Evolution isn't a perfect system. It's a game of repeated "good enoughs". If the genes with a disadvantage get a little lucky with their reproductive odds during the initial generations of the mutation, there's no reason a fully detrimental mutation might not stick around for a while.

Also, humans tend to be the exception to a lot of rules. Our knowledge of medicine (Edit: and agriculture, and a buncha other things) significantly alters our fitness odds, and allows many genes to reproduce that may not have otherwise survived.

So why is it delivered intramuscularly and not into the blood? How does it work when it’s injected into the muscles to spread throughout the body?

Depends how you align them. Conventional wisdom says to add racing stripes first, then line any flaming decals up with them so that all the speed is focused in the same direction.

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>Human chromosome 2 has a vestigial (unused due to no longer being needed) extra centromere and 2 vestigial telomeres found inside the chromosome sequence.

Goddammit that's cool.

I can't be sure of it quite yet, but I have a feeling sequencing the entire genome is the single greatest human breakthrough in my lifetime. I was in middle school when my science teacher told us it had been done for the first time. When I was in college I toured a sequencing facility where it was being done for outrageous cost per sequence on machines bigger than my house. Last year I got my own DNA fully sequenced, every single base pair, for about two day's wage.

Reading your own ancient programming code letter by letter is a weird, almost disassociating experience.

A sex cell has 1 copy of each chromosome. They are created by meiosis, i.e. a classical cell with 2 copies of each splits into 2 sex cells. During this process, each chromosome finds its buddy, so they split nicely and you end up with 1 copy of each, not random half. That would be bad.

In the person with 45 chromosomes (assuming this specific kind of mutation where 1 chromosome is fusion of 2), the combined chromosome pairs up with random one of the smaller ones, and the other is left without buddy. That's bad. If you are lucky, it ends up in the same cell as the other small chromosome. If you are not, it ends up in the other cell.

The article I linked in the first comment has nice pictures illustrating this.

Just to add, children's vaccines are almost always given in the thigh, which apparently reduces common side effects.

I both like and dislike that. Because on the one hand, yeah, you’re not wrong. On the other, it feels a bit like it discourages exploration as a kind of “yeah it just be like that” sort of thing.

The sex chromosomes are unique though. The X chromosome is the only chromosome that is almost fully functional whether there's 1 or more copies. The Y chromosome is not necessary for life, though it does serve a function besides "make boy", as missing it or duplicating it is not a side effect free situation as in XO and XYY like you pointed out.

When you reproduce, your chromosomes are split in half. One gamete will end up with 22 and one with 23. This will only create a viable gamete if the one with 22 includes the extra long boy but more importantly, that the set with 23 doesn't include the extra long boy. Duplicate genes aren't any better. Most trisomy conditions are incompatible with life.

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Why would 45 chromosomes be a problem but not 44?

Chordates (vertebrates and a few close relatives) also went through two rounds of whole genome duplication early on in their evolutionary history (this is the 2R hypothesis, the evidence for which is pretty solid at this point), so while it's not as common or well-tolerated in our clade compared to plants, it's still something that can happen occasionally.

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I'm learning so much through this, thank you!

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> “we’re not entirely sure.”

As someone with a moderate biological education I always assume "if the chances of something are low, just remember evolution has a LOT of time and a LOT of DNA replication events to work with" is the answer to weird questions about evolution.

Building a "reference genome" for a species from scratch is a whole field of science.

When people do "normal sequencing", the genome is broken into an infinity of small pieces. The genome of chimpanzees, gorillas, and orangutans fit so well the human genome, that scientists usually use the human reference genome to study great apes.

Some scientists compared both the human and the chimpanzee reference genomes built independently from scratch, and they found just minimal differences. All this shows that the human chr2 and the great ape chr2a and 2b are almost identical in they just happened to fuse in proto-humans sometime in the last 6 million years.

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Just to be a bit pedantic, the new genes actually have three possible fates: becoming genes with new functions (neofunctionalization), becoming a part of the same pathway where both copies take on part of the work (subfunctionalization), or losing functionality entirely (psuedogenization).

Evolution is cool.

Right, and that seems to illustrate OP's point. Having 44 chromosomes is obviously a pretty big fitness detriment, since it makes it harder to reproduce with other members of your own species. So how did a such a variation in chromosome numbers between species occur in the first place, if evolving it is a detriment?

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