However, I thought I should clear this up. When I made the comment I just saw the headline of the article and the sentence @swamidass quoted. As I mentioned, I hadn’t read the article. And I had just had a baby, so it hit my funny bone to think of comparing an amazing process I had just gone through to scientists excited about yeast evolution.
But my comment wasn’t a parody of a creationist argument, it was a creationist argument as by making that comparison I was poking a little at research that tries to explain origin of life or complexity, in that they have a lot further to go.
@dsterncardinale pointed out flaws he sees in Jeanson’s argument. I guess my joke gets lumped in the same category - comparing development of an organism to evolution of a population. Oh well.
But how much do transposons effect development of organisms and affect phenotypic diversity in populations, that’s what I want to know.
It was both kind of amusing that Dan featured me and also he gave me too much credit. I guess creationists just think alike.
But I also wasn’t sure how @Dan_Eastwood and others took what I wrote. Obviously it hit him a certain way. The amusement for me was that the headline didn’t differentiate what process it referred to and we already know single cells become multicellular forms in development. So I guess I was poking fun at the hype sometimes around research. That’s not the scientists fault. They didn’t write the headline.
On a different note, also now that I know more I need to reread the Jeanson paper mentioned in the video.
I have a question on that - maybe for @dsterncardinale Are mtdna somatic and germline mutation rates expected to be different? Or is there a biological reason for a difference, anything I wouldn’t come across in a quick Google search for the answer?
For several reasons, germline line rates are far far lower than somatic rates. Somatic mutations are no inherited, but germine mutations are. So using rates that approximate somatic mutations where germline mutations should be used is a bait and switch.
Thanks for the explanation, but this part is less helpful than Google not more.
I read the paper though after trying to search for those “several reasons” a bit.
In the Ding et al. (2015) study, the authors examined an order of magnitude more pedigrees than either of the two studies above and scored both heteroplasmic and homoplasmic mutations. Again, I ignored all mutations reported as heteroplasmic. Conversely, the identified homoplasmies were so rare that the authors treated them as essentially inconsequential. Nevertheless, they did sequence the mtDNA of 333 parent-child relationships, and in Table 1 of their paper, they report 7273 homoplasmic variants in the children, of which 7238 were shared with the mother. Thus, 35 (7273–7238) new homoplasmic mutations appeared in the offspring.
Trying to think this through - If Jeanson is only counting homoplasmic mutations, are any artifacts going to be statistically significant? It seems like they’d be super rare to come up - each mtDNA in the cell mutating in the same way, compared to the somatic cells showing homoplasmic inheritance because the mtDNA goes through a genetic bottleneck in the germline? That’s what I made of what I read, but I can never tell whether I’m understanding things correctly.
@dsterncardinale if you’ve already made a video covering this question, please point me to it - I admit I probably tried watching a video of yours on this paper before, but I was probably too tired and went to bed and never came back to this subject. But I’m already learning new things, so that’s fun.
It was a joke. I was making fun what I saw as the hyped-up headline of the article. Development of a baby is way more amazing than the yeast research, which was not that surprising IMO when I read over it. But I was comparing things that shalt not be compared lest I incur the scorn of the evolutionary biologists. Oh well.
I’ll check them out and see if my question got answered. But also interested in the possible general refutations.
One of those is that mutations that affect the germline might have no effect in some somatic cell line. Imagine a mutation that causes a protein critical to brain function to stop working, but the mutation happens in a skincell(somatic cell line) that doesn’t express or use this protein for anything. To the skincell this mutation has no effect, and therefore doesn’t affect the fitness of the organism, so isn’t selected against. But had it happened in a gamete the organism that could go on to develop from that simply couldn’t survive. There must be a large host of such mutations that matter a lot and have strong fitness costs to offspring of organisms that suffer them in germline cells, but have little to no effect in somatic cell lines. That’s one reason why somatic mutation rates are higher than germline.
And note that the germline for mitochondria is exclusively female. If the rate of mitochondrial evolution is tied to the rate of cell division (and it seems to be across species, at least), then the germline rate through oogenesis should be lower than that seen in spermatogenesis.
I don’t know if you made a typo or didn’t read carefully. I looked up the definition of homoplastic and obviously that doesn’t apply here. What I had quoted from the study is that Jensen only counted homoplasmic mutations (we now know our somatic because someone emailed the author of the study). In @dsterncardinale video that my post was featured in, he was criticizing Jeansen for explaining that the numbers he used may not indicate the actual germline rate unless three generations were counted. My understanding of homoplasy is that those are only mutations that are shared among all of the mitochondria in the cell (cells?) that was/were sampled. So I was trying to differentiate how that wouldn’t be similar to the germline rate because how would it be possible to have a homoplasmic pedigree mutation unless it happened in the germline?
This would be a reason why it could be different because the study doesn’t seem to use female children only.
But if there are other reasons why a homoplasmic pedigree mutation rate would be different than a germline rate, that’s what I was trying to ask. But I don’t know if I understand the biology correctly because there could be something big I am not understanding.
@Rumraket thanks for your explanation. I had read some about selection and mitochondria but your explanation makes it much more practical to understand.
@dsterncardinale I listen to the 5 minute video and watched the debate with sft so far. Debate was great; you both are very good at what you do. It didn’t get too in the weeds so that I got a population genetics headache. Makes sense why you have popular YouTube channels.
It’s so much worse than just somatic vs germline. You need the germline cells to actually become ova, which most fail to do, which must become a zygote, which must develop to reproductive age, successfully reproduce, and then that lineage must persisit to the present. Jeanson ignores all of this.
But it DID persist to the present. I assume they sample real living people. So that’s why I’m asking.
I assumed @John_Harshman was saying males may possibly inherit more mitochondrial mutations than females. But maybe I should have looked up those terms first, because I might have assumed very wrongly.
Or maybe what you said is not irrelevant, you just used the wrong word AGAIN? Lol, at this point I can’t tell. I made the “t” uppercase so you can see why I’m confused. I get that homoplasy can be in the germline or somatic cells.
Ok fine, but it’s pretty irrelevant to the conversation.
@dsterncardinale I should read more carefully too. It looks like you are also refering to three generations. So Jeanson doesn’t ignore all of that because he brings it up! It’s trying to have it both ways - he’s both bringing it up and ignoring it…you could better say he just shouldn’t have used the data?
But…since no one is explaining to me so far where my logic is incorrect I can only assume at this point the homoplasmic pedigree rate may not be the same as a germline rate because we don’t know how many of the offspring sampled went on to have daughters…perhaps that can be inferred by looking a typical population to see if it’s statistically significant…
Putting aside that the data Jeanson uses (Ding, 2015) was two generations, not three, three generations doesn’t solve the problem, because in order for a mutation that occurs at a specific point in time to exist in the present, it needs to survive through every generation since it occurred, and we know that doesn’t happen. Natural selection exists. Genetic drift exists. That’s why there’s a mutation rate (the rate at which mutations occur) and a substitution rate (the rate at which mutations accumulate). Only a substitution rate is useful for calculating the time to a most recent common ancestor. Jeanson uses a one-generation mutation rate and just extrapolates it backwards, which, lol no.