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Why Some DNA Is Selfish
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Uploaded: | 2021-06-03 |
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MLA Full: | "Why Some DNA Is Selfish." YouTube, uploaded by SciShow, 3 June 2021, www.youtube.com/watch?v=hixBGjM7Ld8. |
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APA Full: | SciShow. (2021, June 3). Why Some DNA Is Selfish [Video]. YouTube. https://youtube.com/watch?v=hixBGjM7Ld8 |
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SciShow, "Why Some DNA Is Selfish.", June 3, 2021, YouTube, 10:10, https://youtube.com/watch?v=hixBGjM7Ld8. |
Your DNA is a part of you, but it might not share your sense of who's numero uno.
Hosted by: Michael Aranda
SciShow has a spinoff podcast! It's called SciShow Tangents. Check it out at http://www.scishowtangents.org
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Support SciShow by becoming a patron on Patreon: https://www.patreon.com/scishow
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Huge thanks go to the following Patreon supporters for helping us keep SciShow free for everyone forever:
Silas Emrys, Drew Hart, Jeffrey Mckishen, James Knight, Christoph Schwanke, Jacob, Matt Curls, Christopher R Boucher, Eric Jensen, Adam Brainard, Nazara, GrowingViolet, Ash, Laura Sanborn, Sam Lutfi, Piya Shedden, KatieMarie Magnone, charles george, Alex Hackman, Chris Peters, Kevin Bealer, Alisa Sherbow
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Sources:
https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1007700
https://www.nature.com/articles/284604a0
http://www.sas.rochester.edu/bio/labs/WerrenLab/My%20Papers/2001_Hurst&Werren.pdf
https://www.jstor.org/stable/10.1086/656220?seq=1
https://link.springer.com/article/10.1007/s00439-012-1257-0
https://link.springer.com/protocol/10.1007/978-1-4939-9074-0_6
https://www.jci.org/articles/view/116400/pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874221/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3013285
https://link.springer.com/referenceworkentry/10.1007%2F978-3-642-16483-5_3360
https://www.genome.gov/genetics-glossary/Crossing-Over
https://embryo.asu.edu/pages/meiosis-humans
https://www.annualreviews.org/doi/abs/10.1146/annurev-genet-112618-043905
https://www.sciencedirect.com/science/article/pii/B9780123014634500061
https://pubmed.ncbi.nlm.nih.gov/23242375/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133486/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5959745/
https://www.sciencedirect.com/science/article/pii/S0960982218313642
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701898/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3338262/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1201875/pdf/519.pdf
https://www.sciencedirect.com/topics/neuroscience/selfish-dna
https://www.genetics.org/content/172/2/1309
https://bio.libretexts.org/Bookshelves/Human_Biology/Book%3A_Human_Biology_(Wakim_and_Grewal)/24%3A_Ecology/24.04%3A_Community_Relationships
https://medlineplus.gov/genetics/understanding/basics/noncodingdna/
https://www.cell.com/current-biology/comments/S0960-9822(12)01154-2
https://www.researchgate.net/publication/235907922_Largest_and_Smallest_Genome_in_the_World
https://www.theguardian.com/science/2013/feb/24/scientists-attacked-over-junk-dna-claim
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439153/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4014423/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619371/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4859970/
https://www.cell.com/cell-metabolism/pdf/S1550-4131(19)30120-2.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5857283/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7061985/
Image Sources:
https://www.storyblocks.com/video/stock/double-helical-structure-of-dna-strand-close-up-animation-s-xhcmjp8k8r4yuhn
https://www.istockphoto.com/photo/dogs-gm463752425-32802234
https://www.istockphoto.com/photo/yellow-wheat-field-gm1152174842-312490894
Hosted by: Michael Aranda
SciShow has a spinoff podcast! It's called SciShow Tangents. Check it out at http://www.scishowtangents.org
----------
Support SciShow by becoming a patron on Patreon: https://www.patreon.com/scishow
----------
Huge thanks go to the following Patreon supporters for helping us keep SciShow free for everyone forever:
Silas Emrys, Drew Hart, Jeffrey Mckishen, James Knight, Christoph Schwanke, Jacob, Matt Curls, Christopher R Boucher, Eric Jensen, Adam Brainard, Nazara, GrowingViolet, Ash, Laura Sanborn, Sam Lutfi, Piya Shedden, KatieMarie Magnone, charles george, Alex Hackman, Chris Peters, Kevin Bealer, Alisa Sherbow
----------
Looking for SciShow elsewhere on the internet?
