Several themes have been doing the rounds lately. The origin of organelles, standards of evidence, common descent, the role of phylogenetic analysis, and the meaning of ‘prediction’ in science. Here’s a case study/rambling discourse that links a few themes.
Researching an answer to a separate question (I do try), I was struck by a thought about RecA. RecA (also going by the names RAD51, Dmc1 and RADA in different groups, for historical reasons) is a ubiquitous group of proteins involved in homologous DNA repair. That’s a process whereby a break in DNA can be ‘patched’ if a homologous sequence can be located. Matching sequence either side of the gap is aligned (by nothing more sophisticated than the binding energy of DNA complementarity) and then a DNA polymerase template-copies from the intact strand to the broken one between the two complementary sequences. Both accidental and deliberate breaks are repaired by this, hence it is involved both in maintaining DNA integrity and in the more ‘orchestrated’ process of crossover formation in meiosis.
Because this process relies on quite a high degree of complementarity, it works best on sister chromosomes – those recently replicated, within the current cell cycle, and hence clearly commonly descended. This is all a prokaryote has to work with, outside of instances of LGT. In eukaryotic diploids, the donor for repair can be the homologous diploid chromosome (that’s a terminological confusion: the chromosome pair with the greatest amount of homology is actually not the homologous pair, but the sister pair). But even in diploids, the sister is ‘preferred’ for repair – when not available, the normal repair pathway is ‘nonhomologous end joining’, which simply splices the break. An exception to this is during crossover of meiosis. Most crossovers form between homologues, not sisters.
So, thinks I, if chloroplasts and mitochondria evolved from bacteria, their RecA equivalents should be more like those of bacteria than archaea. To the internet!
It so happens that all these proteins are, in the modern eukaryote, held in nuclear DNA. So in a plant, you’ve got your RAD51s, plus Dmc1 specific to meiosis, but you’ve also got RecA proteins targeting, respectively, mitochondria and chloroplasts. RECA1 heads for chloroplasts, RECA3 for mitochondria. There’s also RECA2 which goes to both.
More specific and comprehensive phylogenetic analysis reveals quite a complex picture. Nonetheless, the Lin paper notes a ‘striking’ sequence similarity between the recA genes of plants and protists and those of the bacteria from which they are presumed to have come. There is a healthy 61% sequence match between RECA1 and the RecA of cyanobacteria. Sequence identity for RECA3/bacteria is not so high, but interestingly, Arabidopsis RECA3 can complement E. coli deficient in bacterial recA. E. coli are Gammaproteobacteria, not Alphaproteobacteria as is thought to be the group from which mitochondria came, but still not a million miles away. That’s not conclusive of a common origin, but is a noteworthy fact, consistent with structural conservation.
And that, really, is where I was headed. I started from the hypothesis that mitochondria and chloroplasts originated as bacteria. A prediction of that hypothesis is that organelle-targeted proteins would be expected in general to align more closely with bacterial than with archaeal or non-organellar eukaryote proteins. That prediction has been borne out. The hypothesis has been strengthened by that observation. How can that be? I did the same a few days ago with N-formyl methionine as translation initiator. Maybe I’m cherry-picking, but there are no searches I’m not mentioning that drew a blank. This is the sum total of my ‘research’: two things that it occurred to me to look for, and I found them both.
Also of interest to me, given the conviction explored in my ‘Evolution of Sex’ paper that meiosis is foundational to the modern eukaryote clade, is the finding that Dmc1 apparently evolved very early during what it pleases me to call ‘eukaryogenesis’. Whether it preceded or succeeded the mitochondrial endosymbiosis is not clear, which is one reason I don’t think of endosymbiosis as definitively the origin of the eukaryotic cell, whatever lols may accompany someone finding an author who does just that (Hi, Mung!).
Another point to ponder: homologous recombination relies upon a physical analogue of the algorithmic alignment performed during sequence comparison. It is only by anchoring matching sequences that ‘differences’ – in repair, the missing vs the intact sequence – can be located. Molecular differences between taxa are trumpeted by Creationists, but they are located in much the same way. The question remains: where does the alignment come from? In the case of sister chromosomes, it is non-controversially common descent – the sisters arise in the same cell cycle. In the case of diploid homologues, again not too controversial – the bases of the haploid chromosomes in gametes can reasonably be assumed to have a common origin in template-copies originating in an ancestral cell. But somehow, for the Creationist, this logic breaks down somewhere not clearly specified outside of the species. Alignment suddenly stops being common descent and becomes the completely indistinguishable ‘common design’. I don’t see why.
