Junk DNA... It's a Thing
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- čas přidán 21. 08. 2024
- The concept of junk DNA - the notion that some portion of the genomes of every organism is non-functional - has been around for over 60 years. And yet, many people, including some biologists, don't seem to understand it. In this video, I review the history of the concept, including framing junk DNA in an ecological and population genetic lens, demonstrating that it's virtually guaranteed to exist. We also take a deep dive into the infamous ENCODE controversy, discussing notions of biological function, and the many methodological, statistical, and conceptual errors of the consortium.
• The Onion Test & Genom...
#junkdna #evolution #education
Links to @CreationMyths ongoing feud with the Discovery Institute over junk DNA:
• DEBATE: Is the Human G...
• The Discovery Institut...
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References and further reading:
Graur, D., Zheng, Y., Price, N., Azevedo, R. B., Zufall, R. A., & Elhaik, E. (2013). On the immortality of television sets: “function” in the human genome according to the evolution-free gospel of ENCODE. Genome biology and evolution, 5(3), 578-590. (academic.oup.c...)
Palazzo, A. F., & Gregory, T. R. (2014). The case for junk DNA. PLoS genetics, 10(5), e1004351. (journals.plos....)
Doolittle, W. F. (2013). Is junk DNA bunk? A critique of ENCODE. Proceedings of the National Academy of Sciences, 110(14), 5294-5300. (www.pnas.org/d...)
Kellis, M., Wold, B., Snyder, M. P., Bernstein, B. E., Kundaje, A., Marinov, G. K., ... & Hardison, R. C. (2014). Defining functional DNA elements in the human genome. Proceedings of the National Academy of Sciences, 111(17), 6131-6138. (www.pnas.org/d...)
Lynch, M., & Marinov, G. K. (2015). The bioenergetic costs of a gene. Proceedings of the National Academy of Sciences, 112(51), 15690-15695. (www.pnas.org/d...)
Lynch, M., & Conery, J. S. (2003). The origins of genome complexity. science, 302(5649), 1401-1404. (doi.org/10.112...)
Ohno, S (1972). So much "junk" DNA in our genome. Brookhaven Symposia in Biology. 23: 366-70.
Moran, L. A. (2023). What's in Your Genome?: 90% of Your Genome Is Junk. University of Toronto Press.
The segment about bacteria essentially being pigeonholed into simplicity by selection itself was super interesting and thought provoking. Makes me even more curious about the exact conditions surrounding the origins of more complex cells
Well, bacteria didn't evolve into more complex cells. The consensus view is that bacteria entered the simple archaea cells and evolved into the specialized organelles we see in eukaryotes today.
This is a fantastic, thorough explanation! I just finished reading Moran's "What's in your genome?" and this was a delicious dessert to that.
I am one of those with molecular genetics training and virtually no population genetics training beyond HWE. I have a newfound appreciation of the field because of your channel. Keep these bangers comin'!
We're born too late to explore the planet, born to early to explore the universe, but we're born just in time to explore the wild frontiers of the creationist blogosphere.
We're the lucky ones.
Just took an undergrad genomics course, senior/grad level, and I didnt know much of what was being discussed, especially in the first part. Thanks for the amazing lecture!
Super video again, Sir. I will have to rewatch it, but for sure its worth the time. Have you ever thought of dividing it up into smaller sections? Could help digesting it. Anyway: great work, thank you!
Wow, absolutely fantastic video. I learned so much. And just in time, as I am working on a video about ERVs myself!
Zach, what a great video. Your grasp of the history, the interplay between biologists and biochemists, along with your popgen expertise is so valuable. You need to write a book or two! ;)
Not just excellent, a basically perfect introduction to the topic, Zach!
I'm really looking forward to your video!
I've recently read Larry Moran's book on the topic
Great video!
Very very minor technical issue: the audio levels of your mic and the intro music are a bit off: I got a bit of a jump-scare when the music started 😅
One of the reasons I gave up creationism was the overwhelming amount of transposable elements. I got my PhD and lost my God.
@@TeatimeMindfulness some gave up evolution due to order and planning of cellular systems, I wonder whose reason is more fundamental.