Facebook: http://www.facebook.com/scishow
Twitter: http://www.twitter.com/scishow
Tumblr: http://scishow.tumblr.com
Instagram: http://instagram.com/thescishow
----------
Sources:
https://journals.plos.org/plosgenetics/article?id=10.1371/journal.pgen.1007700
https://www.nature.com/articles/284604a0
http://www.sas.rochester.edu/bio/labs/WerrenLab/My%20Papers/2001_Hurst&Werren.pdf
https://www.jstor.org/stable/10.1086/656220?seq=1
https://link.springer.com/article/10.1007/s00439-012-1257-0
https://link.springer.com/protocol/10.1007/978-1-4939-9074-0_6
https://www.jci.org/articles/view/116400/pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2874221/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3013285
https://link.springer.com/referenceworkentry/10.1007%2F978-3-642-16483-5_3360
https://www.genome.gov/genetics-glossary/Crossing-Over
https://embryo.asu.edu/pages/meiosis-humans
https://www.annualreviews.org/doi/abs/10.1146/annurev-genet-112618-043905
https://www.sciencedirect.com/science/article/pii/B9780123014634500061
https://pubmed.ncbi.nlm.nih.gov/23242375/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133486/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5959745/
https://www.sciencedirect.com/science/article/pii/S0960982218313642
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701898/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3338262/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1201875/pdf/519.pdf
https://www.sciencedirect.com/topics/neuroscience/selfish-dna
https://www.genetics.org/content/172/2/1309
https://bio.libretexts.org/Bookshelves/Human_Biology/Book%3A_Human_Biology_(Wakim_and_Grewal)/24%3A_Ecology/24.04%3A_Community_Relationships
https://medlineplus.gov/genetics/understanding/basics/noncodingdna/
https://www.cell.com/current-biology/comments/S0960-9822(12)01154-2
https://www.researchgate.net/publication/235907922_Largest_and_Smallest_Genome_in_the_World
https://www.theguardian.com/science/2013/feb/24/scientists-attacked-over-junk-dna-claim
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439153/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4014423/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619371/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4859970/
https://www.cell.com/cell-metabolism/pdf/S1550-4131(19)30120-2.pdf
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5857283/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7061985/
Image Sources:
https://www.storyblocks.com/video/stock/double-helical-structure-of-dna-strand-close-up-animation-s-xhcmjp8k8r4yuhn
https://www.istockphoto.com/photo/dogs-gm463752425-32802234
https://www.istockphoto.com/photo/yellow-wheat-field-gm1152174842-312490894
[intro ].
For decades, some scientists and authors have argued that your genes are out for only themselves, even though they are... part of you. But, like, your genes are in your cells.
So, if natural selection is any guide, your well-being should be their top priority. However, according to the selfish view, genes are driven to survive. And their need to survive causes them to make organisms do everything from mating to eating.
So how are they betraying you from within? Well, whether or not all genes are selfish is up for debate. But in recent decades, scientists have discovered that some DNA really is selfish.
In fact, it’s so selfish it does whatever it can to multiply, even if that doesn’t help or even if it actually hurts its host. They’re like the roommate who doesn’t pay rent and also breaks your stuff. These rogue genetic elements might be calling the shots in your cells right now.
And while they may be causing you harm, they also made humans and other organisms what they are today. There are a few different types of selfish genetic elements, each with their own tricks to subvert the rules. One trickster DNA sequence is called transposable elements or transposons.
