Most of what I said comes from scientific reviews, so not super layman friendly.

The tree of life web project is maybe something I can point to if you are interested in phylogeny.

Otherwise, all I can say is look at papers using BEAST2, which is, from what I understand, the main tool used for inferring a philogenetic tree from DNA sequences.

Indeed, generation time is one of the big things to take into account. That's why in the early days, the estimates that the genetic clocks gave was only good enough for closely related species.

But the method has come a long way. They have "relaxed clocks" now, which take into account generation time and stuff (it's all Bayesian statistics which I don't really understand). When they compare to known fossil records, it broadly agrees. But I think even now you'd expect it to be more accurate when comparing rodents together than the whole of arthropods for example.

Excellent question. That's because the inactivation is not complete, and up to 25% of the genes on the inactivated X can be expressed.

Some of these are in the pseudoautosomal regions (PAR). Autosomal is the big word for "not sex chromosome", the PAR are regions on the X and Y which behave like autosomes and not sex chromosome, because they are shared between X and Y.

And also in the rest of X sometimes genes can get reactivated because no rules can ever be simple in biology.

That's only one of the many challenges faced by molecular clocks, although really not the biggest one. By construction you're looking at the neutral mutations, at as many loci as possible. Modern, Bayesian statistical methods can account for different clock speeds in different genes and different species, and of course sequencing is cheaper than ever.

> the genes effectively 'compete' for which one is encoded

Either you have in mind something very specific, or this is generally false.

Monoallelic expression is more of the exception than the norm, and is generally not responsible for dominance of traits. It happens for the ~200 imprinted genes, the X-linked genes (because of the X-chromosome inactivation you describe), and as far as I'm aware a handful of other genes.

I think you're missing the key point of dosage compensation. Having 4 copies of a chromosome means 4 times (a priori) the amount of RNA/protein, most of the time bringing you into toxic territory. X is an exception as you say because X-chromosome inactivation ensures there's always only one X getting expressed.

I'd chalk up the survivability of Y duplications more to the fact that it has so few genes than the fact that those genes are transcription factors (i.e. genes that go activate other genes elsewhere).

I mean, the data presented here suggests that ENA is basically nepotism with extra steps.

Although the extra steps are possibly of importance. ENA entrance exam is reputed to be extremely hard regardless of cooptation, at least being born from a diplomat is not enough.