The technical term is syncytium.
Some other people mentioned a couple of things, but the placenta is particularly interesting because there is evidence that is arose as a result of co-option of a viral gene. Some modern viruses cause syncytium formation in host cells as part of their life cycle.

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.

All things being equal (with no regulation etc.) two copies of a gene are going to make twice as many mRNA transcripts and twice as many proteins as a single copy.

So gene dosage essentially.

Having too many copies can be damaging or lethal to an organism, especially in complex delicate situations during development.

This is a gross oversimplification (and not something that actually happens), but what if your brain was trying to make itself two times bigger than what your skull could contain?

You can imagine all sorts of processes going out of whack in a single cell, let alone when they have to interact in complicated ways.

There are other ways evolution could have dealt with it, but we have evolved to have around two functional copies of a gene on the autosomes (with a few recessive completely non-functional genes here are there), but that is quite a bit different than having a two fold difference across the entire X- chromosome.

Once the system we have evolved, it would be very difficult (practically impossible) to change the regulation of almost every single gene on the X-chromosomes, let alone change the regulatory scheme of every genes on the autosomes.

So yeah it is conceptually weird, but the barriers to doing something different in evolutionary terms are too high or too unlikely for it to have occurred in humans. Biology does not have to make sense from the standpoint of how a reasonable person might design a thing.

Even in tightly regulated genes, it can take more energy to regulate for two copies than one, which would be exacerbated across the entire X-chromosome. Again, we have evolved in such a manner that we are regulating our two copies of autosomal genes appropriately, which is evident by the fact that we are here.

Edit: this is over generalized for all animals. There are some other methods of dosage compensation in animals. Drosophila just doubles expression on an X chromsome, instead of inactivating one. There are some other methods of dosage compensation in other animals, especially those with different type of sex chromosomes.

It isn't clear that there was a specific entity that could be widely considered alive that suddenly appeared one day at all.

There could have been millions of years of complex processes going on which was sort of a gradient from "definitely not alive" to "definitely alive".

Microbes can accept genetic information much more readily than animals do with unrelated forms, and all sorts of genes have probably disappeared in the last billion years. How would one define not ancestral to modern life vs ancestral.

Even if all the genes of some creature are no longer extant, they could arguably have shaped the evolution of genes that still are,so there is still some remaining influence.

Dosage compensation. Autosomes are always at two copies, the X chromosome can be one or two. "Bad" recessive genes on an autosome can be masked to varying degrees by good copies. It makes more sense to have two copies rather than one for the most part for everything with paired chromosomes apparently.

The "dosage" for a XY chromsome carrier and XX chromosome carrier is kept even by an X chromosome inactivation.

There are other ways around this that could have evolved, but this is what we have.

Bacteria often have multiple copies of their genome, which can vary wildly depending on growth state and other things, so they have other compensatory systems.

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To be nit picky, there is a pseudo-autosomal portion of the Y chromosome, and there are a small amount of genes that aren't inactivated on the "inactive" X.

Yes, in addition to what others have mentioned the other way to do it is to make a virus that can *only* replicate in cancer cells.

So the cancer cells aren't being directly targeted, but the mutant virus can't replicate in normal cells. Presumably when the virus enters non-cancerous cells it just gets quietly degraded during general protein and nucleic acid turn-over

This may sound weird at first. However, There is some overlap with the way some cancer cells and some viruses need to be able to disrupt the cell to replicate effectively.

Most cells in an adult are senescent or dividing very slowly, so all the machinery for DNA replication and spare bases are are at low levels.

Cancer cells divide by definition, and viruses tend to evolve to sort of force cells into dividing or dividing faster, so that they will then be able to replicate faster.

If these things get "turned on" when they shouldn't most cells will commit suicide (apoptosis) with the help of "checkpoint proteins" and other mechanisms. Cancer cells tend to have mutation in these checkpoints (which is why they don't commit suicide).

So one can imagine a scenario where you have a cancer with a known checkpoint mutation, and a virus that targets the same checkpoint protein (with one of the viruses numerous genes/proteins).

If you remove or mutate the gene in the virus that targets that checkpoint, the virus will only be able to replicate in cells that have a defective checkpoint.

I saw talks back in the late 90s where they had a few great results with inoperative head and neck tumors, but there were too many complications and deaths.

Yeah, I thought so too. Then again, there are some enzymes that somehow outperform the theoretical maximum diffusion constant. Something about formate as a substrate.

I'm terrified if I talk about this some jerkwad will make some association with a vaccine or aquarium cleaner, and I don't like responsibility.

That is how I read it, but I really like bourbon. like a lot. I like bourbon.

Interestingly, there are some very weird things that could happen with that rate.

An extreme example I know of is Xenopus oocyte maturation. Oocyte maturation goes through a number of steps, in one of those the oocyte basically hoards a whole bunch of mRNA but doesn't do much with it (for like days), then at the next stage it makes a whole lot of protein but little mRNA.

So in this (somewhat extreme) example calculating the rate of proteins made per transcript is going to yield very different answers, and is also going to obscure what is really going on in the cell.

This is an extreme example, but I'm sure you can see the difficulties.

I would tend to think that has a worse chance at a useful and glib answer (although you may find some). For anything practical, that rate might not be super informative about what is going on.

It is harder to study because of differences in protein degradation rates and other things. High absolute numbers of a protein made per hour with a high decay rate can have the same ratio as a slow synthesis and slow degradation rate protein, There are a number of other technical challenges. Although there are certainly rates known for some individual mRNAs, and have been for some time, it is harder to look at that on the whole genome

That being said, the paper below suggests one to millions per generation (Figure S1 supplemental), which they define as a minimum of about 21.5 minutes (varies substantially).

The paper below is an E.coli example. It may very quite a bit in other organisms and cell types in multicellular organisms at least. life stage etc.

"Quantifying Absolute Protein Synthesis Rates Reveals Principles Underlying Allocation of Cellular Resources" https://www.sciencedirect.com/science/article/pii/S0092867414002323

It varies considerably for a number of reasons.

Transcript lifetime is generally regulated directly by degradation in a time dependent manner. There are regulated in many others ways as well including miRNAs, and probably at least half a dozen other things.

According to the below example the median half-life of a transcript was 7 hours, with a few mRNAs under an hour. This may be very different than for bacteria, or various cell types etc.

How many proteins are made per transcript before degradation is also liable to be very different for reasons like, for example, codon usage (rarer codons tend to have smaller tRNA pools) so it will take longer to translate and thus there will be fewer proteins, and any number of other things.

Database for mRNA half-life of 19 977 genes obtained by DNA microarray analysis of pluripotent and differentiating mouse embryonic stem cells

https://pubmed.ncbi.nlm.nih.gov/19001483/

NO, this is not true.

CRISPR has it's basis in bacteria adaptive immunity. There are many similar systems.

https://geneticeducation.co.in/how-does-the-crispr-mediated-adaptive-immune-system-work-in-bacteria/

Adaptive immunity mediated by antibodies and specific types of immune cells, maybe, but that wasn't the question.