They’re found in a huge variety of organisms. And they’re considered selfish because they can jump around the genome. Let’s unpack that idea for a bit.
You can think of your genome as a book that provides instructions. And each of your genes is like a single sentence in that book. Now, imagine some of those sentences could say, “I don’t want to be in chapter 3.
I want to be in chapter 1.” And then they moved.~ That’d be selfish, because the sentence doesn’t care about the integrity of the whole book. Just itself. That’s basically what transposons do.
These so-called jumping genes are categorized into two types. Class I transposons, also known as retrotransposons, jump around by copying and pasting themselves. Class II transposable elements are similar, but they cut and paste instead of copy.
They actually snip themselves out and insert themselves in another spot. Now, cells can silence or reduce the activity of transposable elements, like by sticking certain molecules onto the DNA to keep it in check. So a lot of the time these jumping genes don’t cause any problems.
And genomes seem to tolerate them. In fact, up to 80% of the genomes of many animals and plants are made of transposable elements. Which is a pretty big chunk of a genome.
For example, a kind of retrotransposon known as LINE-1 elements make up 17% of the genomes of humans and some other mammals. Most LINE-1 elements never wake up and do their thing -- they’re almost like fossils. But researchers think some LINE-1s are highly active, and that they play a role in disease.
These selfish genes have been linked to cancer, hemophilia, and age-related conditions like neurodegeneration. In a 2019 study published in Cell Metabolism, researchers wanted to investigate the role of LINE-1s in age-related disease. So, they looked at mice bred to lack a gene that’s thought to help cells resist wear and tear.
These mice tend to experience remarkably premature aging. The researchers found that these mice showed higher LINE-1 activity and damaging inflammation in their cells. But when the scientists curbed the activity of these selfish genetic elements, the mice fared a lot better.
That brings us to another kind of selfish
DNA: segregation distorters. These genetic elements interfere with the process of making sex cells so they become overrepresented in cells like sperm and eggs. It’s like stuffing the ballot box with lots of votes for themselves, while preventing other votes from getting in. Sex cells like sperm and eggs are called gametes.
The process of making them through cell division is meiosis. And here’s how it’s supposed to work. Humans have two sets of 23 chromosomes, one from each parent.
Meiosis starts with a two-set cell, which duplicates its genome and results in one big fat cell with two identical sets of two chromosomes. Then they split into two daughter cells, and split again into two more daughter cells to make four sperm cells. The process is the same for egg cells except three of the resulting four cells are scrapped, leaving one plump ovum.
Each gamete ends up with different combinations of genetic material from each would-be grandparent. But the general rule is that DNA from either grandparent has an equal chance of making it into a gamete each time meiosis happens. There are a few ways segregation distorters mess with this rule, and it’s been observed in several organisms.
Like, some chromosomes with selfish genetic elements can control their movement during egg formation and ensure they end up in the one cell that doesn’t get sacked. And segregation distorters called killer meiotic drivers go one step further:. They detonate any gamete that they don’t make it into.
Some of these DNA villains are linked up with a gene that encodes a toxin... and only they have the antidote. Any cells that don’t get the distorter gene and its antidote get poisoned and die. It’s a cell-eat-cell world out there.
One type of these killers has been observed in mice. These meiotic drivers aim poison at sperm cells’ tails, which are in charge of paddling the sperm to the egg cell. Sperm that don’t inherit the killer and its antidote can’t swim.
So they can’t fertilize the egg and get passed on. Killer meiotic drivers have also been observed in insects. A 2018 study in the journal Current Biology looked at genetic sequences from booklice and found that females with a distorter in their sex chromosomes never have sons.
So, if that distorter gene became common enough, females could run out of males to mate with. This scenario has been modeled in a few lab experiments in which groups of insects have wiped themselves out. Though it hasn’t been observed in the wild so far.
Genetic elements that seem like segregation distorters have also been observed in humans. But scientists are still teasing out the details about what they are and what impact they might be having. At least they don’t think we’re at risk of going the same way as booklice.
