I'm sure you're familiar with this image or others very like it. It's the biological tree of life showing the relationship between the major domains and kingdoms. You'll note that plants and animals are actually quite close together, and far removed from the two groups of prokaryotes. Were there separate seed populations of prokaryotes, one for plants, and another for animals shouldn't we expect to see these pools group with their descendent multi-cellular forms?
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.
I don't see why you feel chance is an insufficient factor?
quote: 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.
I think we have to eliminate the argument that it is easier for a hypothetical designer to produce a working single-called organism than it is for evolution. That really isn't the point under discussion.
The real issue is whether building in a rhodopsin homolog makes it significantly more likely for eyes to evolve when compared with an alternative organism produced solely by evolution. Remembering that we can't rely on any part of the gene surviving other than those parts essential for function it isn't at all clear that front-loading offers much help. You NEED a strong overlap between the function and usefulness for vision for the argument to work, but you also need this overlap to be specific to rhodopsin. If the overlap is a direct consequence of function - a point that you haven't addressed - then alternatives to rhodopsin would likely have the same usefulness, and there would be no need for any more evolution in that case, either.
quote: From Wikipedia: "Bacteriorhodopsin belongs to a family of bacterial proteins related to vertebrate rhodopsins, the pigments that sense light in the retina." (Emphasis added)
Wikipedia disagreeing with itself would support my point of uncertainty, so this quote doesn't really help (even if it does mean an evolutionary relationship which isn't explicitly stated).
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.
Well no they wouldn't, 'cos of not having a common ancestor. They might be genetically similar, but they couldn't be genetically related.
Not meaning to dodge this question, but I think Mr Jack has answered this question succinctly.
He may have been succinct, but he was also wrong.
Something has to make the difference. This something, by your hypothesis, cannot lie in the genome. Where, then, does it lie?
I'm sure you're familiar with this image or others very like it. It's the biological tree of life showing the relationship between the major domains and kingdoms. You'll note that plants and animals are actually quite close together, and far removed from the two groups of prokaryotes. Were there separate seed populations of prokaryotes, one for plants, and another for animals shouldn't we expect to see these pools group with their descendent multi-cellular forms?
Yes, and based on phylogenetic considerations, I don't think my idea of two different initial populations is tenable.
I don't see why you feel chance is an insufficient factor?
I didn't say it wasn't. But if that's what Genomicus thinks, then he should say so. What I am trying to elicit from him is what he thinks this factor is. It cannot be the genome. It must be something else. I want to hear from him what he thinks it is. If he says "chance" then we can continue the discussion on that basis.
Something has to make the difference. This something, by your hypothesis, cannot lie in the genome. Where, then, does it lie?
Chance. What's stopping animal genes in one lineage from being deleted? What's stopping a plant lineage to start developing, built around plant genes, and thus animal genes would be eliminated in this lineage (or become pseudogenes)?
OK, that's a new factor in your hypothesis. Chance decides it.
But in that case, shouldn't we stop calling your hypothesis front-loaded evolution, when it is, according to you, just how the dice happened to fall? What I understood by "front-loaded evolution" is that the outcome was inevitable. If, instead, it is random, then perhaps you should think of another name for it.
OK, that's a new factor in your hypothesis. Chance decides it.
But in that case, shouldn't we stop calling your hypothesis front-loaded evolution, when it is, according to you, just how the dice happened to fall? What I understood by "front-loaded evolution" is that the outcome was inevitable. If, instead, it is random, then perhaps you should think of another name for it.
Chance has always been a factor in the FLE hypothesis. Biology is a probabilistic science - the outcome was not inevitable, but certainly the odds were considerably in its favor.
Consider the following example: the last common ancestor of plants and animals have genes x (an animal gene) and y (a plant gene). In one of these lineages, a series of mutations occur, generating a new morphological structure such that gene x is necessary for the existence of the new lineage. Gene y is dispensable, and so it is lost in this lineage. An analogous process occurs in a second lineage, albeit in reverse: instead of gene y being lost, gene x is lost.
Now I'm properly confused; I thought the point was that the dice are loaded?
If by "the dice were loaded" you mean the outcome was inevitable, then no. But under the FLE hypothesis, the outcome that resulted was far more probable than in the absence of front-loading. The first genomes anticipated the origin of plants and animals, for example.
Chance has always been a factor in the FLE hypothesis.
Then you would have done well to mention this in your OP instead of waiting 'til now.
But if chance is a factor, then in what sense is evolution front-loaded? If it is purely a matter of chance that evolution produced humans and tigers rather than bumblegriffs and hippodores, then where is the front-loading?
If you wish to advocate for directed panspermia, then let's continue the discussion on these lines. But I don't see how you can argue for front-loaded evolution and also ascribe a highly significant role to mere chance.
Then you would have done well to mention this in your OP instead of waiting 'til now.
Actually, I thought that was sufficiently clear: that the blind watchmaker tinkers with the initial constraints, and it shapes its designs around those initial constraints.
But if chance is a factor, then in what sense is evolution front-loaded? If it is purely a matter of chance that evolution produced humans and tigers rather than bumblegriffs and hippodores, then where is the front-loading?
Multi-cellular life forms, plants and animals, possibly invertebrates and vertebrates; specific taxonomic classes could be anticipated by the first genomes, but they weren't necessarily front-loaded. Still, any "anticipation" would make the appearance of a specific biological feature much more probable. One reason chance is a factor is because you can't stop the blind watchmaker - but you can put it to work for you if you start with right initial constraints.
™ Version 4.0 Beta
(1)
