It depends on the species. Some have them, some don't: https://journals.plos.org/plosbiology/article/figures?id=10.1371/journal.pbio.1001899

My favorite fun fact is that sex determination in birds is exactly opposite to mammals: the females are heterogametic. They are ZW, while males are ZZ.

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Could have evolved to be an environmental variable?

Like when sea turtles lay a clutch of eggs in the sand, the ones closer to the surface sand might be warmer, the ones in the middle might be warmer, ones that hatch closer to dawn might be warmer, etc.

Might just allow for randomness in the sex mix of any individual batch of eggs, that gets smoothed out by the variation across any breeding season.

No “y” chromosomes in fish?

One thing about adaptations is that one mutation away from the parent needs to be at least as good if not better than other siblings.

If it's going to take three generations of mutations to get to an advantage, they probably won't make it.

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Is it an advantage or just “this happened to work out slightly better than the alternatives present at the time”? It’s mostly randomness and a matter of “not so awful it’s untenable” which, over billions of iterations, tends to end up somewhat efficient. To assume that something happens purely because it’s advantageous in a general sense doesn’t really work though. I mean, look at human nasal passages. Horrible, but not so bad it’s untenable.

Edit: to be clear, I say this only to mean that it’s not inherently going to be a logical conclusion we can easily discern. I’m mostly supporting your point.

Clownfish are one such fish. Another species is mentioned in the BBC Earth series, but I'm afraid I don't recall the name or even which episode.

When researching how to sex my pseudomugil illuminatus fry, i came across this article, which talks about one person's experience with different temps. https://www.pvas.com/forum/breeder-s-award-program/spawning-report-pseudomugil-luminatus-red-neon-blue-eyes

Temperature dependent sex determination is fascinating! Just remember, mammals and birds use chromosomal sex determination (meaning sex is genetic) but other mechanisms are quite common across all organisms! Check out the cool graphs at tree of sex http://treeofsex.org/.

There is still a lot of work left to be done on mechanisms of how temperature during incubation leads to different sex ratios. This is a good scientific review on red-eared sliders https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2695493/. The ultimate mechanisms, or why temperature sex determination occurs, is also an interesting evolutionary question. Here is a good starting point for further research: https://sites.utexas.edu/crewslab/files/2016/06/CrewsDVLGen.pdf.

Finally, it’s important to remember that sex is a complex phenotype with many components and is really a shorthand for biologists to describe a common suite of traits. But thanks to sweet, sweet variation there is no one size fits all! In fact, it’s not uncommon for sex to be broken down into at least 5 levels of animal sexuality but that’s just the beginning. Not to mention human-specific levels, such as gender. Just a fun aside, the genderbread person is a nice primer on gender https://www.genderbread.org/

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Temperature affects the rate of chemical reactions.

Complex biological pathways result in more or less of particular hormones being produced at different temperatures. This is useful in cold-blooded organisms, because if the chemistry of some biological function tends to shut down beyond a particular temperature threshold, the organism can incorporate other biological systems that kick in to replace it.

The advantage of having offspring's sex affected in such a way is open to discussion.

Many species of fish do this, in that the temperature will determine the sex of the eggs. Some fish species will also change sexes depending on environmental pressures. Unfortunately I don’t have sources on this for you at the moment.

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Fatal Familial Insomnia (FFI) is a genetic disorder caused by a mutation in the PRNP gene. The PRNP gene codes for the prion protein, thought to be involved in copper signaling and cell adhesion. For the mutation itself, at position 178, asparagine (N) replaces the wild type aspartic acid (D); D178N is the correct notation. However, what determines if someone shows the pathology of FFI or familial Cruetzfeldt-Jakob (fCJD), depends on another position on the mRNA that’s translated. The D178N mutation must be coupled with a methionine at position 129; this site is the valine/methionine polymorphism site.

Homozygotes at codon 129 show a shorter disease duration, more severe insomnia, and the disease is mostly restricted to the thalamus.

Heterozygous at codon 129 show a longer disease course and other symptoms, such as ataxia and dysarthria; the disease is not restricted to the thalamus, and can spread to other parts of the brain, such as the cerebral cortex.

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It’s just a problem with the interactions between cells, it sounds like. You’re correct, X Inactivation virtually completely disables one X chromosome, it just happens after cells have divided several times, so some clusters of the developing embryo have one X chromosome while other clusters have the other chromosome.

This is so damn interesting. I would have never seen anything like this in my normal studies. I never would have thought heterozygous could be worse.

There are lots of clues. One of the simpler ones is counting seasons. I've only seen ice cores from the Arctic, which don't go as far back, but just looking at them you can tell summer ice from winter ice. Counting the layers give you years. There are also more accurate ways to measure the difference (you can look into what delta 18Oxygen means).

You will lose count if there was a period where summers got warm enough to melt more ice than was formed during the winter, but you can then use the other methods to try and correct for that.

Even so, being of by a 100 years isn't too bad when you are counting 100000.

More terrifying. Ebola Zaire had a 90% case fatality rate when discovered.

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