Course free for everyone forever:
David Fanska, Andrew Woods, Sean Saunders, DL Singfield, Ken Davidian, Stephen Akuffo, Toni Miles, Steve Segreto, Kyle & Katherine Callahan, Laurel Stevens, Burt Humburg, Aziz Y, Perry Joyce, Scott Harrison, Mark & Susan Billian, Alan Bridgeman, Breanna Bosso, Matt Curls, Jennifer Killen, Starstuff42, Jon Allen, Sarah & Nathan Catchings, team dorsey, Bernardo Garza, Trevin Beattie, Eric Koslow, Indija-ka Siriwardena, Jason Rostoker, Siobhán, Ken Penttinen, Nathan Taylor, Barrett & Laura Nuzum, Les Aker, William McGraw, Vaso, ClareG, Rizwan Kassim, Constance Urist, Alex Hackman, pinapples of solidarity, Katie Dean, Stephen McCandless, Thomas Greinert, Wai Jack Sin, Ian Dundore, Caleb Weeks
__
Want to find Crash Course elsewhere on the internet?
Instagram - https://www.instagram.com/thecrashcourse/
Facebook - http://www.facebook.com/YouTubeCrashCourse
Twitter - http://www.twitter.com/TheCrashCourse
CC Kids: http://www.youtube.com/crashcoursekids
There’s nobody else in the world exactly like you.
Not your sibling, not your third grade classmate who copied everything you did. Not even comically evil alternate universe you…at least hypothetically. But, how?
I mean, if we’re all made of the same biological stuff as not only each other, but also E. coli, then…how is it that we turn out genetically unique? [as Papa Sammy] Well…buckle up, Sport. Hopefully this isn’t your first time hearing this but you were brought into the world by sexual reproduction. And sexual reproduction…doesn’t make clones — no matter how much people tell you that you have your mother’s nose. See, even identical twins have a bunch of slight genetic variations.
Instead of making clones, sexual reproduction combines genetic information from two organisms, with each contributing half their genome. Which results in offspring with a remix of both parents’ DNA. This remix is made by some reproductive DJ cells called gametes, which carry genes from one generation to the next. And to produce gametes, we need a special type of cell division: meiosis. Hi, I’m Papa Sammy, your friendly neighborhood bug dad, and this is Crash Course Biology. Yooooo DJ Gamete, hit me with that stanky theme music! [THEME MUSIC] [As Dr. Sammy] Thanks, Dad.
When a cell reaches the stage in its life cycle where it needs to create more cells, most of the time it does a little division dance called mitosis. The dance has several steps, but essentially, copied DNA splits apart, eventually parting ways into twin cells. This copy-and-paste process means that most of our cells contain identical copies of all of our genes, neatly packaged into bundles called chromosomes. But those gorgeous gametes are different.
For starters, they form in just one part of the body: the gamete-making factories called the gonads. In humans, the female gamete — which is called the ova or egg — gets made in a gonad called the ovary. The male gamete, called the sperm, forms in gonads called the spermary, just kidding they’re called testes. But there’s another big reason gametes are unlike any other cells in your body. See, most of your cells are diploid, meaning “double.” Diploid cells contain two pairs a pair of each chromosome, and each of those pairs is homologous – which means they’re matching, but not identical.
In humans, that adds up to 23 pairs, and 46 chromosomes in all. Homologous chromosomes are a lot like shoes. If you have a pair of Chucks, you’ve got a left one and a right one — matching, but not identical. That makes them homologous. If you had a pair of the same right-footed Chucks, those would be identical, but not matching.
So, not homologous – and also not comfortable. And just like I need more than a pair of Chucks for a functioning foot wardrobe, you need homologous versions of each type of chromosome to make your cells functional. But gametes are different! Sperm and egg cells need to be single and ready to mingle. They need to fuse with another gamete during sexual reproduction. So they’re haploid—meaning they contain half of each homologous pair and a full set of genes but only one copy (or allele) of each gene.
That way, when one gamete meets another, they can join forces to make a baby with the complete number of chromosomes. Since it takes two different gametes, a sperm and an egg, to make a baby, they have to be haploid. If they were diploid, and contained the full set of chromosomes each, the fertilized egg would end up with twice as many chromosomes as it needs. And since different species have different numbers of chromosomes, most can’t reproduce outside of their own kind. Like, ducks tend to have 80 chromosomes, and turtles, depending on the species, have between 28 and 66.
