It is an interesting page and with quite intriguing results.
My first reaction is that “many genes” doesn’t necessarily mean a horizontal
spread, it could be vertical ie beginning at the lens and extending down
into the eye substructures.
This would give a narrower bandwidth, a pyramid with the lens still near the
apex.
I’m still “evaluating” the potential of the quotes in my last post and then
I’ll look at “backcrossing” (if necessary, as usual I haven’t heard of it
before).
Jorolat
sigh
I am actually doing a PhD right now in the molecular genetics of eye specification and development.
This pathway is rather remarkable – many of the genes involved in the so-called Retinal Determination Network (RD network), discovered in fruit flies, are conserved in all organisms with eyes. These genes, if mutated in the fruit fly, lead to a no-eye phenotype. Pax-6, mentioned above, is the vertebrate homolog of Drosophila eyeless. In mice, Pax-6 mutants are termed small eye (Sey). In humans, it leads to aniridia.
Eye development is dependent on a very complex genetic network, of which the RD genes are only part. They act as a central pillar. In Drosophila and other organisms, they are activated and modulated by secreted factors like dpp, an TGF-beta homolog. These secreted factors in vertebrates are involved with formation of the crystalline lens, which receives and in turn secretes FGFs and expresses FGFRs.
What am I getting at here?
There is nothing about blind cave fishes, or lens explants rescuing them that is not explainable by natural selection or known developmental genetics. They even lend strong support to those existing theories. There is no need for Baldwin effects or AONEs or other Lamarckian theories to explain it.
The OP betrays a fundamental misunderstanding of natural selection.
A particular trait need not have any positive value to the survival of the organism to be retained. Only if it has a negative affect on the reproductive capability of the organism will it be selected against.
In other word, vestigial traits are traits which may have “fallen into disuse,” but have not been “bred out” of the organism because their retention causes the organism no reproductive harm.
Hi Lissener,
It’s not that I want to argue the point (owing to “doubts” about conventional theory) but I have read (I think!) that natural selection can account for vestigial eyes by something along the lines of they require too much “energy” to maintain.
I’m intrigued by what you have said - you appear to be saying that there is no direct reason to select against the eye as, presumably, fish can mate whether their eyes are open or shut. Does this mean, according to theory, that vestigial eyes shouldn’t be occurring?.
I’m further intrigued by the fact you have posted an almost identical message to the Evolutionary Benefit for Schizophrenia debate. Which one was your post meant for, or is it applicable to both?
Jorolat
ps for Choosybeggar & Edwino,
I’m still ploughing my way through a lot of new stuff and hope to post again in a few days.
Jorolat–
I posted my response here first, then saw the other thread and adapted what I’d just written for that thread.
To answer your question, “. . . you appear to be saying that there is no direct reason to select against the eye as, presumably, fish can mate whether their eyes are open or shut. Does this mean, according to theory, that vestigial eyes shouldn’t be occurring?”
There’s no direct reason to select for or against any trait. If the eyes are useless to an animal who spends all of its time in total darkness, then there is no evolutionary pressure to retain, much less improve them. And if there’s a mutation that makes them less efficient, there’s no evolutionary pressure to breed that new trait out of the population. Now, if there were a mutation that made the gills less efficient, that would be much more likely to be bred out. So the eyes may deteriorate over time simply by default. And if efficient eyes do draw more “energy,” or resources, from the organism, then there might well be evolutionary pressure to select for the occasional mutation that contributes to their deterioration.
But again, there’s really no such thing as a “reason” for any evolutionary trait, except the “reasons” that are constructed, after the fact, by humans, to try to understand what evolutionary pressures might have made this or that random mutation useful to the organism. To use the word “reason” for this is to get uncomfortably close, in my opinion, to Lamarckianism, which I feel has been convincingly disproven.
Sometime last week as I was researching eyeless cavefish on the net I made a startling discovery!!!
These things are available to the casual enthusiast. Here is a commercial looking site that has a page about them. Presumably folks who buy these things don’t maintain them in the dark. And presumably, some enthusiats allow them to breed.
So Jorolat, knowing your penchant for experiments that have been done for you, it should be quite simple to find out the results of these breeding experiments. Would you be convinced that the environment plays no direct role in selecting which genes to mutate if blind cave fish remain blind even when bred in a lighted environment?
I’ve worked in the aquarium trade for large chunks of my adult life. Tank-bred Blind Cave Tetras are widely available, and I think there are a couple other blind cave fish out there as well.
Hi Edwino,
Within this complexity a number of articles speak of the cascade of regulatory genes controlling structural development. It is the relationships of this hierarchy, particularly the “vertical” component, that I am interested in.
Apparently Pax 6 is one of the homeobox genes that have been highly conserved throughout evolutionary history. In terms of theory wouldn’t it be slightly paradoxical if any of these genes were responsible for, or connected with, the beginning (ie at or near the top the cascade) of eye degeneration?
Jeffrey says:
If its not too naive an approach I basically want to find the top of the tree and how wide the canopy is, if that makes sense. Limited time, web articles presuming varying degrees of knowledge and not quite what I want, are making it heavy going though.
Jorolat
Sadly, no - I don’t do logic 
In an earlier post you asked “BTW what in the hell do the last three cites of your last post have to do with the OP?”
It seems I’ve been approaching vestigial organs from the wrong angle. Eye degeneration doesn’t happen in isolation, in some cavefish there is a reduction in that part of the brain connected with seeing and there are other changes with a more general distribution among cavefish species.
A chap called Romero (Here and Here) has been using the hypothesis that “changes in behaviour precede morphological ones”. I should have thought of it sooner, he’s said he’ll send me reprints of 3 articles I’m interested so I’m hoping he doesn’t forget.
