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MLA Full: "Why Are All Humans Unique? Meiosis: 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). Why Are All Humans Unique? Meiosis: Crash Course Biology #30 [Video]. YouTube. https://youtube.com/watch?v=pj1oFx42d48
APA Inline: (CrashCourse, 2024)
Chicago Full: CrashCourse, "Why Are All Humans Unique? Meiosis: 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

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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!