All of this explains why some scientists compare selfish genes to parasites. These genes hang out in their hosts and take advantage of them, sometimes causing harm. And the fact that they’re so successful at replicating and competing means there are a lot of them.
Which is why some scientists think they might hold a clue to the mystery of so-called junk DNA. For decades, scientists have grappled with a conundrum:. Why does the majority of the human genome not seem to do anything?
The best-known function of DNA is to code for proteins. But most of our DNA doesn’t do that. So scientists have nicknamed this seemingly useless stuff junk DNA.
Shockingly, around 98% of the human genome is non-coding. Even weirder, the genome of a particular single-celled amoeba is 100 times bigger than ours. Some researchers have suggested that selfish genetic elements can explain the mismatch between genome size and the perceived complexity of organisms.
Basically, they argue that much of that so-called junk DNA is also selfish DNA. And it’s simply there because that’s what selfish DNA does — take up as much space as it can without contributing. But whether this junk DNA is really junk has been a matter of extremely heated debate.
In 2012, results were published from an international research effort called ENCODE, which aimed to identify all the functional genetic elements in the human genome. They suggested that up to 80% of the human genome isn’t junk at all -- that is has some function. They also proposed that selfish genetic elements that were once non-functional can gain function.
We know that non-coding DNA performs lots of regulatory functions, like directing genes to turn on or off. So, if so-called junk or selfish DNA is performing important management functions, then it’s not actually junk, and maybe it’s not really selfish. But not everyone accepts these global claims of “function,” so a lot more research is needed before we can say for sure.
But scientists are fairly sure that selfish genetic elements have inadvertently driven evolution. See, there are cases in animals where a transposable element squeezing into place has been associated with changes that didn’t have terrible consequences. Like in dogs, which have the most diverse traits among land mammals, from the lanky bodies of some breeds to the lengthy snouts of others.
Scientists think that transposable elements in mammals like dogs provide lots of raw material for evolution to act on. For instance, research has suggested that mutations in these long sequences can affect traits like the patterns on their coats. ~. And they may make a difference in human immunity.
A 2020 study suggested that transposons contribute to the activation of multiple genes involved in human white blood cells fighting off common infections. Another arguably good deed of selfish DNA is that it may have played a role in driving the emergence of different species. Researchers have suggested that selfish genes, and the organism’s attempts to fight back, can evolve together and contribute to reproductive isolation, or the prevention of interbreeding between populations.
Basically, if you have a selfish gene, you may also have an unselfish one evolve alongside it to suppress it and prevent bad stuff like toxicity from happening. That can happen in one population but not another, making them gradually more distinct from one another. This is especially apparent to plant breeders working with crops like maize, wheat, and rice.
When two purebred crops are crossed, seeds that inherit a selfish element without the corresponding suppressor will actually die. Meaning they can’t interbreed on their own.~ And populations separating from one another is how you get new species! So there you have it.
Selfish genetic elements started out being thought of as genetic oddities with little significance. And now they’re considered major players in the diversity and function of life on Earth as we know it. It all goes to show that, in life, you sometimes have to take the bad and the ugly with the good.
Selfish genetic elements are associated with disease and potential extinction, which is pretty unsettling. But also, if selfish DNA makes us what we are, and it makes dogs what they are, which is awesome, then we’ll take the creepy with the cute. Thanks for watching this episode of SciShow.
If you like what we do, and want to help us do more of it, you can become a channel member. All you have to do is click the join link below this video, and you’ll get access to some fun perks, plus bragging rights. And if you’re already a member, thanks so much for your support. [ outro ].
For decades, some scientists and authors have argued that your genes are out for only themselves, even though they are... part of you. But, like, your genes are in your cells.
So, if natural selection is any guide, your well-being should be their top priority. However, according to the selfish view, genes are driven to survive. And their need to survive causes them to make organisms do everything from mating to eating.
So how are they betraying you from within? Well, whether or not all genes are selfish is up for debate. But in recent decades, scientists have discovered that some DNA really is selfish.