Jorolat
Oh right - thanks
Jorolat
jorolat:
The Pax6 homologs of Drosophila are genes called eyeless (ey) and twin of eyeless (toy). I address fruit flies because the pathway is most described in them (and that is the primary focus of my PhD). They are indeed highly conserved in development, along with much of the retinal determination network – genes like sine oculis (Six genes in mouse), eyes absent and dachshund.
Both toy and ey are very early specifiers of the eye fate in the fruit fly. Both of them begin delimiting the eye primordia in embryonic development. toy appears to be upstream of ey but there is no loss of function data.
The question of what turns on ey and toy is currently being researched both in our lab and several others. Good candidates would be the secreted patterning factors responsible for positional information in the fruit fly embryo. These, along with their transduction machinery, are also highly conserved in evolution.
I do not find it paradoxical at all the Pax6 genes or their close interactors are involved in eye degeneration. Most genes are utilized in many different developmental functions. Genes in the RD network, especially in fruit flies, tend to be limited to eye devlopment – some mutants of eyes absent, sine oculis, eyeless, and some others run around perfectly happily with no eyes. This to me means that if you lose selection pressure on the eyes, mutations in these genes are not overtly detrimental (since they have a specific effect on the eyes).
Couldn’t agree more. I’d say something like 47.5[sup]o[/sup] would be better.
You familiar with the phrase, “The cells that fire together, wire together?”
It is an established fact that many aspects of CNS development and organization do not occur in the absence of sensory input.
Take the clinical condition called ambliopia. It occurs in individuals with a unilateral visual deficit. If the deficit goes uncorrected during a critical developmental window (ages 2-10, IIRC), vision in the afflicted eye becomes permanently impaired, irrespective of subsequent correction.
The permanent deficit is thought to be caused by poor development of those regions of the brain concerned with processing the visual stream from the affected eye. The reason that the deficit becomes recalcitrant to correction after a certain age is there exists a limited developmental window of maximal synaptic plasticity in the CNS. Once things become hardwired to a greater or lesser extent, improvements in the quality of the datastream (ie. fitting with glasses) cannot effect visual improvements.
There are countless other examples of stimulus-induced CNS development; I don’t see how the existence of this phenomenon in cave fish supports your position.
This abstract Genetic Control of Development of the Mushroom Bodies mentions that ey & toy, etc., are expressed in the developing mushroom bodies of Drosophila which in turn reminded me of Jeffrey’s comment:
“the antagonism between the pax6, pax2, and midline signaling genes, …appears to be responsible for the regression of eye development in cave fish.”
Is it possible, in principle, that the pax 6, pax 2, and midline genes, each have a minor modification such that only when they come together in the eye is regression caused leaving their expression elsewhere unaltered?
Jorolat
Thanks for the info [b[Choosybeggar**, I’m still exploring…
Jorolat
ps I made it 180 degrees
I forgot about the mushroom bodies – indeed some of my buddies are in fact working directly on this. I should be ashamed. dac actually has roles in leg and genital disc development as well (it wasn’t on my list). ey, eya, and perhaps so are also expressed in the brain. It doesn’t change the fact the phenotypes of certain alleles of these genes (except dac to date) cause happy, eyeless flies.
It is possible, in theory. Both genes could have a borderline phenotype – they are both broken, but do not show a phenotype alone. In combination, they can show a phenotype. We see this on occasion, and it is difficult to rule out this possibility in a non-genetically manipulated organism like the cave fish.
Generally, if you break a developmental process, cell death results. This is the default pathway for any tissue in the body which lacks an intact developmental endpoint. This is what happens in the cave fish. Somewhere, the eye development cascade is broken. Apoptosis (programmed cell death) results. Jeffrey is studying the apoptosis, as well as where the developmental pathway is broken. As I mentioned, this organism is not able to be manipulated genetically, so it is quite difficult to tell where the pathway is busted:
“…the antagonism between the pax6, pax2, and midline signaling genes, which appears to be responsible for the regression of eye development in cave fish.”
There is nothing special about the “antagonism” here – these genes all specify different parts of eye development and they antagonize each other to make specific domains of eye development (Pax6 in the retina and lens, Pax2 in the optic nerve, etc.). Regression is just caused by the pathway being broken at some point, and the apoptosis which follows.
I forgot the last half of my above post:
Nothing about eye-specific alleles, apoptosis, or borderline phenotypes which signifies the particular genetic change was “environmentally mediated” : these are all well-known genetic phenomena which often result from random mutation.
So, the vestigial eyes in this case resulted from random mutations in genes encoding them simply because selection pressure was lost. Accumulate enough random mutations on now evolutionarily neutral parts of the genome, and you get eyeless cave fish. Mutations in those regions occur at the same rate, and get passed on at the same rate. The selective advantage/disadvantage of receiving a mutation in those regions change with environment, however. The environment never affects the genome directly in this example.
The only effect of the environment is in removal of selection pressure. An analogy:
Imagine a game of darts where you are playing Cricket (15-20 and bull count, if you hit something 3 times, you can score, if your opponent then hits something 3 times, the number is blocked and no one scores). You and your opponent are playing poorly so that darts are landing totally randomly. You hit 20 three times. 20 now becomes extremely important. All hits of 20 will be noticed. Your opponent hits 20 three times, and 20 just becomes another “dead” area of the dartboard.
This is the way I think of selection pressures – nothing about your dart throwing or the dartboard has changed, just the particular value you place on the wedge. Nothing about the mutation rate or the genome changes when the environment changes, just the particular value you place on the particular mutation.