A problem with molecular evolution?

Have you considered the possibility of a beginning with external gonads, which a body cavity later evolves around to protect, or alternatively that the gonads simply over generations gradually migrate into an already existing cavity (such as near some waste-dispelling orifice) during development, and later specialize into full-blown reproductive organs?

Have you considered analyzing this question in the light of at least some understanding of the cellular basis of life, and the processes of development of multicellular organisms, such as cell division, cell differentiation, tissue formation, cell/tissue migration and so on?
I mean, instead of thinking about this problem with this plumber-like mindset, where organisms in your mind seem to be sort of “assembled” from these inert and rigid components such as “tubes” and “eggs” that can be added or subtracted, instead of growing and changing gradually in shape and function?

Do you have any openings in your body? What are their functions?


I’m pretty sure it’s also where he deposits knowledge he’s informed about here, as it never seems to stick around for long.

we can speculate a lot about what may have happened in the past, but i prefer to stick with reality, and in reality we have many cases which A depend on B and vice versa. so why should we believe against reality?

Pretty sure everyone believes in what they think is reality.

That said, we don’t ignore reality - we accept and you ignore

Radiometric dating, dendrochronology, ice cores, lake varves
Genetic evidence, molecular clocks
Geologic evidence
Distant starlight evidence including basic trigonometry, white dwarf cooling, globular cluster ages

Among many many other pieces of evidence.

So really, you should take your own advice; what conclusions can we derive from the evidence?

Have you ever heard of a sponge?

We evolved from a sponge-like common ancestor, y’know.

What is a cnidarian, and what are bilaterians?

How is radial and bilateral symmetry controlled genetically?

You seem extremely confused again now. Nobody disputes that there are many examples of systems where one thing A depends on another thing B to function. What they are disputing is that this co-dependence relationship means the A+B system cannot evolve.

But we know that such relationships can evolve. We know examples where A has some ancestor from which A evolved, and B has some ancestor from which B evolved, and that they then later became dependent on each other to function.

For example this:


Many cellular processes are carried out by molecular ‘machines’— assemblies of multiple differentiated proteins that physically interact to execute biological functions18. Despite much speculation, strong evidence of the mechanisms by which these assemblies evolved is lacking. Here we use ancestral gene resurrection911and manipulative genetic experiments to determine how the complexity of an essential molecular machine—the hexameric transmembrane ring of the eukaryotic V-ATPase proton pump—increased hundreds of millions of years ago. We show that the ring of Fungi, which is composed of three paralogous proteins, evolved from a more ancient two-paralogue complex because of a gene duplication that was followed by loss in each daughter copy of specific interfaces by which it interacts with other ring proteins. These losses were complementary, so both copies became obligate components with restricted spatial roles in the complex. Reintroducing a single historical mutation from each paralogue lineage into the resurrected ancestral proteins is sufficient to recapitulate their asymmetric degeneration and trigger the requirement for the more elaborate three-component ring. Our experiments show that increased complexity in an essential molecular machine evolved because of simple, high-probability evolutionary processes, without the apparent evolution of novel functions. They point to a plausible mechanism for the evolution of complexity in other multi-paralogue protein complexes.

And this:


Human muscle-type acetylcholine receptors are heteropentameric ion channels formed from four evolutionarily related subunits, which assemble with a specific stoichiometry and arrangement. It has long been thought that each of the modern-day subunits are required for function. We dispel this notion by first showing that an ancestral β-subunit can replace both the β- and δ-subunits in human acetylcholine receptors. We then identify a single historical amino acid substitution that eliminates the ability of the ancestral β-subunit to functionally replace the human δ-subunit. Our work experimentally demonstrates how acetylcholine receptor subunit complexity could have evolved and uncovers a form of contingency that is unique to heteromeric protein complexes, in which mutations that “lock in” individual subunits determine future evolutionary paths.


Human adult muscle-type acetylcholine receptors are heteropentameric ion channels formed from four different, but evolutionarily related, subunits. These subunits assemble with a precise stoichiometry and arrangement such that two chemically distinct agonist-binding sites are formed between specific subunit pairs. How this subunit complexity evolved and became entrenched is unclear. Here we show that a single historical amino acid substitution is able to constrain the subunit stoichiometry of functional acetylcholine receptors. Using a combination of ancestral sequence reconstruction, single-channel electrophysiology, and concatenated subunits, we reveal that an ancestral β-subunit can not only replace the extant β-subunit but can also supplant the neighboring δ-subunit. By forward evolving the ancestral β-subunit with a single amino acid substitution, we restore the requirement for a δ-subunit for functional channels. These findings reveal that a single historical substitution necessitates an increase in acetylcholine receptor complexity and, more generally, that simple stepwise mutations can drive subunit entrenchment in this model heteromeric protein.

And many others, such as the evolution of increased complexity in hemoglobin also discussed on this website not long ago.

So this is actually the reality.

ok, so lets take that case, since it will be easier to show where the problem is. first of all, in this case we start with a globin and end up with 4 globins. so im not sure its even IC system in first place. we also dont know if the globin itself can evolve stepwise. actually, we dont even know if the globin sub-parts can evolve stepwise, such as the Heme molecule for instance:

(image from wikimedia)

If we don’t know then you have no argument.

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but we do know that at least now they need each other. and we know that for about million such cases. so the burdon of proof is on someone who claim that such a system can evolve stepwise, and not the opposite.

And we do know that things that depend on each other can evolve by having different ancestral functions, so that fact alone does not represent any challenge to evolution.

So the burden has been answered in principle, you’re just demanding we show how everything evolved. Suppose I answer for the evolution of porphyrin biosynthesis pathway you’ll just move on to some other thing and demand that be answered too. If we don’t know everything, then (to you) we don’t know anything.

And so we’re left chasing the goalposts until the end of time.


It is only problematic for the claim you made in the opening post. It isn’t problematic for evolution.

The production of aldosterone is a new function, and our whole point is that IC systems are not always IC when they emerge.


we dont know that but assume that. so again: we assume against reality here.

actually no. you only need to show how even a single complex IC system can evolve stepwise.

if we will remove the aldosterone what will happen to the creature?

Do you accept that producing aldosterone was a new function?

if we believe in evolution? of course.

So we have a new function, and the new steroid bound to an existing protein. Problem solved.

not if the creature cant survive without it. in that case i will ask how he became dependent on it. in addition, i will ask how the first hormone/hormone receptor ever evolved.

You can remove whatever genes or interactions that stop them from being dependent on the new steroid.

I suppose that you won’t believe that the Romance Languages evolved from Vulgar Latin unless we can show you the first human that used language.

so we need to believe that at least one hormone (the first hormone ever) appeared at the same time with its hormone receptor?

No. Why would we? As we see with aldosterone, there can be a new metabolic pathway that creates a new small molecule that can bind to an already existing protein.

We do know that. We’ve literally watched it happen in real time in the laboratory(Cit+ phenotype in the LTEE, for example). And many such events can be reconstructed by phylogenetic methods to show that, in demonstrable empirical reality, the inferred ancestors were functionally capable of contributing to the fitness of living organisms, and how mutations altered their functions so they became dependent on each other for their later functions.

That’s what was shown in all those ancestral sequence reconstruction articles I’ve linked. They show how systems that consist of two or more things that today depend on each other to function, used to consist of fewer things, that these fewer things functioned in a different way back then, and they show HOW they changed and acquired their modern functions through mutations and selection.

So no, you’re just blatantly wrong. YOU are denying reality here.

We have done so in principle. That’s all that is necessary. I don’t need to count to a million to know that I can do so because I can count to 100, or 1000.

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