Certain commentators seem surprisingly agitated about pursuing the idea that there is no ‘theory of evolution’. Some mean there is no single theory, although on examination the things they see as separate are frequently simply different components of the same broad process. Or, alternatively, they are referring to evolution in other senses, or in non-biological contexts. Others say there is no theory at all, as if that against which they argue does not even exist.
A theme has emerged that TSZ is somehow suppressing their concerns. So, in the spirit of suppressive dictatorships everywhere, here is a thread for people to say whatever they want about this vital topic. Hopefully without pasting in vast swathes of something already posted elsewhere – a link will suffice.
Here, for my part, is my very broad summary of ‘the’ theory of evolution: Genetic changes (mutation, recombination) are subject to a sampling process, correlated to a greater or lesser extent with their effects on survival and reproduction. This process leads to a simultaneous increase and decrease in frequency for the variants in the population, through to, in the limit, extinction or fixation of a variant. This process proceeds indefinitely, subject to the fuel of new variation. All commonly accepted*** ‘theories of [biological***] evolution’ of which I am aware place emphasis on different components, influences and consequences of this basic process. None, so far as I am aware, are at odds with it, which might be expected if there really were ‘different theories’.
*** The caveats are inserted to try to head off anticipated ‘gotchas’, in a possibly forlorn attempt to reduce opportunities to make semantic capital out of a phrase whose intent should be easy enough to understand without them. This is not ‘biologism’: the ToE which upsets people is (are?) the generally accepted biological one.
If they are related by inheritance it is.
Read this explanation and/or draw the diagram yourself.
Walter, please read Denton’s “Evolution: a theory in crisis” he explains it all- nested hierarchies are the product of a mind. Ancestor-descendant relationships do not form a nested hierarchy. And just because a nested hierarchy can be depicted as a branching tree that doesn’t mean all branching trees are nested hierarchies. Both Wagner and mayr have said that evolution doesn’t expect one because evolution is too messy and complex a process.
If they are related by inheritance it is.
Read this explanation and/or draw the diagram yourself.
Wrong- ancestor-descendant relationships do not for nested hierarchies. Your parents do not consist of nor do they contain you. A parent population does not consist of nor contain its daughter populations. See Knox “The use of hierarchies as organizational models of systematics” Biological Journal of the Linnean Society (1998)
What do chimeras do to the nested hierarchy?
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC34369/
Patrick,
“Nested hierarchy” refers to the way taxonomic groups fit neatly and completely inside other taxonomic groups. For instance, all bats (order Chiroptera) are mammals. All mammals are vertebrates. Likewise, all whales (order Cetacea) are also mammals, and thus also vertebrates.
Given transitional forms we would not see groups fitting neatly inside of other groups. Even Wagner said so in “Arrival of the Fittest”. Why do you ignore him? Email him and ask him what he meant. I dare you, however by doing so you will owe me an apology.
Mung,
Combine in one cell the gene trees of two lineages – much like sex, but a bit less frequent.
Yea verily, it’s powers are eerily Godlike. Amen.
https://www.theguardian.com/science/2008/feb/09/natural.selection
Utterly magical. And untestable.
Only if your god is a genocidal maniac. Oh, wait….
You keep repeating that. It keeps making no sense.
Cite, please.
I already cited Wagner, Patrick. Turn off your selective reading and try again. Nested hierarchies require neat, distinct sets. Transitional forms, by their very nature, would blur all lines of distinction. Pages 9-10 of “Arrival of the Fittest” full quote posted above- in a post that you responded to. And that tells me you don’t want a discussion you just want to impose your will regardless of how wrong it is
Wagner’s quote
I read that. It doesn’t say what you claim it does. There is nothing in that quote that supports the nonsensical idea that transitional forms pose a problem for nested hierarchies.
Maybe Frankie could draw out an image and post it as a visual aid so we can understand what the problem actually is. I imagine also in the process he’ll realize he’s wrong so there’s zero chance of seeing such a picture from him.
Or am I wrong Frankie?
Well, no. I’m sure the long lived machine intelligences that either succeed us or we become will be able to observe such changes. And then, no doubt, the other AI’s, the ones that thought that pennies don’t add up to pounds will hang their heads in shame.
The point is that there are many people who have dedicated their lives to making it less magical, by unpicking it and understanding it. And then there’s you.
Wonder if Munkie will bother to update his internal understanding now.
Mung,
Very little is testable, it seems, according to some rather stringent criteria regarding what a ‘test’ involves.
I think they replicate unsuccessfully.
These elements seem to be very important to the Alan Fox theory of evolution, not so much for the Allan Miller theory of evolution. So it’s not a knock on the OP, it’s a knock on your theory of evolution.
Incompatible with what? Each other?