So they could never produce viable offspring. Just one of the many reasons why we’ll never have real-life turtle-ducks. But how do our bodies—and for that matter, ducks, turtles, and everything else that reproduces sexually—make cells with half the normal number of chromosomes? Well, to get our gametes game on, we’ve got to wrench those homologous pairs apart in a process called meiosis.
While similar to the process of mitosis, meiosis is a double round of cell division that produces four new haploid cells after each cycle. It starts with a special reproductive cell, called a germ cell. The germ cell hangs out in the gonads, making one copy of each of its chromosomes. Once all of those copies are made, meiosis is ready to begin. It’s broken down into two stages, meiosis I and meiosis II, and each stage contains five phases of activity: prophase, metaphase, anaphase, telophase, and cytokinesis. Back in the mitosis episode, we used “Pass me a taco, chef” to remember these phases.
And it works for meiosis as well. It all starts with Prophase I, when each copied chromosome pairs off with its homologous match—so, left shoes with right shoes. Sometimes at this point, the chromosomes swap sections of DNA by exchanging alleles, which are like different flavors of a gene.
This process is called, dramatically enough, crossing over. And it’s super important because when and if these cells get passed onto offspring, that exchange of alleles helps ensure genetic diversity. I’ll get back to that in a moment. Next up is Metaphase I, when long fibers called spindles start reaching out to the chromosomes “hey, ummm I just saw you at the metaphase plate and I just thought I’d reach out”.
These spindles pull the chromosomes into a row across the cell’s center at random, until they look like they’re ready for a line dance. Cha cha now y’all! Then, in Anaphase I, the spindle tugs the chromosome pairs apart, so they’re now on opposite ends of the cell, clustering into two separate, randomized bunches.
Then, with Telophase I, a membrane seals each group into a separate nucleus. All animal, plant, and fungal cells have these nuclei that contain their chromosomes. So, this is the step in division where the offspring cells are starting to actually look like cells.
Cytokinesis takes over at that point, pinching the groups off into two separate cells, each new cell with only half the chromosomes the original cell started with. In Meiosis II, the five phases roughly repeat. The chromosomes clump together in Prophase II. But because the homologous pairs already split, there’s nobody to pair off with this time.
Metaphase II lines those lone chromosomes up across the center of both cells once more, until Anaphase II wrenches them in half. Their halves drift to opposite ends of both cells so that Telophase II can wrap them into four separate nuclei. Then cytokinesis pinches the jelly-ish stuff around those nuclei, until we end up with four separate haploid cells. Each has some—but not all—of the same DNA, and the gamete gambit is complete. Most of the time, meiosis runs smoothly.
But sometimes, chromosomes fail to split apart at the right phase. We call this nondisjunction. When it occurs, gametes end up with extra or fewer chromosome copies than usual.
Those gametes could still merge with another gamete that has the usual haploid number. And that fertilized cell can even sometimes develop into living offspring. But the offspring will have a different number of chromosomes than what’s typical for their species. Often they’ll have traits associated with those extra or missing chromosomes. Other times, though, the math just doesn’t work out, and the fertilized cell doesn’t develop at all.
In humans, one of the most widely known examples of a chromosomal condition brought on by nondisjunction is Down syndrome, which is caused by an extra copy of chromosome 21. In this case, Down syndrome comes with visible signifiers. But sometimes, having an extra copy of a chromosome doesn’t cause any noticeable change. For instance, people with trisomy X have an extra copy of the X chromosome, and for many, it results in no symptoms.
At this point you might be thinking, “Wow, there’s a lot that goes into this meiosis business. Somehow making an identical clone of yourself sounds easier than this sexual reproduction thing!” After all, some corners of the kingdom of life do simply clone themselves when they reproduce. We’ll get into more of that in episode 47. But there’s an evolutionary reason we aren’t all just carbon copies of our parents.
And it all comes back to our old friend genetic diversity, evolution’s way of not putting all your eggs in one basket. At the species level, having babies with different DNA is kind of like selling multiple kinds of chips in your corner store. Like, you could sell only Cheddar & Sour Cream Ruffles. I mean why not, they have it all!