In fact, it’s so selfish it does whatever it can to multiply, even if that doesn’t help or even if it actually hurts its host. They’re like the roommate who doesn’t pay rent and also breaks your stuff. These rogue genetic elements might be calling the shots in your cells right now.
And while they may be causing you harm, they also made humans and other organisms what they are today. There are a few different types of selfish genetic elements, each with their own tricks to subvert the rules. One trickster DNA sequence is called transposable elements or transposons.
They’re found in a huge variety of organisms. And they’re considered selfish because they can jump around the genome. Let’s unpack that idea for a bit.
You can think of your genome as a book that provides instructions. And each of your genes is like a single sentence in that book. Now, imagine some of those sentences could say, “I don’t want to be in chapter 3.
I want to be in chapter 1.” And then they moved.~ That’d be selfish, because the sentence doesn’t care about the integrity of the whole book. Just itself. That’s basically what transposons do.
These so-called jumping genes are categorized into two types. Class I transposons, also known as retrotransposons, jump around by copying and pasting themselves. Class II transposable elements are similar, but they cut and paste instead of copy.
They actually snip themselves out and insert themselves in another spot. Now, cells can silence or reduce the activity of transposable elements, like by sticking certain molecules onto the DNA to keep it in check. So a lot of the time these jumping genes don’t cause any problems.
And genomes seem to tolerate them. In fact, up to 80% of the genomes of many animals and plants are made of transposable elements. Which is a pretty big chunk of a genome.
For example, a kind of retrotransposon known as LINE-1 elements make up 17% of the genomes of humans and some other mammals. Most LINE-1 elements never wake up and do their thing -- they’re almost like fossils. But researchers think some LINE-1s are highly active, and that they play a role in disease.
These selfish genes have been linked to cancer, hemophilia, and age-related conditions like neurodegeneration. In a 2019 study published in Cell Metabolism, researchers wanted to investigate the role of LINE-1s in age-related disease. So, they looked at mice bred to lack a gene that’s thought to help cells resist wear and tear.
These mice tend to experience remarkably premature aging. The researchers found that these mice showed higher LINE-1 activity and damaging inflammation in their cells. But when the scientists curbed the activity of these selfish genetic elements, the mice fared a lot better.
That brings us to another kind of selfish
DNA: segregation distorters. These genetic elements interfere with the process of making sex cells so they become overrepresented in cells like sperm and eggs. It’s like stuffing the ballot box with lots of votes for themselves, while preventing other votes from getting in. Sex cells like sperm and eggs are called gametes.
The process of making them through cell division is meiosis. And here’s how it’s supposed to work. Humans have two sets of 23 chromosomes, one from each parent.
Meiosis starts with a two-set cell, which duplicates its genome and results in one big fat cell with two identical sets of two chromosomes. Then they split into two daughter cells, and split again into two more daughter cells to make four sperm cells. The process is the same for egg cells except three of the resulting four cells are scrapped, leaving one plump ovum.
Each gamete ends up with different combinations of genetic material from each would-be grandparent. But the general rule is that DNA from either grandparent has an equal chance of making it into a gamete each time meiosis happens. There are a few ways segregation distorters mess with this rule, and it’s been observed in several organisms.
Like, some chromosomes with selfish genetic elements can control their movement during egg formation and ensure they end up in the one cell that doesn’t get sacked. And segregation distorters called killer meiotic drivers go one step further:. They detonate any gamete that they don’t make it into.
Some of these DNA villains are linked up with a gene that encodes a toxin... and only they have the antidote. Any cells that don’t get the distorter gene and its antidote get poisoned and die. It’s a cell-eat-cell world out there.
One type of these killers has been observed in mice. These meiotic drivers aim poison at sperm cells’ tails, which are in charge of paddling the sperm to the egg cell. Sperm that don’t inherit the killer and its antidote can’t swim.
So they can’t fertilize the egg and get passed on. Killer meiotic drivers have also been observed in insects. A 2018 study in the journal Current Biology looked at genetic sequences from booklice and found that females with a distorter in their sex chromosomes never have sons.
