Was there a period where sapiens and neanderthals couldn't interbreed? I guess what I'm trying to understand is what formally makes them different species in the first place.

Seems to me that "hybrids," as a concept, have less to do with biology and more to do with our arbitrary classification of it.

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>I have always wondered if hybridization wasn't actually more commonly possible.

It's incredibly possible. It happens all the time. The only reason you think it doesn't is because the definitions of words.

The entire concept of the taxonomic tree is human made arbitrary decisions. By definition, when hybrids are "common", we group them together as one species.

But like, pretend you are an archaeologist going through bones. Would you call a Chihuahua the same thing as a Rottweiler? That's totally a hybrid. There's so many, we call them all "dogs" and just use a different word: breed.

If that doesn't convince you, look up Ring Species, which are incredibly cool and totally make you rethink how you think about species.

Yes, certainly. That's why there are multiple different prion diseases in humans, such as Creutzfeldt-Jakob Disease, Gerstmann-Straussler-Scheinker Syndrome,Fatal Familial Insomnia, and Kuru.

>Although PrPC is encoded by the host genome, prions themselves encipher many phenotypic TSE variants, known as prion strains. Prion strains are TSE isolates that, after inoculation into distinct hosts, cause disease with consistent characteristics, such as incubation period, distinct patterns of PrPSc distribution and spongiosis and relative severity of the spongiform changes in the brain. The existence of such strains poses a fascinating challenge to prion research.

--Insights into prion strains and neurotoxicity

Seems like it's still contentious, but since avian sex regulation appears likely to be dependent on having two copies of the Z chromosome to induce maleness, the W chromosome that females have is likely to be analogously expendable to the Y chromosomes - so you would see the same patterns just with the sexes flipped?

https://pubmed.ncbi.nlm.nih.gov/28911174/

> prion-strain specific

What is a "prion strain"? Are there different misfolded forms of PRNP?

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I searched the comments and surprised that no one has yet mentioned humans with XXY (Klinefelter Syndrome or KS). It is possible for them to reproduce, although usually with the help of fertility services and fertility rates are extremely low. It is possible for them to reproduce naturally as well though it's pretty rare.

A couple related articles:

https://pubmed.ncbi.nlm.nih.gov/21207006/

https://www.nichd.nih.gov/health/topics/klinefelter/conditioninfo/faqs

Yes, of course they do. Because men have fewer ribs than women, their intercostal muscles work differently. /s

Men are bigger on average, which leads to some differences like higher lung capacity, peak flow etc. But the mechanics of breathing are the same.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5980468/

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Not only that but plants can have different numbers of chromosomes in different parts of the plants due to inaccurate cell wall growth after cell division. It’s how we got seedless grapes, naval oranges and pink grapefruit.

>Temperature-based determination existed before genetic one.

Specifically, there is a hypothesis that the very first amniotes (reptiles, birds, and mammals are all amniotes) used temperature-dependent sex signalling, and only evolved genetic sex signalling later. There is some good support (phylogenetically) that the first amniotes did not have sex chromosomes but used temperature instead...and that sex chromosomes independently evolved multiple times within the amniotes.

The best model for why any species would adopt temperature-determined sex is probably the Charnov-Bull model. Simply put, the model predicts that in some species, the temperature at which they develop and hatch has a different effect on males and females, so temperature-dependent sex signalling gives you the best possible fitness in your males and females. For example, maybe a species lives in a place with cold winters, and lays eggs early in the spring. And let's say that species is best served by more females surviving the winter than males. If females develop in colder eggs, then eggs laid earlier in the springtime nesting season will all be female. That head start means the females will be bigger in the fall when the first frost hits. Males might then develop later in the nesting season and be smaller when the first frost hits, and a few more males may die during the winter, but the species as a whole preserves more females overwinter this way and improves its odds of surviving.

Of course, both can be true; Charnov-Bull could be the reason why the first amniotes used temperature as a sex selector, and part of the reason that some species have kept it to this day...but obviously many later evolved sex chromosomes (including us warm-blooded mammals).

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>Generally, individuals with an odd number of chromosomes are not fertile.

An exception would be a man with XYY syndrome. They have normal fertility rates.

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Red wolves, for example, may be a stable hybrid of grey wolves and coyotes.

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I didn't know a mammal could have so few chromosomes, figured only worms and such would have less than 10, but I'm just a layman so guess I could be missing a few chromosomes as well.

Probably not.

> Mother-to-offspring prion transmission appears to be prion-strain specific as evidence in other animal species including humans, Syrian hamsters and sheep infected with the classical bovine spongiform encephalopathy (BSE) agent show that progeny from infected females at the moment of gestation do not develop prion disease in the long-term

—Detection of CWD prions in naturally infected white-tailed deer fetuses and gestational tissues by PMCA

As that article and several others show, some prion diseases such as chronic wasting disease of deer can spread from mother to fetus, but there’s no evidence of that ever having happened in humans.

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