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Blind cave fish see the light

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Two blind fish can make sighted offspring.

“The offspring of crossbred blind cave fish see like their surface-dwelling cousins.

The results in Current Biology 1, show that the two populations took different evolutionary paths to blindness.

“We’ve basically shown that these different populations have converged upon the same outward appearance independently, and that they use different genes to do it”, says Richard Borowsky of New York University.”

This is the type of thing that RM and NS can do. I would say that they lose different genes to become blind, not use different genes.

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Mutations can break things easily; it's much harder to make things. There are many possible ways a mutation could break eyesight (think of all the causes of human blindness for comparison). So ‘when you cross them, the genetic deficiencies in one lineage are compensated for by strengths in the other, and vice-versa.’ The evos would be onto something if they could find a mutation that could generate sight de novo, instead of merely allowing already-existing sight information to be expressed. See CMI's article Let the blind see … Breeding blind fish with blind fish restores sight. Jonathan Sarfati
this should be useful http://bric.postech.ac.kr/biotrend/science/science_view.php?nNum=91917 ari-freedom
I would also want to see PaV's evidnece relating to a mechanism whereby disuse of eyes is the trigger for eye-development repressing RNA to bee transmitted to its offspring. Clarence
Well, PaV - show us your evidence. And also how it would explain the data in the paper (e.g. how you get 12 estimated QTLs if the inheritance isn't genetic, and also the pattern of complementation). Bob Bob O'H
Bob #25: Here's a "just-so" story: through disuse of the eye, some type of RNA is transmitted to the progeny that is capable of repressing eye-development during embryonic growth. In the two populations, the RNA and its method of repression is slightly different. Since the genes needed for eye development are at no time absent, when these different populations are crossed, the differing RNAs don't interact in the same way as in each native population, and eyes develop. I like my "just-so" story better. PaV
Vision is supposed to be very energy intensive, so another reason NS would tend to favor fish without the visual apparatus is that they would tend to have more metabolic energy to devote to food gathering, reproduction, etc. magnan
I wish to concede a point about natural selection in this situation. I read an article that mentioned that fish eyes are subject to injury and infection, and that injury especially in total darkness would be greater as the fish can't avoid running into cave walls and the like. Injury of course leads to infection and infection to death. So natural selection very likely is favoring fish with no eyes over those with eyes. That said, whether the visual system is functional or not is still irrelevant. Loss of the whole eye and replaced by a tougher covering would be the thing that was favored. It seems reasonable to presume that eyesight was lost much more quickly than the whole eye as the visual system could be damaged in many ways that don't completely remove the eyeball. DaveScot
Bob O'H asks "What about three blind mice?" If one of those three get their vision, the other two will disappear, because the first will "See how they're one." Q
Oh, but I should mention the real question that lies unanswered from the story:
Two blind fish can make sighted offspring.
What about three blind mice? Bob Bob O'H
PaV - no it's not a just-so story. The point of the work and the paper is that we now have the evidence (and, as I pointed out, sight was only partially restored in the cross where they found the QTLs). Bob Bob O'H
"Loss of sight is caused by fixation of different alleles in different populations. If these are recessive, then crossing different populations will lead to full restoration of the phenotype." Is this a "just-so" story? PaV
Another spin on this story is that Dawkins was right when he said evolving vision is really easy because it occurred 60 times in evolutionary history. ;-) idnet.com.au
PaV - Yes, the blindness was overcome in one cross. This is not uncommon in genetics, and it well understood - it's called complementation (we were taught about it at undergraduate level). Loss of sight is caused by fixation of different alleles in different populations. If these are recessive, then crossing different populations will lead to full restoration of the phenotype. In the cross where they found the 2 QTL, the gene effects were estimated to be mostly additive, i.e. function was partly restored. If it was Lamarckian, how would they find 12 QTLs? And why would they find it in the crosses between individuals from different populations, but not from the same population (check the table in the online supplement)? Bob Bob O'H