As a chip, cheddar and sour cream is living its best life! But then you’re really banking on the cheddar and sour cream fans, and you’re in dire straits if tastes change or there’s suddenly a massive shortage. But if you also stock Cool Ranch Doritos, salt and vinegar chips, and Fuego Takis for good measure, you appeal to broader tastes. And it’s more likely your store stays in business.
Anyway, there’s a similar evolutionary strategy going on with genetically unique offspring. Meiosis mixes and splits DNA, making gametes that are ready to combine chromosomes with other gametes. That keeps things spicy—but more importantly, it sustains genetic diversity. Having offspring that aren’t exactly like you increases the odds that some of them will be able to survive, reproduce, and pass on their genes — even if surprises pop up in the environment.
Meiosis actually has a few different tricks for ensuring genetic diversity. Like, remember how crossing over sometimes happens during Prophase I? Homologous pairs swap sections of chromosomes, like I trade Pokémon. By the way, I’m looking for a shiny Scyther if anybody’s got the hook-up.
Except chromosomes are actually trading alleles from both parents. So when each pair splits, the individual chromosomes have a totally new combination of both parents’ DNA. That’s because not only are gametes different from the starting cell, but they’re also all different from each other, even if they started from the same cell.
Genetic variation is also helped along by the aimlessness of the process during Prophase I. When chromosome pairs line up across the center of the cell, preparing to shift to either side, the direction that these pairs line up is random. And, the direction one pair takes doesn’t influence any other; we call that independent assortment.
Even when meiosis is over, random fertilization keeps building on that potential for variation. This describes the randomness of which particular egg ends up fusing with which particular sperm. Myths about “the fastest” swimmers fertilizing the egg aren’t true. In fact, the fertilization process is basically a giant lottery—it’s mostly down to chance.
And in humans, the particular combination of chromosomes in that egg and that sperm each represent just one of eight million possible arrangements. That’s not even counting any additional unique combinations that might have happened during crossing over. And when egg and sperm combine, those possibilities compound. You’re not just one in a million.
You’re one in…64 trillion, give or take a few. Without meiosis, you wouldn’t be you. Gametes are the only meiosis-made cells in our bodies, and it’s because of that process that you’re not a clone.
You’re unique. So even if you end up with your mom’s nose, or your dad’s debonair smile, thanks to that random recombination of genetic material, your DNA test says you’re 100 percent that bae! And if you think meiosis was a wild ride, just wait until we dig into genetics and start learning how alleles get expressed in traits.
But that’s next time, until then, 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. [As Papa Sammy] 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 folks right here, very nice people.
Now if you want to help keep Crash Course free for everybody, all over the place, you can join our community on Patreon. All right bye now, I’ll see y’all later. Don't you be a stranger now!
Not your sibling, not your third grade classmate who copied everything you did. Not even comically evil alternate universe you…at least hypothetically. But, how?
I mean, if we’re all made of the same biological stuff as not only each other, but also E. coli, then…how is it that we turn out genetically unique? [as Papa Sammy] Well…buckle up, Sport. Hopefully this isn’t your first time hearing this but you were brought into the world by sexual reproduction. And sexual reproduction…doesn’t make clones — no matter how much people tell you that you have your mother’s nose. See, even identical twins have a bunch of slight genetic variations.
Instead of making clones, sexual reproduction combines genetic information from two organisms, with each contributing half their genome. Which results in offspring with a remix of both parents’ DNA. This remix is made by some reproductive DJ cells called gametes, which carry genes from one generation to the next. And to produce gametes, we need a special type of cell division: meiosis. Hi, I’m Papa Sammy, your friendly neighborhood bug dad, and this is Crash Course Biology. Yooooo DJ Gamete, hit me with that stanky theme music! [THEME MUSIC] [As Dr. Sammy] Thanks, Dad.
When a cell reaches the stage in its life cycle where it needs to create more cells, most of the time it does a little division dance called mitosis. The dance has several steps, but essentially, copied DNA splits apart, eventually parting ways into twin cells. This copy-and-paste process means that most of our cells contain identical copies of all of our genes, neatly packaged into bundles called chromosomes. But those gorgeous gametes are different.
