This is just a fact. All life that we know of has the same origin. Common descent is a core tenet, and one of the best established facts, of modern biology (https://doi.org/10.1038%2Fnature09014). For there to have been multiple distinct ancestors, we would need to see some relevant differences in the core machinery of life. And the fact is that, despite minor variations, we simply don’t see any. The odds of there being multiple distinct ancestors is astronomical, and would fundamentally impact our understanding of modern biology.
> and b) no organism has drifted in the millions of years of evolution
Organisms have drifted. That’s what evolution is. But evolution plays by rules, it can’t just change things willy-nilly. Changes to the core machinery would presumably either break it outright, or be so strongly detrimental as to be purified away almost immediately. Of course many genetic changes are deleterious to some extent but most effects can either be buffered for a short time because they are minor, or they confer some other advantage. In the core machinery of the cell this is much (!) less tolerated because even tiny chemical inefficiencies would immediately be amplified millionfold. Odds are, the DNA/RNA core machinery of all life sits in a steep local optimum. It’s not necessarily a global optimum but it’s essentially impossible to evolve out of because any individual change, or even a handful of coincidental changes, would leave the organism a lot worse off.
but that doesn't mean it's been proven through experimentation, does it? isn't it just an assumption?
what if there's something akin to mathematical uniqueness in the mechanics of the core machinery?
I mean it in the sense that it's either the way it is, or it's not really viable over a long enough period of time? such that it could have multiple origins which all nontheless converge into the same core mechanism?
It’s not an assumption, it’s backed up by excellent evidence — see the paper I linked.
> what if there's something akin to mathematical uniqueness in the mechanics of the core machinery?
Well that’s clearly not the case, we can trivially (…) design self-replicating machines that have completely different mechanics, as a thought experiment. More to the point, we can change parts of the machinery. For instance, we can take the universal genetic code and, with effort, change it into something completely different (by just swapping all codons around). The result is just as viable, but doesn’t exist in nature. In fact, the observed universality of the genetic code, in itself, is already seen as sufficient evidence for common descent (and then some).
Or, some would argue, evidence of a common designer.
The question seems the same as, could an AI in a virtual world deduce or prove its artificialness or the reality outside the virtual?
To me that’s more interesting than the simple credulity implied by moon cheese.
It's taken that (known) modern organisms descend from a common set of ancestors, but the tree of life isn't a tree. Organisms diverged and merged multiple times along the way to the modern world.
It says nothing about how that/those points of common descent came to be.
What originally constituted living things probably weren't very good at living by modern standards. They probably leaked like sieves, and they probably traded RNA, polypeptides, and other small molecules back and forth.
When was this soup alive, and when wasn't it? I suspect it's just a continuum, and that complicated soup probably went back and forth across that grey zone of living-nonliving many times.
That’s correct but I don’t see what this has to do with my comment. It’s still a fact that all modern life, at some point, came through the same individual organism (EDIT: this should be population) which, furthermore, already possessed the fundamental machinery of DNA replication, RNA transcription and protein synthesis (amongst other things).
EDIT: I misunderstood. Yes, you’re right: due to lateral gene/molecule transfer, it’s not certain that the last universal common ancestor was an individual cell, and at that time the label “individual” probably didn’t make much sense (although the paper I linked argues strongly that it was in fact one single cell).
This is a contentious statement that I don't think is established - a fact that the grandparent comment is trying to raise.
I don't think there are any known to be radically different. Note that it's possible that life arose several times but only the lineage of that one cell survived, perhaps? In any case, it's not like there's been no variation.
Now, here's a mystery (AFAIK): Just where is the genetic code stored? I seem to recall reading an article a while back about how while this seems like an easy question it's actually not known. I can't seem to find it at the moment, though. Anyone know more about this?
In terms of potential errors in gene expression, the genetic code is rarely discussed as a potential source of error.
It's just difficult to study for various technical reasons related to how we sequence it.
Sometime the mistranslation is even intentional! (https://www.ncbi.nlm.nih.gov/pubmed/25220850)
As you mentioned though, there are also quite a few safeguards.
* tRNA synthetase example: https://www.ncbi.nlm.nih.gov/pubmed/27226603
* trans-editing factor example: https://www.ncbi.nlm.nih.gov/pubmed/28737471
Damaged tRNA is even repaired (a bit, sometimes). (https://www.ncbi.nlm.nih.gov/pubmed/28901837)
From an interesting (2018) review of tRNA in general (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6103721/):
> Surprisingly, a perfect proteome is not a pre-requisite for cellular viability even in the context of human cells. Lant et al. demonstrated that a single tRNA mutant can lead to significant mistranslation in human cells [17]. This was accomplished by expressing an Ala accepting tRNAPro G3:U70 variant in HEK 293 cells. The authors visualized a rate of ~ 3% mistranslation using a novel green fluorescent protein (D129P) reporter that fluoresces in response to mistranslation at proline codons. In contrast to previous studies in yeast [18], human cells in culture did not mount a detectable heat-shock response and tolerated the mistranslation without apparent impact on cell viability.
Translation errors also exist, and some people hypothesise that there is selective pressure on protein-coding genes to reduce this source of errors by selecting codons in a way that reduces the error rate (potentially by slowing down the polymerase). This results in something known as “codon bias” but so far there is no good evidence that codon bias has an actual effect on error rate (it does have an effect on correct protein folding), or is selected for (http://dx.doi.org/10.7554/eLife.27344, http://dx.doi.org/10.1371/journal.pgen.1006024).