That’s like asking why geology didn’t predict the himalayas. Geology predicts mountain ranges, but it doesn’t predict a particular layout of the continents that make up the surface of a planet. Like, 3 billion years after this planet forms, it will have this layout of tectonic plates. Nobody has knowledge at that accuracy and level of detail to be able to make predictions like that.
That is the same with evolution. In the same way, evolution predicts gene and organelle loss in some lineages, it just doesn’t make specific predictions about which particular lineages. We don’t have the kind of information that allows us to predict the history of life at that resolution.
Part of the hypothesis of endosymbiosis for mitochondria and chloroplasts is that many of their genes were horizontally transferred to the archaeal host genome. Supposedly there are some strong selective reasons why this would be favored as opposed to having the organelle retain it’s full genome.
No. The nuclear DNA repair came from archaea. The mitochondrial DNA repair came from the mitochondrial eubacterial ancestor.
Introns gradually proliferated. They still do. We understand how they do this. What’s the problem?
We know of several examples of homologous genes with different numbers of introns. We know many examples of introns that are clearly related and have accumulated both in number and through suffering mutations iteratively over geological time. The picture you paint here is itself a form of cherry picking, as you actually leave out all the interesting details about introns that reveal their history as evolving entities.
The argument you are advancing here can only be maintained when you deliberately ignore the actual properties of introns, and focus only on the fact that they exist.
ok, but how do the repair enzymes know that?
So they just got lucky? I am asking how they know which chromosome to go to in order to find a replacement sequence. And then where to look on that chromosome. And then how this all came about starting with a bacteria without any chromosomes at all. It’s just all so very … miraculous. 🙂
Simply magical.
So it was excised from one DNA strand and then inserted into a different DNA strand, with the DNA strand being imported into the nucleus from outside the nucleus? And in the meantime, everything just kept working just swimmingly.
That’s your story?
Now that would be a miracle. 🙂
You’ve shown a willingness to be reasonable, so let me try this out on you. How do we know there has been gene and organelle loss? How is it that such knowledge, once gained, became a prediction of evolutionary theory?
Because I don’t think it’s a prediction at all. I think it’s an observation. There’s no principle of evolutionary theory that I am aware of that predicts that entire organelles will be lost. Enlighten me?
No. I ask again: Do you have any idea at all what Theobald did? Have you even read the paper?
And archeon. Another type of prokaryote besides bacteria.
If eukaryotes today are an indication, then it was probably the case that when an archaeal cell was invaded by a bacterium, the bacterium lived as a parasite inside it and would grow and divide several time such that the archaeal cell would contain multiple bacteria that would diffuse slowly around in the cytoplasm.
That way when the archaeal cell divided, chances are both new cells would have mitochondria inside them. Then the process would repeat, as the archaeal host slowly would grow, along with it the mitochondria inside would divide multiple times and take up whatever free space they could, such that when it came time to divide again for the host, it again would have so many mitochondria that when it split, both “halves” would have some inside it.
This is basically what happens in eukaryotes today. Some eukaryotic cells today contain thousands of mitochondria. It was probably never 1:1. Even if only a single bacterium originalla invaded an archaeal cell, that parasitic invader would grow and divide multiple times inside the archaeal cell.
Current thinking is that the invader might originally have been a parasite that wasn’t even advantageous to the host (there is some debate over this).
But as phoodoo will tell you, some times the shitty ones are just lucky, and the best ones are just in the wrong place at the wrong time. It’s true. The biggest strongest tiger can end up in a landslide and get buried, leaving the significantly less awesome tiger as the sole survivor. It’s not particularly miraculous.
The host was an archaea, not a bacterium.
Same in that they both initially had ATP synthase. Archaea have ATP synthase just like mitochondria do.
Unneeded genes are not retained by natural selection and so are lost to inactivating mutations and eventually through deletions.
Yes and they probably just happened one at a time over millions of generations.
Yep, pure blind dumb luck, and natural selection.
With natural selection, not all that miraculous to be honest.
No. Probably just copied, not excised.
