Submitted by nodeciapalabras t3_ylu0ir in askscience
byllz t1_iv2wsb4 wrote
Reply to comment by RhabarberJack in Why don't we have Neandertal mitochondrial DNA? by nodeciapalabras
It is one family of mitochondria, but there are random mutations that happen regularly. Through tracking these mutations, you can tell how closely different people are related to each other, matrilineally speaking.
poop_face_monster t1_iv39hcf wrote
Do any of these variations [edit: mutations] change the form/fit/function of the mitochondria?
It seems to me that any marginal improvement there would yield a pretty significant boost to fitness.
(Thank you for fielding Qs. I’m only a moron, but this thread is brilliant.)
PontificalPartridge t1_iv3gjd8 wrote
Probably. Some mutations are good, some bad. If it provides selective advantage for ATP exchange then over a long period of time that mutation could become prevalent if that ATP exchange could become more common if it meant more breeding.
It’s worth noting that modern humans don’t necessarily rely on ATP exchange for “breeding” at this point. The movie idiocracy is an extreme example. But our survival selection method is pretty close to societally based at this point
Edit: for most of human history there are probably some tangible selective advantages to some mitochondrial mutations, just like anything else. I don’t have any specifics
morgrimmoon t1_iv4gyjt wrote
Quite a few of these mutations impact mitochondria in a negative way. For example the LHON mutation often causes blindness, but only in about 30% of carriers (so there's probably some environmental or non-mitochondrial DNA factor that "activates" it).
Since cells have multiple mitochondria, and since the non-mitochondrial DNA rules most of the cell, it can be tricky to determine what any mutation does and having it may not cause a change for all carriers. So it won't have as strong a selection pressure as it may intuitively seem, and any fitness improvement may still take a long time to spread thru a population.
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