@@Philalethes101I'd like to hear who exactly looked at the evidence of evolution and gave up on it. Because the only groups who deny evolution do so based on faith and not science.
@@Philalethes101 Nope, literally no one who has studied evolution has given up on it except if they’re very religious, nice try tho.
@@laserfan17 I could make a similar argument, all who studied evolution in depth and still believed it happened are deluded, demonstrably deluded just like the guy above, using insignificant evidences to believe in evolution, while ignoring the fundamental evidences that if true , would proof evolution to be false.
It seems to me the size of a genome of an organism is also reflective of how long that lineage has existed on Earth and has been collecting viral DNA inserts. Lungfish have been around 400 million years and one species has 14x the genome of Humans.
Nope! For two key reasons: 1) all extant genomes have been evolving for the same amount of time, even if not independently they've had the same opportunities for expansion/contraction; 2) the most ancient, independently evolving clades have the smallest genomes (e.g., prokaryotes and many unicellular eukaryotic lineages). And some lineages, like the Canadian shovel bug I mentioned in this video, expanded its genome by 7 billion bases in less than 10 million years since it split from its most recent ancestor. Similarly, the Texan shovel bug reduced its genome by ~4.5 billion bases in the same time.
Genome size is predicted by rates of transposon proliferation (i.e., mutation) and drift, not by the age of the lineage.
Hi Dr. Zack great to see you again we missed you a lot..... I have some question about Junk DNA : 1_ can we claim that the seemingly useless portion of our Genome have a buffering function against mutation loads? ... 2_ or can we say Junk DNA is actually a setting for de novo variation (if yes that could be considered a function for it self )..... And my last question " do we have also junk proteins? If we have, it would be hard for me to belive that it a (slightly, randomly fixed deleterious mutation) I think it would be severely deleterious mutation specially if we have about 90% of noisy transcripts!!!
For (1) and (2), the answer is no - both require that natural selection has foresight and that some closely related organisms need substantially different amounts of mutational protection than others. Prokaryotes, for example, have very little junk DNA; are we to assume they just don't need protection from mutation? Or that they don't require extra DNA just for the sake of "variation"?
Any excess DNA that doesn't serve a function in the immediate generation to the individual that possesses it is deleterious because it costs ATP to maintain it even if in some future generation it could prove useful. Natural selection can't look into the future - it's extremely short-sighted.
To your last question - we absolutely do have junk proteins, these are pseudogenes. As I show in the video, duplicate genes can persist by mutation pressure alone, and so long as they have an intact promoter they can be transcribed and occasionally translated. Whether this is costly depends on the total cellular budget of ATP, which is large in multicellular eukaryotes, ensuring that junk proteins persist.
@@talkpopgen Why would we have to assume foresight? I think we just need to assume that Prokaryotes have in general a efective population size bigger than Eukaryotes that would relax natural selection and increase the impact of genetic drift for Eukaryotes. That will create great differences on the evolutionary path of each lineage. They won't reproduce as often, they will grow more, the overal impact of mutations will be less noticeable, etc... eventually as mutations build up the impact would be greater, especially if its a biochemically active sites that will eat up more resources and ATP and that will be selected against. In general, the impact in fitness have to be higher to be selectable in eukariotes.
So, if our cells are mutations, each being slightly deleterious, but not enough to be eliminated by natural selection, how do eukariotes, and by extension multicellular organisms, manage to survive? One can consider each of these mutations as a local problem with an associated cost to the fitness of the organism. When we consider that natural selection operates on each individual mutation, the cost of a single mutation (or “local problem”) may not be sufficient for its elimination. Instead, it appears that eukaryotic cells have what is known as “global solutions” to these local problems. The size of these similar problems may "justify" antagonistic pleiotropic cost of selecting a general silencers for retrotransposons or other major threat. In a way that woundn't be favourable for a Prokaryote.
There are a lot of features that evolved by drift and mutation accumulation, and then was coopted later by selection into a new adaptative function. Selection is a great recycler and eukaryotes have a lot of junk for her to work with. Introns are a great example of this. It would be great to see if we cut out Most of the non functional genome, what would happen with the mutation rate of the organism's functional region. But I couldnt find such paper.