Yeah pretty much. There are many ways this could have happened. It doesn’t even have to be through DNA. It could be transcribed in the bacterium into RNA, that RNA is then lost for whatever reason (there are many known) into the host cytoplasm. And this RNA could then be reverse-transcribed back into DNA and incorporated in the host genome by repair mechianisms that fix what-looks-like-broken DNA. Prokaryotes do this. Our own genomes do this. Some transposons take advantage of such mechanisms to move around and proliferate.
Or one of the several invading bacterial cells could undergo apoptosis, or just plain fall apart, or get killed by the host and disintegrate, for whatever reason (hey, it could suffer a lethal mutation) and release it’s genetic material into the host, where local DNA repair mechanisms would mistake them for damaged host DNA and incorporate them. There isn’t anything about this that is “miraculous” or “magical”. The exchange of genetic material between prokaryotes isn’t unusual or unlikely. At all.
There might not have been any nucleus at the origin of endosymbiosis.
They don’t know anything, they’re enzymes, not sentient. They just work on things that are sufficiently similar. It happens to be the case that they are similar BECAUSE they are homologous.
Who got lucky? Your question doesn’t make sense in context.
They don’t know anything. Molecules interact at varying degrees of mutual attraction and repelling through their overall 3dimensional shape, and their local polarity and charge. The repair enzyme “fits” with the shape of DNA and only activates when certain structural conditions are met. It doesn’t “know” anything any more than the south pole of a magnet “knows” to attract the north pole of another.
There was a bacterium without a chromosome of some sort? How do you know this? Where did you get this remarkable insight into early life?
I can see how it would look like that when you know seemingly nothing at all about chemistry.
Should I take this to mean you refuse to answer them?
Yes. yes. By bacterial host I didn’t mean the host was a bacterium but that the host was hosting a bacterium.
… mitochondria and chloroplasts originated as bacteria, engulfed by what?
Thank your for clarifying the host was an Archeaon.
Occam’s Razor sez excised. Why explain something by two events when one will do? If merely copied now you still have to explain the disappearance of the sequences from the DNA of the bacterium. And you have to do it for both mitochondria and chloroplasts. Excised is better. 😉
Does it really matter? Will it kill you if I don’t?
I have to hand it to you Sal…You really nailed it with the prokayote >eukaryote gene supposed evolution… It can’t be any clearer than that…
Whoever can’t see it that it couldn’t evolve, he is lying to himself…For that, he can go straight to hell…if it existed…
Great job Sal!!! Your further arguments on the theme are not necessary…
Well first you build a phylogeny by taking shared genes and making your tree from that data. And then you probably try to estimate where the root of that tree is. This then is your guiding genealogy that tells you who is more closely related to who.
Then you look at the patterns of presence and absense of other genes (or organelles).
If all but one of your extant taxa have chloroplasts (say), yet your phylogeny clearly indicates that the organism without chloroplasts is closely related to another one with chloroplasts, and the one with chloroplasts in turn is also closely related to another with chloroplasts, and so on and so forth, then you’d infer that the one without it lost them.
Something along those lines.
Okay now I see. I suppose you are right in the sense that evolution doesn’t say “there will be loss of organelles” in that way.
I think it is actually a more general prediction that apply to basically any aspect of organismal physiology. Sort of like this: if the conditions that favor the retaining of the entity are no longer met, and of course if the entity isn’t critically necessary to survival, then it will be eventually lost as deleterious mutations are no longer filtered out.
Like how the blind cavefish eventually lost their sight because they live in complete darkness and neither they, nor any of their food or predators, have any sort of bioluminesence.
I think this is ad hoc. Why should I believe it reflects what actually happened?
So this parasite grew and multiplied and never harmed the host, even though this host/parasite combination is totally new. The engulfing host never starved, never burst, everything was just peachy. Smells just like a miracle.
It just so happened that the bacterium replicated much faster than the host. Another miracle.
And since we’re now in the business of copying sequences from these parasites into our archeal DNA, it just so happened that the DNA sequence for RecA was only copied once. Another miracle.
Hallelujah!
Wave the magic wand of natural selection!
I think it’s time we change the name evolution to miraclelution…
Further, the ancestral acheaon already had it’s own DNA repair enzyme, but it didn’t work so good on mitochondrial DNA. Better to snip, copy, paste, voila!
Why wasn’t the host’s DNA simply duplicated and changed to become what was needed? Natural selection could have done that, right?
At this level of story telling I honestly don’t know how to tell the difference.
Rumraket claims something happened by pooftery and then natural selection came by to make it not pooftery, but rather pooftimation. How does he know? He doesn’t.