You seriously think we can’t find two theories that are incompatible with each other within the broad scope of evolutionary theory?
Some people think it’s more important than others. But it’s not like the two views actually conflict with each other, right.
Given the length of time life has existed on planet earth, perhaps there should be something in the theory to explain that observation.
There is, it’s called random genetic drift
Mung,
You’re getting the idea!
I’d be interested to see what you came up with. So far (that sentence is another example) there seems blanket incredulity at the very idea, but I still don’t know what you are getting at. Drift and selection aren’t incompatible, for instance, but I accept that might be what people mean. Hard to tell if they won’t say so.
The opportunity to provide substance once again goes begging. Pretend the ball is my face, and have a punt.
DNA_Jock,
Human DNA has a repair mechanism and retroviruses write into human DNA. Do you have experimental evidence that the human repair mechanism does not repair retroviruses? If you do then do you have evidence that these retroviruses don’t have a limited life?
This part does:
In an essentialist world, the essence really is the species. Contrast this with an ever-changing evolving world, where species incessantly spew forth new species that can blend with each other. The snake Eupodophis from the late Cretaceous period, which had rudimentary legs, and the glass lizard, which is alive today and lacks legs, are just two of many witnesses to the blurry boundaries of species. Evolution’s messy world is anathema to the clear, pristine order essentialism craves. It is thus no accident that Plato and his essentialism became the “great antihero of evolutionism,” as the twentieth century zoologist Ernst Mayr called it.– Andreas Wagner, “Arrival of the Fittest”, pages 9-10
Nested hierarchies require that clear, pristine world, Patrick. You cannot get distinct sets from “evolution’s messy world”.
Linnaean taxonomy is the observed nested hierarchy. It doesn’t have anything to do with evolution.
Added:
Regardless of what is eventually learned about the evolution of Clarkia/Heterogaura, the complex nature of evolutionary processes yields patterns that are more complex than can be represented by the simple hierarchical models of either monophyletic systematization or Linnaean classification. page 34, Eric B. Knox, “The use of hierarchies as organizational models in systematics”, Biological Journal of the Linnean Society, 63: 1–49, 1993
Why would they conflict? No one questions NS or drift, the disagreement is about their prevalence
DNA_Jock,
Human DNA has a repair mechanism and retroviruses write into human DNA. Do you have experimental evidence that the human repair mechanism does not repair retroviruses? If you do then do you have evidence that these retroviruses don’t have a limited life due to genetic breakdown?
“I’ve read some words on the internet and my incredulity floweth over but I’m not going to actually research anything or understand it deeply. PS you’re wrong”
Mung,
The elements you consider present in the ‘AF theory’ but missing from ‘mine’ are not, in fact, missing at all. I don’t mention phenotype or heritability, or selection or drift, by name, but they are certainly there.
colewd
HPV (may cause cancer later in life) and Hepatitis B come to mind are examples of prophage viruses which integrate into the hosts genome. HIV is a retrovirus that DNA repair fails to remove from the hosts genome as well as HTLV-I and HTLV-II
Harshman’s here. Ask him about the debate over bird origins.
Feduccia is best known for his criticisms of the widely held view that birds originated from and are deeply nested within Theropoda, and are therefore living theropod dinosaurs. He has argued for an alternative theory in which birds share a common stem-ancestor with theropod dinosaurs among more basal archosaurian lineages, with birds originating from small arboreal archosaurs in the Triassic.
No, dazz, random genetic drift is not a theory that explains the longevity of life on earth. Is there any particular reason that rather obvious fact gets left out of the theory? Just taken for granted?
Mung must think he’s really impressing Frankie and Phoodoo with these childish semantic games.
LMFAO, you’re so funny. Oh! you weren’t joking this time? Ouch
Mung,
That’s what you mean? There is no [a qualifier might be useful here if that’s what people really mean] theory of evolution because there are uncertain nodes? I’m stunned. Let’s teach the controversy then; nothing else for it.
Is there any way to resolve this conflict? Any way at all? Is it testable?
Interestingly, while HIV has an RNA based genome, the mechanism by which it inserts in the host genome involves recruitment of DNA repair pathways in the host. But this is not so as to “keep the HIV genome intact”, since technically it isn’t really broken. Rather, when the HIV’s reverse-transcribed cDNA is incorporated in the host genome, the junctions at the site of insertion are incomplete and need to be “filled in”. The host cell detect these incompleted junctions as “damage” and “repairs” them, at which point the viral genome has now become part of the host genome.
So it really gets a matter of technicality. Simplistically, the HIV genome is replicated successfully without falling apart, it doesn’t need to be “repaired” by host DNA-repair because DNA-repair is somehow critical to keep the DNA intact indefnitely.