However, I believe my third link is about environmental stress triggering intentional mistranslation (mRNA to protein). From that paper's figure 3:
> Proteins arising from “statistical proteomes” have various folding and binding properties, resulting in phenotypic diversity in the host organism.
I haven't bothered to pull up the related references (5 obvious ones) to assess their strength though.
The papers you linked seem to be claiming that codon encoding preferences (which vary by gene category) are in fact due to (or merely correlated with?) GC content in mammalian genomes (as opposed to a number of other previously proposed mechanisms). This is surprising because individual tRNA abundance varies by cell state and type, so that would have been the obvious (but apparently wrong) explanation. It's doubly surprising because a number of single celled organisms utilize the mismatch between codon preference and tRNA availability in order to regulate protein translation, but these papers are claiming that's not a significant factor in mammals.
tRNA gene expression varies by cell state, but isoacceptor abundance is in fact very stable (at least in mammals). Meaning, if you have a set of tRNA genes which all code for, say, Ala_AGC, the sum of the gene expression of all these genes is relatively stable, even if their individual expression varies (http://dx.doi.org/10.1101/gr.176784.114l; full disclosure: I’m an author on this and one of the previously linked papers).
Why individual tRNA gene expression varies, and how the cell regulates the overall stability, is unclear (my personal pet theory is that secondary tRNA function as regulatory RNA, in the form of tRNA-derived fragments, causes the need to regulate tRNA genes, see e.g. http://dx.doi.org/10.1016/j.cell.2017.06.013).
> It's doubly surprising because a number of single celled organisms utilize the mismatch between codon preference and tRNA availability in order to regulate protein translation
It’s not that surprising: gene regulation happens fundamentally differently in eukaryotes and prokaryotes, and even differently in different classes of eukaryotes. The effective population size (= evolvability) and genome complexity seems to play a role here. Simply put, higher animals have much more powerful and precise ways of controlling gene expression (enhancers and histone control). Regulation at the translation level is comparatively slow and wasteful (it’s several steps further down the line of the gene->protein production process).
The synthetases are also encoded in DNA, so the fundamental point, that the code is encoded in DNA, stands.
On the other hand, once a certain layer of functionality exists, and starts being used to build on top of, that layer will resist change, because any variation will throw off so many higher level processes it's unlikely to be viable.
Why?
Life happens rarely enough; even in the 'optimal' conditions of the primordial soup, it's still a pretty miraculous occurrence for a cell to spontaneously form. Then consider this:
- The first cell was probably not 'good' at surviving, even in those conditions. It probably sucked at it, and was just barely good enough at doing it to reproduce a little and evolve a little.
- So, a cell which is actually good at surviving is pretty much guaranteed not to form spontaneously. Meanwhile, the lineage of the first (shitty) one has evolved to be pretty damn good at it.
- If a new cell tries to form, even if it's better at surviving than the Original cell, it'll probably get instantly outcompeted by its progeny.
Voila, single ancestor cell.
> b) no organism has drifted in the millions of years of evolution.
Why should they? There's no pressure to.
This would answer why most are using it now. If other cells uses a different mapping that's less optimal, they'll have a harder time to reproduce, and thus lose out over time.
https://www.jstor.org/stable/26047680?seq=1#page_scan_tab_co...
https://wps.prenhall.com/wps/media/objects/12330/12626747/my...
_Encoding_
Methionine is one of only two amino acids encoded by a single codon (AUG) in the standard genetic code (tryptophan, encoded by UGG, is the other). In reflection to the evolutionary origin of its codon, the other AUN codons encode isoleucine, which is also a hydrophobic amino acid. In the mitochondrial genome of several organisms, including metazoa and yeast, the codon AUA also encodes for methionine. In the standard genetic code AUA codes for isoleucine and the respective tRNA (ileX in Escherichia coli) uses the unusual base lysidine (bacteria) or agmatine (archaea) to discriminate against AUG.[15][16]
The methionine codon AUG is also the most common start codon. A "Start" codon is message for a ribosome that signals the initiation of protein translation from mRNA when the AUG codon is in a Kozak consensus sequence. As a consequence, methionine is often incorporated into the N-terminal position of proteins in eukaryotes and archaea during translation, although it can be removed by post-translational modification. In bacteria, the derivative N-formylmethionine is used as the initial amino acid. [0]
This is not a necessity. It is entirely possible life on earth was formed multiple times, completely independently and our lineage simply out-competed other sort(s) of life; and somehow we lost the evidence of it, or couldn't find it yet. As it's suggested by other comments, it's a well established fact that the life we know of share the same single origin (this organism(s?) is called the "Last universal common ancestor" or LUCA [1]); but that doesn't mean there has been a single sort of life our lineage ever interacted with, it just means our lineage was the only good-enough life for the conditions on earth for most of the geological periods.
[1] https://en.wikipedia.org/wiki/Last_universal_common_ancestor
https://en.wikipedia.org/wiki/Human_mitochondrial_genetics
Genetic Code Variants
For most organisms the "stop codons" are "UAA", "UAG", and "UGA". In vertebrate mitochondria "AGA" and "AGG" are also stop codons, but not "UGA", which codes for tryptophan instead. "AUA" codes for isoleucine in most organisms but for methionine in vertebrate mitochondrial mRNA.
wikipedia cites to https://www.ncbi.nlm.nih.gov/Taxonomy/Utils/wprintgc.cgi?
[1]: https://en.wikipedia.org/wiki/Tierra_(computer_simulation)