I agree that explanation superficially appears simpler.
But I’d still say copied is more likely, because after all the whole chromosome is copied every cell division. And cell divisions happen all the time, whereas single-gene excision and reintegration is rather unusual. And you don’t have just a single organelle from which you want to remove the unnecessary gene, you probably have dusins of them in the host. So that’s a lot of targeted excision you need to invoke. One for each invader.
As for the loss of the gene in the organelle that’d just be deleterious mutations being favored by selection. Here’s why: It takes time and energy to replicate DNA. So when a single eukaryotic cell contain several organelles each with their own genome, it costs a lot of energy if they all have their fully intact ancestral genomes. For that reason, if any of the organelle genes are transferred to the nucleus, they only need to be copied once when the host itself divides, as opposed to copied many many times when all the organelles divide. Following such a transfer, the organelle genes are no longer required, and so deleterious mutations can accumulate in them, and eventually they get lost to the occasional deletion mutation. And every single deletion is beneficial, as it deletes unneeded DNA that otherwise would cost energy to copy.
My guess is that probably the entire invader chromosome was originally transferred and fused with the host genome. And the host retained the genes from that invader chromosome that were beneficial to have there, while the rest detoriated to deleterious mutations and deletions. And the invaders gradually lost theirs as they no longer needed them since they were now present in the host. And the few that remained in the organelle invader remained because their presence there was fundamentally necessary for their continued existence.
Yes it matters, as you keep using a word you refuse to define. How are we to make sense of what you say if you don’t explain how you understand that word?
Amazing what we can agree on when we assume the other is capable and willing to be reasonable. 🙂
How about gene loss? We infer it has taken place. But does that make it a prediction of the theory? Can we also agree that evolution doesn’t say “there will be loss of genes” in that way?
From where I stand it’s difficult to even say that evolution predicts that if something is unused it will be lost. You seem to be wanting to hang on to that.
If that’s the case, how does one explain junk DNA?
Let’s say that humans lost their ability to hear God’s voice because they stopped using that ability. Since the ability doesn’t exist, there’s no evidence for it. So you can never verify the “prediction.”
And take vestigial organs. They are still there. They haven’t been deleted. But the evolutionist can always claim that they are in process of being deleted. So counter-evidence (it’s unused but not gone) is taken as evidence (it will be gone, just believe!).
So I think claiming evolution predicts anything with regard to disuse is on very shaky ground.
ETA: It was there once, but now it is gone. It would not be gone if it was in use. Therefore it must not have been in use.
Because that’s what happens today, so why not?
There are degrees of harm. You probably carry parasites right now, and yet here you are. You might even have children, and they might have parasites too.
It is actually not in the interest of parasites to kill their hosts. If they do, they lose their host!
Cells come in different sizes, and the smaller ones usually replicate faster than the bigger ones for the simple physical reason that it takes more time to biosynthesize more material.
This is really not all that miraculous. Have you ever had lice? Not that miraculous in my view.
What do you mean only once? What you’re saying here doesn’t make sense. Why would it have to happen more than once?
As opposed to waving an actual magic wand that can just make shit appear from non-being, yes!
Yes and I appreciate that. I will go to bed now though, so answers for the rest of your questions will have to wait for tomorrw. Good night.
You know of a case where the DNA of a human parasite has been incorporated into the nuclear DNA of humans and subsequently lost from the DNA of the parasite?
Also, the claim that it is happening today is suspect. We are speaking of an intra-cellular parasite. You have a candidate in mind?
The fairy-tale of multiverse pretty much says exactly that…
If you have enough universes and in each one of them enough potties, s..t is bound to appear in one of them…no actual wand waving required…lol
I have always been intrigued by why atheists/evolutionists have so much more faith than many believers…I have tested it many times over the years…They are willing to believe any bs as long as it doesn’t lead away from materialism and, Darwin forbid, to ID/God…Today’s exchange is the very proof of that…
Perhaps Rumraket can produce some evidence to substantiate his claims. I’m willing to wait and see.
Yeah…evidence as he sees it…“it evolved” don’t wet your appetite… 😉
Well, perhaps ingestion of bacteria by archaea happened all the time. Perhaps there was nothing at all unusual about it. If there’s evidence that someone wants to present, I’m all ears.