This is the only channel where I start each video with aggressive headbanging
I know it's not the right genre, but my thought was "Junk DNA? More like PUNK DNA, amiright?"
Would you classify a gene as junk or garbage if it's a gene that is deleterious, but selection can't get rid of it?
Like medeia genes in beetles, where the presence of the gene in the mother is toxic to all her eggs that didn't inherit the medeia allele, but is harmless to her offspring that carries the gene? It decreases fertility (killing part of the Punnet square), and so increases in frequency in the offspring. But it doesn't help with anything else, it's just a selfish element that lashes out violently if you try to breed it out.
All non-functional DNA, in the strictest sense, is deleterious, because it costs the cell energy to replicate. Junk DNA is that which the cost of maintenance doesn't exceed 1/2N, so selection cannot purge it. Garbage DNA does exceed 1/2N, and is expected to eventually be purged by selection. In this way, if a population grows in size, a region that was once junk can become garbage, and vice versa (if the population shrinks).
@@talkpopgen but this example of garbage is removal-proof because it cheats selection.
I'm referring to "Maternal effect dominant embryonic arrest" (there's a Wiki page for it, it's a selfish genetic element in flour beetles)
@@borisbauwens7133 So this is functional because it is being favored by selection insofar as it increases in frequency (even if at the cost of population growth). It's actually one of the coolest cases that prove selection cares about relative fitness more than absolute fitness. I'd also point out that this is an allelic variant of a region that presumably alters its function but doesn't case it to cease having function. Garbage DNA singularly reduces fitness, both absolute and relative.
god i love this channel so much
Utterly fascinating stuff well delivered
I am so excited
53:28 "To suggest anything else is an insult to the _sacred memory of Darwin._"
Our Darwin, who art in the British Museum, hallowed be thy name...
I’m curious about something. C value is obviously evidence of junk, but it also seems to be good ammo against creationism. Should t the same created kind have same size genomes? 4,000 years isn’t a lot to diversify. The salamander doesn’t just have a much larger genome than us, the different species have a wide range of c values. There’s a whole database of animal genome sizes. Just pick a kind and see the ranges.
Yep. In the shovel bugs, for instance, it means that genomes have had to expand/contract by some 12 billion bp in only 4,000 years. This is especially difficult for creationists in that these animals are diploids, so it's not like they have evidence of recent whole genome duplication.
@@talkpopgen I've always wonder why creationists even use the "waiting time problem" as an argument. If there's no time in the hostory of the universe for a new gene to arise, how can all species of the same "kind" evolve from the same "kind" in just 6000 years?
Thank you!!!!!
53:15
But Thomas Jukes also wrote in the same letter :
"Various people have tried to think up possible functions for the regions of DNA that do not code for anything as far as is known. Roy Britten says that such DNA has a regulatory function."
Does this mean that Thomas Jukes believed that non-coding DNA had no function?
Curious about the HeLa cells that have diverged form normal human cells. Is this any help in ideas about how cells might have originated in the first place. That part caught my attention and you just moved on - ha! I need more!
Great video..i learn so much from your videos..your pop genetics videos have helped me alot.. requesting you to make a video on 2 locus selection model ..Thank you
Question. Not so much the onion problem, but the two onion problem. if mutation rate, population size, selection...etc, effects genome size why do two presumably 'ecologicall'y' similar onions have such vastly different genomes (is it a ploidy thing?). Love your videos
You might would think ploidy drives it, but the polyploids on average have similar or smaller genomes than diploids (doi.org/10.1093/aob/mcab155 ). I couldn't find any quick references for standing levels of genetic diversity across onion species (which would tell us if they differ in population size), but I can explain the difference in genome size in the shovel bugs.