Rather, due to the way the foreign DNA is inserted in the host genome, the two junctions where both ends of the virus genome meet up with the host genome, are missing bases on one strand. These two pieces are what is being detected as “damaged”. But nevertheless, DNA repair mechanisms are in fact involved in HIV replication.
None of this constitutes evidence for colewd’s misconception that indefnite DNA replication is impossible without repair-enzymes. It’s about successful integration into the host’s genome, not about keeping the viral genome from detoriating due to deleterious mutations.
Interestingly also, to the extent that a host genome does keep a viral insert error-free while in its DNA, this does allow such inserts to be used as markers in phylogeny, just like SINEs. Cue a rearguard action from Sal as he notes that science marches on and these inserts are really all functional too!
eta – italics for emphasis!
The funny thing about viruses is they don’t replicate the same way cells do, in the sense that one splits into two (and can do so repeatedly). Rather, when a cell is invaded by a virus, it can produce hundreds of new viruses from that initial invasion of a single cell, since the cell effectively becomes a factory for producing new virus. The virus basically hijacks the cell cycle, turning it towards virus-manufacture instead of replication, growth and division. This is one of the reasons viruses can escape genetic meltdown due to large mutation rates, because some of them produce so many offspring for every cell invaded that even though their mutation rates are very high, chances are with so many new viruses produced there will still be plenty of them without strongly deleterious or lethal mutations. This shows there’s a fecundity aspect to replication whereby deleterious mutations can be escaped from.
Basically for retroviruses, mutations are due to the error rate of reverse-transcriptase and the host’s RNA-polymerase (or in the case of DNA-based retroviruses, just DNA-polymerases and integrases). While both of these do make mistakes, and while this is why virus mutation rates are comparatively high (even higher than the most error-prone prokaryotic replication), the particular life style of viruses make it possible for them to escape error catastrophe through extremely high fecundity.
I suspect colewd had this misconception that a virus (for example), would invade a cell, which produced one new virus, which invades a new cell, which produces another new virus and so on (or something along this line).
In this view, if that was really how the virus life-cycle worked, deleterious mutations would quickly accumulate and the viral genome would succumb to deleterious mutations eventually. But since that’s not how it happens, there is no in principle barrier to indefinite viral replication unaided by mutation-detection and repair machinery.
Yes, as Rumraket notes, retroviruses make use of repair pathways to integrate, and an integrated retrovirus will “benefit” from the host’s repair mechanisms if the infected cell divides. These facts might rescue colewd’s objection, if only the vast majority of replications in the retrovirus life cycle were DNA -> DNA host cell replications. But they are not. Each infected cell produces over 10,000 new virions.
You ask “do you have evidence that these retroviruses don’t have a limited life due to genetic breakdown?”
Yes: they’ve been around a while. As have RNA viruses, like HCV and yellow fever, which are also crappy replicators.
Precisely, and the same logic applies to the early replicators that colewd believes are impossible. So long as 1.001 out of their thousands of progeny work, they can carry on.
It is no wonder that biologists think life started as a kind of “viral” stage. Tiny genomes (in principle, to begin with no larger than a single gene), enormous fecundity and high mutation rates. This would also promote a comparatively more powerful exploration of the local sequence space.
But, I can already hear the objection. “If we came from viruses, why are ….”
Rumraket,
Yeah, and given such high fecundity and mutation rate, even a mutant that is an order of magnitude worse will eventually “find” the back-mutation, unless its more vigorous cousins completely deprive it of resources…
Which brings us to the next big driver of adaptation: predation.
We generally think of predation-by-engulfing, but viruses show the power of predation-by-insertion and hijacking. Maybe the progenitors of modern viruses carried a lot more machinery with them, but discarded it as surplus to requirements, so they could spend more time transducing. 😉
Where did you get your replicators from? And how can you get from molecular replicators to biological reproduction?
So to say that a virus is replicating could be seen as an equivocation or as just plain wrong?
Mung,
Splitting hairs, I’d say. One could reduce it, pointlessly, to say the only thing that is replicating is polymerase itself. The rest of the genome is just along for the ride.
Is “virolution” another theory of evolution?
Virolution is the product of Dr Frank Ryan’s decade of research at the frontiers of this new science – now called viral symbiosis – and the amazing revolution that it has had in these few years.
Rumraket,
Personally, I’m waiting for … “if this isn’t settled, there is no theory of evolution”.
Allan Miller,
Damn! Mung got in first.
Mung,
No. It’s a source of variation, coming under the heading ‘recombination’ in my brief sketch.
DNA_Jock,
Do you have evidence that that stand alone cells can survive for extended periods without repair. Would that include both bacteria and yeast types? If you have answered this my apologies. I am not trying to make an argument, I just would like your opinion here.
Mung,
Here’s a slightly less “breathless” exposition of his thesis.
Enjoy!