Perhaps there is convincing evidence that after ingestion of bacteria by archaea the bacteria replicated more quickly than the host leading to multiple copies of the bacterium in each host before the host ever replicated. If there’s evidence that someone wants to present, I’m all ears.
But if Rumraket is just tossing out hypotheticals that cannot be substantiated by any actual evidence, well, we can all play that game. I say goddidit!
All the major features of the eukaryote cell were already present before eukaryotes began to diversify into the extant phyla we see today. There is absolutely no evolutionary reason why this should be so.
It just happened, that’s all.
What happened to the “partial-eukaryotes”? No one knows. Did they ever actually exist? No one knows. Should we just believe without evidence? Apparently so.
To believe that all the major features of the eukaryote cell all came together in one fell swoop is to believe in miracles. The alternative is to believe in the gradual evolution of the eukaryote ancestor by gradual accretion of the elements of the eukaryote cell even in the face of the lack of evidence for such a gradual accretion.
Pick your poison.
According to Esser et al. (2004) there has been extensive transfer of genes of mitochondrial origin into the eukaryote nuclear genome.
Numerous happy accidents. Miracles multiplied.
Wave that magic wand of “natural election’ to make it somehow go away. It’s still magic. Even assuming that natural selection favored each and every move of a gene from a mitochondrion to the nuclear genome is itself an invitation to believe in magic.
#DontStopBelieving
https://www.yeastgenome.org/reference/S000121900
The ancestral complexity of the cytoskeleton in eukaryotes leaves a huge gap* between prokaryotes and the earliest eukaryote we can reconstruct.
– Gaspar Jekely
* insert God here
Perhaps it was just an analogy.
You’re confused. The particular statement of mine to which you are responding, is itself a response to you questioning my explanation that the organelles in eukyotes today exist in large numbers inside the eukaryotic cell.
There is not one mitochondrion for every eukaryotic cell. There are hundreds, some times thousands.
The context of our conversation is this:
Rumraket: If eukaryotes today are an indication, then it was probably the case that when an archaeal cell was invaded by a bacterium, the bacterium lived as a parasite inside it and would grow and divide several times such that the archaeal cell would contain multiple bacteria that would diffuse slowly around in the cytoplasm.
Mung: I think this is ad hoc. Why should I believe it reflects what actually happened?
Rumraket: Because that’s what happens today, so why not?
Mung: You know of a case where the DNA of a human parasite has been incorporated into the nuclear DNA of humans and subsequently lost from the DNA of the parasite?
Since it is now clear we were talking about your question regarding the presence of organelles in both cells following cell division of the host, it isn’t suspect. Mitochondria really do divide many times so they exist in hundreds inside eukaryotic cells. Today. Your own cells right now, every single one, contains hundreds of mitochondria. So when one cell splits in two it’s pretty much unavoidable that the offspring will contain some of them.
I suppose we are talking specifically about the gene loss in the invading cells following transfer of genetic material to the host genome here.
As far as I am aware, and to be honest this is at the limits of my own understanding, there are some metabolic and population genetic models which indicate that this (gene loss in the invader) really is what would happen if the invader transferred genetic material to the host. The metabolic cost of replication and genetic load under the strength of selection and… stuff like that, predicts gene loss in the invaders. Don’t ask me about the details of those models because I can’t answer it. You’d have to talk to an expert there.
Well that part is simply unavoidable. Mutations happen all the time, they’re unavoidable. And some of those mutations will happen in genes that affect some phenotype. And a large fraction of those mutations are deleterious, they “erode” the function.
Not a bad question at all and in fact that is one of the first objections the ultra-adaptationists invoked back when the debate about junk-DNA first started. Why would there be junk if extra genetic material not in use is deleterious?
The answer has multiple prongs that has to do with both the type of genetic materials that make up junk (pseudogenes, dead gene-duplications. (retro)transposons, introns, retroviral insertions and so on), and with the strength of natural selection and the genetic load.
Some of that genetic material is parasitic DNA that proliferates faster than natural selection can get rid of it (among other reasons because it exploits normal cellular mechanisms for DNA repair and reintegration). Like transposons, and self-splicing and inserting introns.
Some of that junk-DNA is recent stuff, so there just hasn’t been enough time to erase it.
And there’s the whole population size, strength of natural selection and genetic load factors.
