An ID hypothesis: Front-loaded Evolution

You stated in Message 64

Actually, the capacity for eye development is encoded at the root of the phylogenetic tree of life. Pax6 is a gene involved in eye development, for example. When you BLAST (blastp; default search parameters) the protein encoded by Pax6 (accession number: P63015) against the domain Prokaryota, you get significant hits (E-values < 1e-05). A PSI-BLAST search would almost certainly uncover hits with even greater significance. This suggests that eyes (and other major organs in Metazoa) were anticipated by the first genomes.

In Message 70 I tackled your "front-loaded eye" statement by pointing out that the similarities found by BLASTP are found only in the regulatory part of the protein,he helix-turn-helix.

In Message 80 I again requested you address the above.

In Message 80 Wounded King requested that you address this.

In Message 114 Mr Jack brings up the same thing.

You responded to that by saying

In fact, I'm more than willing that the matches don't indicate front-loading.

Doesn't that contradict your statement in Message 64? Are you now withdrawing your claim that the BLASTP results suggest that eyes were anticipated?

All I see is that a method of control of gene expression is required in prokaryotes and this helix-turn-helix arrangement has remained a mechanism of control in higher organisms.

Are you now withdrawing your claim that the BLASTP results suggest that eyes were anticipated?

Yes.

Thanks Granny Magda. I'm looking at his blog now.

It is interesting and you're right, probably another thread concerning theism, ID and science and how to go about them from the best angle/s.

Thanks, and now i'll bow out of the discussion here.

Alternatively, the front-loading designers could have designed such a population from the start: where some cells have genes for plants, and others have genes for animals.

Well, this would be a bit of a climb-down. Are you going to give up on common ancestry?

Yes, but front-loading isn't about pre-programming something. It's about "stacking the deck," and anticipating the rise of plants and animals, for example. Simply put, if we start with an origin population of cells, which contain genes necessary for the development/function of plants and animals; next, this initial population separates into two populations. Then, deletion events in one population removes the animal genes, say, so that we just end up with plants.

But you're still not drawing a picture.

This "deletion event" happens to plants, but not animals. When they start off with the same genome. What causes this to happen?

If you want to stick with common ancestry, then there must be some causal factor other than the genome that makes the "deletion event" occur.

Well, what is it?

If you do wish to abandon common ancestry then we have a whole 'nother discussion on our hands.

In Message 70 I tackled your "front-loaded eye" statement by pointing out that the similarities found by BLASTP are found only in the regulatory part of the protein,he helix-turn-helix.

There's a small typo on your part here, which I shall correct for clarity's sake, the regulatory part of the protein is not the helix-turn-helix. You mean the DNA binding part. The regulatory part would be the part that actually interacts with other proteins to enhance or suppress transcription.

Fair enough, I'll admit that my experience is mostly based around comparative genetics amongst metazoans. The only bacterial sequences I generally encounter are in plasmids.

TTFN,

WK

Well, not when seen in the context of other biological features. In my little essay, I showed how (a) it is feasible for specific proteins to be front-loaded; (b) it is feasible for specific molecular machines to be front-loaded; and (c) how specific biochemical pathways can plausibly front-loaded. Thus, demanding that I explain the origin of the eye through FLE seems to be pushing the goal-posts back. The FLE hypothesis is just in its infancy; demanding that we produce a teleological hypothesis for the origin of the eye, at this point, seems a little premature, to me at least.

Well, you know, if you want to develop the hypothesis, and you find you need another few years to get it right, then you go for it. As I said, I do admire your ambition. You're almost certainly wrong, but science would not progress unless people pursued seemingly crazy ideas. I've pursued a few of those myself.

But, you can't expect anyone to accept your ideas when they're in their present half-formed condition. All I can do is wish you the very best of luck. But if you can't explain the evolution of the eye, then presently we have to say that your hypothesis has failed to do what it is meant to do, namely explain evolution.

It's about "stacking the deck," and anticipating the rise of plants and animals, for example.

Alternatively, the front-loading designers could have designed such a population from the start: where some cells have genes for plants, and others have genes for animals.

Obviously your argument in favour of front-loading requires an entity or entities to "anticipate", to be the "front-loading designers". It now seems that it may require constant intervention in the form of "tinkering".

I'm not sure I understand why you propose this when we have an explanation which accounts for all the diversity without invoking a tinkerer? Is there specific evidence that you have which demonstrates that tinkering occurs and therefore natural mechanisms are insufficient?

There seems to be about two lines missing from my post! That'll teach me to rush things and not proof-read. My laptop keyboard is rbbish nd I kep losing letters, clauses and sentences because I'm not hitting them hard enough. I'e not bothered to check this post so you can se whtIm p against

This "deletion event" happens to plants, but not animals. When they start off with the same genome. What causes this to happen? If you want to stick with common ancestry, then there must be some causal factor other than the genome that makes the "deletion event" occur. Well, what is it?

I don't see that this necessarily holds. Gene deletion happens, neither we nor Genomicus are going to dispute that, right? You don't need a special causal factor to account for the deletion. What you need is some kind of selective filter that will mean that your front-loaded genes end up in the right "buckets" but that isn't particularly difficult to explain either - it simply requires that the "animal" genes work well together and the "plant" genes work well together and straightforward selection will do the rest.

The problem, as I see it, is rather more fundamental. If there are to be pools of front-loaded animal and plant genes which are whittled down to the correct sets in animals and plants we should see there being more genes in prokaryotes than in plants and animals rather than less. And we should see distinct, non-overlapping, sets of genes present in plants and prokaryotes; and animals and prokaryotes - but there's no evidence of that either.