So, if that distorter gene became common enough, females could run out of males to mate with. This scenario has been modeled in a few lab experiments in which groups of insects have wiped themselves out. Though it hasn’t been observed in the wild so far.
Genetic elements that seem like segregation distorters have also been observed in humans. But scientists are still teasing out the details about what they are and what impact they might be having. At least they don’t think we’re at risk of going the same way as booklice.
All of this explains why some scientists compare selfish genes to parasites. These genes hang out in their hosts and take advantage of them, sometimes causing harm. And the fact that they’re so successful at replicating and competing means there are a lot of them.
Which is why some scientists think they might hold a clue to the mystery of so-called junk DNA. For decades, scientists have grappled with a conundrum:. Why does the majority of the human genome not seem to do anything?
The best-known function of DNA is to code for proteins. But most of our DNA doesn’t do that. So scientists have nicknamed this seemingly useless stuff junk DNA.
Shockingly, around 98% of the human genome is non-coding. Even weirder, the genome of a particular single-celled amoeba is 100 times bigger than ours. Some researchers have suggested that selfish genetic elements can explain the mismatch between genome size and the perceived complexity of organisms.
Basically, they argue that much of that so-called junk DNA is also selfish DNA. And it’s simply there because that’s what selfish DNA does — take up as much space as it can without contributing. But whether this junk DNA is really junk has been a matter of extremely heated debate.
In 2012, results were published from an international research effort called ENCODE, which aimed to identify all the functional genetic elements in the human genome. They suggested that up to 80% of the human genome isn’t junk at all -- that is has some function. They also proposed that selfish genetic elements that were once non-functional can gain function.
We know that non-coding DNA performs lots of regulatory functions, like directing genes to turn on or off. So, if so-called junk or selfish DNA is performing important management functions, then it’s not actually junk, and maybe it’s not really selfish. But not everyone accepts these global claims of “function,” so a lot more research is needed before we can say for sure.
But scientists are fairly sure that selfish genetic elements have inadvertently driven evolution. See, there are cases in animals where a transposable element squeezing into place has been associated with changes that didn’t have terrible consequences. Like in dogs, which have the most diverse traits among land mammals, from the lanky bodies of some breeds to the lengthy snouts of others.
Scientists think that transposable elements in mammals like dogs provide lots of raw material for evolution to act on. For instance, research has suggested that mutations in these long sequences can affect traits like the patterns on their coats. ~. And they may make a difference in human immunity.
A 2020 study suggested that transposons contribute to the activation of multiple genes involved in human white blood cells fighting off common infections. Another arguably good deed of selfish DNA is that it may have played a role in driving the emergence of different species. Researchers have suggested that selfish genes, and the organism’s attempts to fight back, can evolve together and contribute to reproductive isolation, or the prevention of interbreeding between populations.
Basically, if you have a selfish gene, you may also have an unselfish one evolve alongside it to suppress it and prevent bad stuff like toxicity from happening. That can happen in one population but not another, making them gradually more distinct from one another. This is especially apparent to plant breeders working with crops like maize, wheat, and rice.
When two purebred crops are crossed, seeds that inherit a selfish element without the corresponding suppressor will actually die. Meaning they can’t interbreed on their own.~ And populations separating from one another is how you get new species! So there you have it.
Selfish genetic elements started out being thought of as genetic oddities with little significance. And now they’re considered major players in the diversity and function of life on Earth as we know it. It all goes to show that, in life, you sometimes have to take the bad and the ugly with the good.
Selfish genetic elements are associated with disease and potential extinction, which is pretty unsettling. But also, if selfish DNA makes us what we are, and it makes dogs what they are, which is awesome, then we’ll take the creepy with the cute. Thanks for watching this episode of SciShow.
If you like what we do, and want to help us do more of it, you can become a channel member. All you have to do is click the join link below this video, and you’ll get access to some fun perks, plus bragging rights. And if you’re already a member, thanks so much for your support. [ outro ].