The problem with your analogy here is that there are no such things as mutations and selection in it. There are some very basic physical facts that predicts the gradual and eventual loss of pretty much any unnecessary organic material:
1. It costs energy to carry around and to copy it when reproduction takes place.
2. Mutations happen in the genes that are involved in the existence and maintenance of that organic material. And among those mutations are both deactivating mutations and deletions. Invariably, the genes will turn off as their expression is no longer maintained, and deletions will eventually after enough time delete all traces of their existence.
There are exceptions (the material is in some sense selfish and can replicate faster than the “host organism”). And there are factors that affect the rate of loss (mutation rates, cost of maintenance and replication, population size). And then there are pleiotropic effects of genes and mutations where something is maintained in existence because the genes that control it also control other still important biological functions, so if mutations were to happen in those genes, while it would delete unneeded material, would also affect another function critical to survival.
And some times we can even construct phylogenies of the gradual loss of the entity in question and see how it degrades over time independently in multiple lineages. Like the pseudogene GULOP that was used to biosynthesize vitamin C somewhere around 65 million years ago. This gene still exists in all primates, and we can see how some mutations have accumulated in it over time. How some exons (coding regions) were gradually lost to chance deletions, and how other mutations introduced premature stop codons and so on.
Here’s a nice article on that: http://www.evolutionarymodel.com/pseudogenes.htm
I don’t. And I think you’re wrong when you say that.
And again, this can actually be modeled by taking some very simple observational facts. It follows. It has been observed in laboratory populations (loss is happening in Lenski’s long-term evolution experiment with E coli, as unneeded genes in E coli that don’t see use in the simple and constant flask-environment, are gradually lost to deletions and inactivating mutations). And we can see the phylogenetic signal of gradual loss for many such disappearing entities in the diversity of life. Like GULOP.
It’s not on shaky ground, it’s an empirical fact that can’t be rationally denied.
Why is there not?
Says who?
This thread was started because someone found another small piece of that evidence.
Some times we are in the unfortunate situation that we are trying to explain the result of a historical chain of events we can no longer see. So the best we can do is work with what we have, what we know, and try to predict what follows, and test it against future observations (like Allan did with this thread). If this isn’t good enough for you, then so be it. Then you will forever be without an explanation for the origin of the eukaryotic cell since you apparently reject observational hypothesis testing.
There’s no reason to think it had to happen iteratively, though that can’t be ruled out. You observe the genes are present in the host, and absent in the endosymbiont. And the genes still in the symbiont are more similar to eubacteria, and the genes in the host are a mix of genes that are similar to both bacteria and archaea.
That is the pattern you have. With that kind of data the hypothesis that it happened interatively is equally consisten with the hypothesis that a single large transfer happened.
And I’m still not clear what you mean by a miracle. You keep using a word that, superfically, doesn’t seem to really mean anything other than “unlikely”. So an unlikely event happened. And so what?
What is magic? That genetic material can be copied and transferred? That a cell can divide inside another? By what definition of magic? What is magic to you? Just something you don’t understand, or something you don’t believe?
Why? Try to explain why, and start by defining what magic is.
Mung,
Which god?
Cytoskeletal homologues have been found in archaea. I think this was quite recently.
You know of a case where the DNA of a human parasite has been incorporated into the nuclear DNA of humans and subsequently lost from the DNA of the parasite?
Yes. Trypanosome cruzi
Also, the claim that it is happening today is suspect. We are speaking of an intra-cellular parasite. You have a candidate in mind?
see above
Ed Yong blogged about this:
http://phenomena.nationalgeographic.com/2010/02/14/genes-from-chagas-parasite-can-transfer-to-humans-and-be-passed-on-to-children/
Thanks PeterP.
The claim is that such a parasitic invasion would be non-fatal and a symbiotic relationship would be born.
It is interesting that the DNA comes from the mitochondria.
Do you know what an event horizon is? That’s how they describe what took place before the LECA. We just don’t know and we can’t see.
Now you can continue to believe what you like, and tell stories all you like, but they are not evidence-based theories.
This doesn’t mean that goddidit. It just means that we’re ignorant. And we ought not pretend to know more than what we can currently know just because we need for something like our story to be true in order to be an intellectually fulfilled atheist.
Be a scientist, not a teller of tales. As long as you continue to tell tales I’ll be here to laugh at them, sure. I know they are just tales. Surely you know it too.
It’s not an analogy! It’s a counter-analogy.
Breath-giving cooperation: critical review of origin of mitochondria hypotheses
Jesus ,mung.
Lucky for all of us Mung is here to keep everyone honest eh?