For starters, they form in just one part of the body: the gamete-making factories called the gonads. In humans, the female gamete — which is called the ova or egg — gets made in a gonad called the ovary. The male gamete, called the sperm, forms in gonads called the spermary, just kidding they’re called testes. But there’s another big reason gametes are unlike any other cells in your body. See, most of your cells are diploid, meaning “double.” Diploid cells contain two pairs a pair of each chromosome, and each of those pairs is homologous – which means they’re matching, but not identical.
In humans, that adds up to 23 pairs, and 46 chromosomes in all. Homologous chromosomes are a lot like shoes. If you have a pair of Chucks, you’ve got a left one and a right one — matching, but not identical. That makes them homologous. If you had a pair of the same right-footed Chucks, those would be identical, but not matching.
So, not homologous – and also not comfortable. And just like I need more than a pair of Chucks for a functioning foot wardrobe, you need homologous versions of each type of chromosome to make your cells functional. But gametes are different! Sperm and egg cells need to be single and ready to mingle. They need to fuse with another gamete during sexual reproduction. So they’re haploid—meaning they contain half of each homologous pair and a full set of genes but only one copy (or allele) of each gene.
That way, when one gamete meets another, they can join forces to make a baby with the complete number of chromosomes. Since it takes two different gametes, a sperm and an egg, to make a baby, they have to be haploid. If they were diploid, and contained the full set of chromosomes each, the fertilized egg would end up with twice as many chromosomes as it needs. And since different species have different numbers of chromosomes, most can’t reproduce outside of their own kind. Like, ducks tend to have 80 chromosomes, and turtles, depending on the species, have between 28 and 66.
So they could never produce viable offspring. Just one of the many reasons why we’ll never have real-life turtle-ducks. But how do our bodies—and for that matter, ducks, turtles, and everything else that reproduces sexually—make cells with half the normal number of chromosomes? Well, to get our gametes game on, we’ve got to wrench those homologous pairs apart in a process called meiosis.
While similar to the process of mitosis, meiosis is a double round of cell division that produces four new haploid cells after each cycle. It starts with a special reproductive cell, called a germ cell. The germ cell hangs out in the gonads, making one copy of each of its chromosomes. Once all of those copies are made, meiosis is ready to begin. It’s broken down into two stages, meiosis I and meiosis II, and each stage contains five phases of activity: prophase, metaphase, anaphase, telophase, and cytokinesis. Back in the mitosis episode, we used “Pass me a taco, chef” to remember these phases.
And it works for meiosis as well. It all starts with Prophase I, when each copied chromosome pairs off with its homologous match—so, left shoes with right shoes. Sometimes at this point, the chromosomes swap sections of DNA by exchanging alleles, which are like different flavors of a gene.
This process is called, dramatically enough, crossing over. And it’s super important because when and if these cells get passed onto offspring, that exchange of alleles helps ensure genetic diversity. I’ll get back to that in a moment. Next up is Metaphase I, when long fibers called spindles start reaching out to the chromosomes “hey, ummm I just saw you at the metaphase plate and I just thought I’d reach out”.
These spindles pull the chromosomes into a row across the cell’s center at random, until they look like they’re ready for a line dance. Cha cha now y’all! Then, in Anaphase I, the spindle tugs the chromosome pairs apart, so they’re now on opposite ends of the cell, clustering into two separate, randomized bunches.
Then, with Telophase I, a membrane seals each group into a separate nucleus. All animal, plant, and fungal cells have these nuclei that contain their chromosomes. So, this is the step in division where the offspring cells are starting to actually look like cells.
Cytokinesis takes over at that point, pinching the groups off into two separate cells, each new cell with only half the chromosomes the original cell started with. In Meiosis II, the five phases roughly repeat. The chromosomes clump together in Prophase II. But because the homologous pairs already split, there’s nobody to pair off with this time.
Metaphase II lines those lone chromosomes up across the center of both cells once more, until Anaphase II wrenches them in half. Their halves drift to opposite ends of both cells so that Telophase II can wrap them into four separate nuclei. Then cytokinesis pinches the jelly-ish stuff around those nuclei, until we end up with four separate haploid cells. Each has some—but not all—of the same DNA, and the gamete gambit is complete. Most of the time, meiosis runs smoothly.