The Texan one (H. allardi) has a genome 2.5 Gb, while the Atlantic one (H. canadensis) is 14 Gb. But they differ dramatically in how much genetic diversity they have, with the Texan one having almost twice as much. So selection can "see" more mutations in H. allardi than H. canadensis. Furthermore, there's some evidence that H. allardi's genome was recently purged of transposons, and this appeared to have occurred when it colonized brackish bay areas. We hypothesize this is due to increased thermoregulatory pressure, which intensified selection for genomic streamlining (doi.org/10.1093/jcbiol/ruab042 ).
Hi, I have heard somewhere, hope I understood it correctly, that there are supposed to be ERV's that don't fit the pattern. Are you familiar with that?
what pattern ? the expected phylogenetic pattern ?
PTERV-1 and HERV-K-GC1 are the one's that creationists claim do not fit the tree as far as i've heard are u referring to the one's i mentioned or something else
@@NANOG-P8 i don't know which ERV'S but I guess that it's just a creationist propaganda.
@@bilal535 herv-k is an interesting case. there's one virus that's present in orthologous loci b/w chimpanzees and gorillas but not humans they instead have the pre integration site. if gorillas diverged before we did then we should have them ( they did diverge before us ) but we don't. that's the argument iam aware of its probably the best example out there but its easily explainable
Neat :)
thank you for the information, watched the whole thing
What would happen if you would culture E. coli in 10 microliter cultures, that are split and refreshed very often, before or during the exponential phase (especially before the sigmoidal part), in rich medium, and look at their genome size over time?
Would the low population sizes and low competition lead to relaxed selection and increased drift, leading in turn to increased genome size?
Or will the deletion bias still be intrinsically larger than insertion bias, and you just get a slightly larger but not bloated genome, at the equilibrium between those two rates?
You didn't specify why these rates are biased: is it intrinsic to the biochemistry of prokaryotes versus multicellular eukaryotes? If it is, my guess is that prokaryotes have more restriction enzymes, and we have more homologous recombination between larger ploidy numbers. So prokaryotes are biased to cutting out stuff, while we do more loopy bendy homology stuff that can increase size by entire big blocks?
Ah great question! So while there may be some intrinsic differences at play, recent work suggests that the rates of indels are actually strongly predicted by effective population size (doi.org/10.1534/g3.116.030890 ), with some unicellular eukaryotes having rates similar to prokaryotes that possess the same Ne. This indicates that these rates are likely shaped by natural selection reducing the mutation rate via improving the efficiency of mismatch repair enzymes, polymerase proofreading, etc. I suggest this might be the case in the video by pointing out that E. coli suffers a high fitness cost for having excess transcripts whereas C. elegans and A. thaliana don't, which is at least indicative of natural selection shaping mutation rates in E. coli while drift dominates in C. elegans and A. thaliana.
@@talkpopgenso the ratio between insertions and deletions is the same for occurence (in prokaryots vs eukaryotes), but becomes different after selection?
Like how the rate of dominant lethal mutations occuring is larger than the observed rate? (Because of literal survivorship bias)
I'm wondering where that pronounciation for "simuler" (similar) comes from :)
East Texas 🙃
thank you so muchhh
Sorry to be the bearer of bad news. Yamashita's team has discovered a function of satellite DNA as required for organisation of cell division (see link at the end). The analogy is like cardboard for amazon packages. These experiments demonstrate NON VIABILITY of future generations of fruit flies when tinkering with binding of 'junk dna' (although there is some complexity there). This has nothing to do with histone DNA exposure. This doesn't dismiss your statistical arguments for variation, drift etc etc but might make them non primary. Probably needs replication, but given what's published, I would bet on their results. Posting the video (because easier to digest) but you can find your way to the papers. czcams.com/video/DNoknezxKrs/video.html Anyway, enjoying your channel, especially Fisher theorems :-)
Yamashita is confused about what constitutes junk DNA. Satellite DNA is mostly concentrated around centromeres and constitutes ~6% of the human genome (or about 180 Mbp). She finds that it's involved in proper chromosome binding, but here's the rub: within humans, there's a ton of variation in genome size, and a strong, positive correlation between genome size and how much satellite DNA you possess. This means that a large portion of satellite DNA exists in excess of what is necessary to promote proper cell division. Any DNA that exists in excess of what is necessary to perform the function is junk. This is akin to saying introns have functions because of alternative splicing: their presence is minimally required and maintained by selection, but they bloat without increasing function because the cost of excess DNA doesn't exceed the drift-barrier. Satellite DNA has some minimal number that must exist, but that they're so variable in size between even related individuals demonstrates they have bloated with junk. Finding function for some doesn't indicate that that function extends to all repeats.