Finally, the idea that plants and animals have particularly distinct genetic sets is fairly untrue. In general we strong homologies between major families of plant and animal genes, but they occur with very different relative importances. For example, I'm currently doing my research project on a MYB transcription factor vital to pollen development. The name 'MYB' derives from 'myeloblastosis' since these genes were first identified in cancer research looking at chickens but, as it turns out, there are only a handful of MYB genes in animals whereas they're a hugely important group in plants, with almost 200 having been identified in Arabidopsis alone. A converse example would be myosin; which has diversified into a huge array of forms important in muscle tissue in animals but is largely confined to its original role, shared with other Eukaryotes, ferrying vesicles around cells in plants.

And, of course, plants and animals are hardly the be-all and end-all of Eukarya. Quite apart from the familiar seaweeds, algae and fungi, there are a host of unicellular eukaryotes.

It was valid enough that Darwin thought it to be worth answering. The usual problem is that creationists quote the argument but ignore the response, giving a deeply misleading impression of what Darwin was saying.

See my response to Dr Adequate, above.

I think that recognising the problems with front-loading, even if they are expressed a little vaguely is an important part of this discussion.

True.

Now this is where we see problems with your arguments. Does designing rhodopsin into the first life significantly increase the chance of eyes evolving ? Nothing you say really addresses this point. You say it does, but it really isn't clear why you think that. Can we really say that rhodopsin specifically would be used ? It's available for co-option, sure, but is it the only possibility ? How likely is it to be the only possibility or even the most available option when eyes do evolve ? We do need to be careful to avoid thinking that the way things work now is the only possible way, especially in the context of this discussion since it would bias the argument in favour of front-loading.

Designing rhodopsin (or a homolog of rhodopsin) in the first genomes increases the likelihood that eyes will emerge precisely because the blind watchmaker doesn't have to tinker around with a totally unrelated protein, gradually transforming it into a protein that can be used for vision. If, however, rhodopsin (and other vision-related proteins) is designed into the first genomes, the fundamental ingredients for eye evolution are already in place, biasing evolution in favor of eye evolution. Few novel genes would have to evolve, and this significantly increases the chances of eye evolution.

Rhodopsin would be available for co-option, but would it be the only possibility? Possibly the blind watchmaker would "generate" a protein that would then be co-opted into a vision-related function. But this would be an extra step: the blind watchmaker would have to duplicate an existing gene, modify it such that its function is compatible with a vision system, and then it'd be co-opted. These extra steps make it less likely for the eye to evolve in the absence of front-loading.

According to Wikipedia (not the best source, I know but usually OK on science and more accessible to the lay public) bacterial rhodopsins may have an evolutionary relationship with visual rhodopsins, but they may not. Doesn't this make it a rather poor example of possible "front-loading" ?

From Wikipedia:
"Bacteriorhodopsin belongs to a family of bacterial proteins related to vertebrate rhodopsins, the pigments that sense light in the retina." (Emphasis added)

Anyways, it was meant as an analogy - just to get the idea across.

Well, this would be a bit of a climb-down. Are you going to give up on common ancestry?

How on earth would this be incompatible in any way with common ancestry? You'd simply design cell population A with genes that would be later used by plants, and cell population B with genes that would be later used by animals. These two populations, on the whole, would be genetically related, with the exception of the different plant/animal genes.

This "deletion event" happens to plants, but not animals. When they start off with the same genome. What causes this to happen?

Not meaning to dodge this question, but I think Mr Jack has answered this question succinctly.

If you do wish to abandon common ancestry then we have a whole 'nother discussion on our hands.

I really don't see how I seem to be abandoning common ancestry.

Obviously your argument in favour of front-loading requires an entity or entities to "anticipate", to be the "front-loading designers". It now seems that it may require constant intervention in the form of "tinkering".

Not at all. Perhaps I'm not being clear here. I'm simply saying that the first life forms that were seeded on earth could contain different sets of genes, one for plants, and one for animals. Evolution would follow from there, shaped around the initial constraints. There is no constant intervention/tinkering from any intelligence.

Well, you know, if you want to develop the hypothesis, and you find you need another few years to get it right, then you go for it. As I said, I do admire your ambition. You're almost certainly wrong, but science would not progress unless people pursued seemingly crazy ideas. I've pursued a few of those myself. But, you can't expect anyone to accept your ideas when they're in their present half-formed condition. All I can do is wish you the very best of luck. But if you can't explain the evolution of the eye, then presently we have to say that your hypothesis has failed to do what it is meant to do, namely explain evolution.

Remember, the purpose of this discussion - at least my purpose of this discussion - and that is for the FLE hypothesis to be refined. Before submitting any FLE hypothesis to the scientific community, it's not a bad idea to see what the bio guys and gals over here at EvC think about the FLE hypothesis, dontcha think? This helps in pointing out the weak spots and strong spots in the hypothesis, and indicates which parts need to be developed more rigorously.

I don't see that this necessarily holds. Gene deletion happens, neither we nor Genomicus are going to dispute that, right? You don't need a special causal factor to account for the deletion.

I didn't say that the causal factor needed to be "special". I just said that there has to be one. Two lineages evolve in different directions. This cannot be solely caused by the same gene passed down from the same common ancestor, or they'd both evolve in the same direction. There must be another causal factor.