But sometimes, chromosomes fail to split apart at the right phase. We call this nondisjunction. When it occurs, gametes end up with extra or fewer chromosome copies than usual.
Those gametes could still merge with another gamete that has the usual haploid number. And that fertilized cell can even sometimes develop into living offspring. But the offspring will have a different number of chromosomes than what’s typical for their species. Often they’ll have traits associated with those extra or missing chromosomes. Other times, though, the math just doesn’t work out, and the fertilized cell doesn’t develop at all.
In humans, one of the most widely known examples of a chromosomal condition brought on by nondisjunction is Down syndrome, which is caused by an extra copy of chromosome 21. In this case, Down syndrome comes with visible signifiers. But sometimes, having an extra copy of a chromosome doesn’t cause any noticeable change. For instance, people with trisomy X have an extra copy of the X chromosome, and for many, it results in no symptoms.
At this point you might be thinking, “Wow, there’s a lot that goes into this meiosis business. Somehow making an identical clone of yourself sounds easier than this sexual reproduction thing!” After all, some corners of the kingdom of life do simply clone themselves when they reproduce. We’ll get into more of that in episode 47. But there’s an evolutionary reason we aren’t all just carbon copies of our parents.
And it all comes back to our old friend genetic diversity, evolution’s way of not putting all your eggs in one basket. At the species level, having babies with different DNA is kind of like selling multiple kinds of chips in your corner store. Like, you could sell only Cheddar & Sour Cream Ruffles. I mean why not, they have it all!
As a chip, cheddar and sour cream is living its best life! But then you’re really banking on the cheddar and sour cream fans, and you’re in dire straits if tastes change or there’s suddenly a massive shortage. But if you also stock Cool Ranch Doritos, salt and vinegar chips, and Fuego Takis for good measure, you appeal to broader tastes. And it’s more likely your store stays in business.
Anyway, there’s a similar evolutionary strategy going on with genetically unique offspring. Meiosis mixes and splits DNA, making gametes that are ready to combine chromosomes with other gametes. That keeps things spicy—but more importantly, it sustains genetic diversity. Having offspring that aren’t exactly like you increases the odds that some of them will be able to survive, reproduce, and pass on their genes — even if surprises pop up in the environment.
Meiosis actually has a few different tricks for ensuring genetic diversity. Like, remember how crossing over sometimes happens during Prophase I? Homologous pairs swap sections of chromosomes, like I trade Pokémon. By the way, I’m looking for a shiny Scyther if anybody’s got the hook-up.
Except chromosomes are actually trading alleles from both parents. So when each pair splits, the individual chromosomes have a totally new combination of both parents’ DNA. That’s because not only are gametes different from the starting cell, but they’re also all different from each other, even if they started from the same cell.
Genetic variation is also helped along by the aimlessness of the process during Prophase I. When chromosome pairs line up across the center of the cell, preparing to shift to either side, the direction that these pairs line up is random. And, the direction one pair takes doesn’t influence any other; we call that independent assortment.
Even when meiosis is over, random fertilization keeps building on that potential for variation. This describes the randomness of which particular egg ends up fusing with which particular sperm. Myths about “the fastest” swimmers fertilizing the egg aren’t true. In fact, the fertilization process is basically a giant lottery—it’s mostly down to chance.
And in humans, the particular combination of chromosomes in that egg and that sperm each represent just one of eight million possible arrangements. That’s not even counting any additional unique combinations that might have happened during crossing over. And when egg and sperm combine, those possibilities compound. You’re not just one in a million.
You’re one in…64 trillion, give or take a few. Without meiosis, you wouldn’t be you. Gametes are the only meiosis-made cells in our bodies, and it’s because of that process that you’re not a clone.
You’re unique. So even if you end up with your mom’s nose, or your dad’s debonair smile, thanks to that random recombination of genetic material, your DNA test says you’re 100 percent that bae! And if you think meiosis was a wild ride, just wait until we dig into genetics and start learning how alleles get expressed in traits.
But that’s next time, until then, 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. [As Papa Sammy] 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 folks right here, very nice people.
Now if you want to help keep Crash Course free for everybody, all over the place, you can join our community on Patreon. All right bye now, I’ll see y’all later. Don't you be a stranger now!