@@talkpopgen thanks for replying. "exists in excess of what is necessary to perform the function is junk" I agree, unless it turns out that the length itself performs a function, not the contents (just like cardboard). Or statistically lends itself for hosting necessary sequences. Of course that's just speculation. Anyway, I did write "This doesn't dismiss your statistical arguments"... so I'm happy :-)
But it's like, maybe not tho.
People are ignoring actual known human history. The actual historical records and DNA migrations show that everyone spread out from Mesopotamia. Ancient history is essential for everyone to know, especially the sixteen original civilizations… from the sixteen grandsons of Noah. Learn ancient history before trying to learn science.
1. The first inhabitants of Italy (K) Tubal
2. Thracians (L) Tiras
3. Mediterranean Greek sea people (T) Javan
4. Siberians & East Asians (NO) Magog
5. West & East Eurasians(P) Meshek
6. Medes (Q) Madai
7. Western Europeans (R) Gomer
8. Hebrews and Arabic (IJ) Arphaxad
9. Elamites (H) Elam
10. Assyrians (G) Asshur
11. Arameans (F1) Aram
12. Lydians (F2) Lud
13. Cushites (AB, C) Cush
14. Egyptians (E3) Mitzrayim
15. Canaanites (E2, D) Canaan
16. Original North African Phoenicians (E1) Phut
The D paternal haplogroup Sino descendants of Canaan migrated from Canaan east to China all the way to Japan and Tibet. The C paternal haplogroup descendants of Nimrod migrated as far as South Asia, the Pacific, Mongolia and all the way to the Americas accounting for the Olmec civilization as well as the Q haplogroup descendants of Madai ancestor of the Medes that crossed the Atlantic to Central America.
The A maternal mtDNA haplogroup belonging to the Semitic N lineage accompanied the Eurasian Q paternal haplogroup to Central America. The C&D maternal haplogroups belonging to the Eurasian M lineage also accompanied the Atlantic crossing of the Q paternal haplogroup Medes and probably the C paternal haplogroup to Central America. The Semitic B maternal mtDNA haplogroup seems to have crossed the Pacific Ocean to South America.
The Mediterranean paternal R1b and the maternal X2a also found in Galilee represent another Atlantic crossing of the Phoenicians in the days of King Solomon considering also the Mediterranean paternal haplogroups of T, G, I1, I2, J1, J2, E and B in addition to the R1b in Native American Populations. J1 and J2 is Arabs and Jews. (I1 is most likely Dan and I2 resembles the movements of the tribe of Asher)
Of course there is also the Cohen modal haplotype of J1 P58 as well which identifies the IJ lineage of Hebrews and Arabs that are descended from Arphaxad. J2 M172 is the largest group of descendants probably of the House of the kings David and Solomon. Now you know a lot more of what is verified human history.
Neanderthals were Eurasians descended from Japheth and Denisovans are a mix of Eurasians and Canaanites and or Cushites descended from Ham.
why don't you try and comment about something relevant to this video, no one is going to read your random, irrelevant thoughts
@@talkpopgen Okay. It’s rather obvious that life can’t make or program itself since energy and matter can’t make or direct themselves.
There is no evolution. It’s nothing more than a bait and switch. Yes, there is variation, yes, there is adaptation, yes, there is responding to the environment and none of that equates to evolution. No, mistakes never write any viable functional programming that’s not there and much less billions and billions of bits of viable functional written programming that’s not there and it never will be there. Evolution is 100% pseudoscience.
Lol, that's like saying that there is buying and selling and money and stock markets, but no such thing as economics :D
My dude, you listed the defining features of evolution.
@@borisbauwens7133 That's what the claim is.
you STILL aren't commenting on anything relevant to this video... wanna try watching it before commenting?