A problem with molecular evolution?

Quite right. Living things that were three-dimensional and, therefore, had an inside existed before living things that laid eggs existed.

This has never been in question, but you’re here to learn things, so there you go. Another thing learned.

do you have an example of hormone that can work without a receptor at all?

so according to your scenario how the first eggs evolved and how the organism lay them?

Define “egg”. Is it something other than any immobile, haploid gamete?

I gave you an example of a new hormone that already had an existing receptor.

I discuss it in this post.

1 Like

Genome duplication provided a mechanism for evolving new receptors, but the order in which the hormones and their receptors appeared remained unknown. Using a sophisticated computational technique and a statistical model of protein evolution, Thornton back-calculated the gene sequence of the ancestral hormone receptor at the root of the steroid receptor evolutionary tree. Analysis of that sequence made its identity clear.

“It’s quite convincing that the ancestral steroid receptor was an estrogen receptor of some sort,” Thornton said, “because its gene sequence is extremely similar to that of the estrogen receptors found today, but it’s not at all like those of the other hormone receptors.” This similarity was particular striking at sites in the sequence that are known to confer the ability to recognize specific hormones and target genes.

The ancient nature of the estrogen receptor suggested a solution to the chicken-and-egg problem. Steroid hormones are produced in a common biochemical pathway in which progesterone is converted to testosterone, which is then transformed into estrogen. Thornton’s results showed that the last hormone in the pathway was the first to have a receptor, a surprising result in a field whose accepted wisdom is that complex systems and structures are gradually elaborated and optimized in a step-by-step fashion.

But this same result suggested a solution to the puzzle, because it implied that less ancient steroid hormones—progesterone and testosterone in particular—had been present as biochemical intermediates before the receptors that recognize them evolved. “Once ancient organisms had estrogen and an estrogen receptor, they had to produce the other steroids in the process of making estrogen. When new receptors were created by gene duplication and then evolved affinity for these steroids, they turned what had been mere biochemical stepping-stones into bona fide hormones,” Thornton said.

“The solution to the which-came-first problem is that the hormones came first, but they had weren’t hormones and had no function per se, until their receptor partners emerged in the vertebrate genome,” Thornton explained.

http://www.columbia.edu/cu/record/archives/vol26/vol26_iss21/2621_Ancient_Estrogen.html

Estrogen itself was derived from an even more ancestral pathway

It was previously suggested that the most abundant metabolites can act as helping hands for pathway evolution, providing readily available substrates for newly arising catalytic activities ( 69 ). Here, we expand this view with a detailed case study showing that newly appearing metabolites can become substrates for older enzymes, leading to both expansion and extinction of pathways. Thus, just as fossils share a combination of characters that are absent in modern organisms, we argue that the actual set of observable metabolites represents only a subset of the full metabolite space. Our method provides the possibility of defining new classes of molecules that can be helpful to orient screens in analytical chemistry and study coevolution between proteins and their ligands.

Fig. 8 Origin of vertebrate estrogens through opportunistic connections from ancient paraestrol synthesis pathways.

Coevolution between metabolic pathways, in colors corresponding to different periods ( A to C ) and steroid receptors of the NR1 (gray) and NR3 (black) subfamilies. We infer that, in addition to the sequential appearance of actual metabolites at different time steps (periods 2 and 3, oxysterols; period 4, progestagens; period 5, androgens), the history of NR ligand synthesis pathways involved metabolites combining features that are separated in actual molecules, such as paraestrols in periods 2 to 4. Those intermediary metabolites may have facilitated a gradual shift in substrate specificity for ancient enzymes, such as the CYP19A aromatase, and hence the building of new pathways through opportunistic connections of old enzymes with new substrates during period 5.

https://advances.sciencemag.org/content/3/3/e1601778

2 Likes

i guess its not. in any case we will need not only a place were the eggs can be formed, but also a hollow passage.

this is a problematic case since that receptor already had the abillity to bind both hormones. so its not even a new function, and thus not even an IC in first place. we only need a single step: to evolve a new hormone.

so how this suppose to work? if they were no hormones yet, and then they evolved into hormones, how they were functional without their receptors evolved yet?

You should notice that under the definition you have agreed on, many single-celled organisms form eggs. No opening, no passage.

1 Like

so how this suppose to work in a multicellular organism?

There are many ways, but a simple and obvious one is that the multicellular organism generally has an opening or two, front and rear.

1 Like

so we still need that opening and a mechanism which produce eggs.

The opening is what multicellular organisms have from the start, and the mechanism that produces eggs is meiosis.

1 Like

what was the function of that opening in first place in multicellular organism?

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?

2 Likes

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:

Abstract

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:
https://www.pnas.org/content/118/7/e2018731118.short

Significance

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.

Abstract

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.

1 Like