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agate_ t1_j8igwtp wrote

Reply to comment by SignalDifficult5061 in Why does X-inactivation happen? by NeedleworkerCapital8

Re “dosage compensation”, is it generally true that more copies of a gene means more gene expression? Aren’t most genes regulated by homeostatic feedback systems?

And what about the many, many plant species that get along just fine with duplicates or triplicates of their entire genome?

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CrateDane t1_j8ix0fy wrote

>Re “dosage compensation”, is it generally true that more copies of a gene means more gene expression?

Yes, it is true to varying extents.

Cancer cells often have genetic errors adding extra copies of oncogenes, which helps boost their growth etc. That wouldn't work if everything just got compensated back to baseline.

>Aren’t most genes regulated by homeostatic feedback systems?

There is a fair bit of that, but it wouldn't necessarily compensate fully. It also wouldn't be uniform, so some genes would have relatively more expression compared to others, which itself could have problematic effects.

>And what about the many, many plant species that get along just fine with duplicates or triplicates of their entire genome?

Well, at least those don't skew the relative dosage of different genes. It's still usually lethal in animals though, so it's an interesting question.

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SignalDifficult5061 t1_j8jramu wrote

nice answers!

I'll just that extra copies of a single autosome (so 3) generally end in embryonic lethality, except for Down Syndrome and a few others very rarely. So dosage is generally important for whole chromosomes.

Extra X chromosomes lead to relatively mild phenotypes vs extra single autosomes, which may relate to X inactivation.

Total genome duplication isn't limited to just plants, and some frogs have up to 12 sets. I don't know a ton about that, other than that often many of those chromosomes aren't fully functional.

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