Bob O'H We can see the shadows moving around. We can tell if they're going left or right; but we're not sure exactly what they are. In the article it says that it took millenia to develop the blindness; yet the blindness is overcome in one cross. What are we dealing with? If 12 genes are involved, were 12 genes lost, causing the blindness; and now, you cross them, and boom, the 12 genes reappear? No, it's obviously the regulation of the genes that is at play here; the authors allude to that when they talk about a developmental program and such. I have a more Lamarckian view of all of this. Great patience will be required before we find out just what these "shadows" are, and what makes them move the way they do. PaV
PaV @ 16 -
This sounds like speculation–and no more–on their part.
No, they actually carried out 2 generations of crosses, for several choices of cross. In one of the crosses, they even estimate that there are 12 genes (well, QTLs) involved. Bob Bob O'H
I would also consider that this may be a nonrandom mutation triggered by the environment ari-freedom
PaV, in 16, mentioned "This sounds like speculation–and no more–on their part." They did do an experiment, it seems. That is more than "no more". I read it as sound science - obsesrve, predict, experiment, confirm or reject the prediction. ----------------------- DaveScot mentions "It’s the absence of natural selection that explains it. Without natural selection acting as a conservative force random mutation runs rampant." If I understand correctly, all of these fish in each cave were blind. That suggests a selective bias towards blindness, and not simply ramant random mutation. Rampant random mutation would suggest a variety of blindess vs vision in the population. Since the bias did preserve one characterstic over another, why is that not an example of "natural selection acting as a conservative force?" Q
Here's the critical passage: "Borowsky and his assistants descended into the caves and fished out different blind populations to cross in the lab. If the fish had the same developmental mutations, the researchers reckoned they would produce blind offspring. Instead, the experiment produced a number of fry with functioning eyes;..." This sounds like speculation--and no more--on their part. PaV
Maybe we’re looking at this thing backwards. Could it be that the blind fish have finally provided an example of a complex system that is partially evolved? Maybe their vision system has been slowly evolving from scratch, and there is just one final mutation needed to complete the system! Let’s free a few million of those blind fish in a body of water outside the cave, and see how long it takes for that final mutation to occur, finally bringing sight to the previously sightless fish. Or is this just an evolutionist’s wishful thinking? Frank
Re #13 Dave, thanks a lot for writing clear explanations that the average layperson can understand. It always bothers me when certain neo-Darwinists, especially biologists act as if one must be a trained biologists to understand this stuff. I am of the opinion that, if a scientist claims to understand a phenomenon but is unable to explain it in a simple language that the average layperson can understand, he/she has no clue as to the nature of the phenomenon. I think this is the best way to distinguish a con artist from an honest scientist. Again, thank you. Mapou
dk So we concede that the lack of light would favor a fish which survives without eyes… or at least that perhaps some other trait is dominant that helps the blind ones survive in the dark better than the ones that have sight. Not at all. Or at least not a significant factor in this instance. Vision, or lack thereof, becomes irrelevant in the dark. Yes, if producing a functional eye takes up more resources than not producing a functional eye then that's something theoretically selectable but it would be a very slow process in that case. In this case the lack of any immediately significant fitness penalty due to blindness allows the vision system to rapidly decay. Selection works against increasing entropy. Take it away and entropy increases at a hugely accelerated pace. The $64,000 question is whether natural selection can completely overcome increasing genetic entropy. The Darwinian faithful believe it can. The rest of us are skeptical at best. I think John Sanford has the most readable and convincing treatment of this question in the book "Genetic Entropy". DaveScot
Fish lose their eyesight in the dark far too quickly to be explained by progressive evolution through random mutation and natural selection. It's the absence of natural selection that explains it. Without natural selection acting as a conservative force random mutation runs rampant. Since random mutations are overwhelmingly deleterious the genes responsible for vision get ruined in a comparative eyeblink of time. If there was some other widely accepted explanation for it then that explanation must be quite dated. I don't think any competent biologist born in the last 100 years would entertain any explanation other than random mutation absent natural selection. DaveScot
So we concede that the lack of light would favor a fish which survives without eyes... or at least that perhaps some other trait is dominant that helps the blind ones survive in the dark better than the ones that have sight. Conversely how do we know that the presence of light doesn't have some effect on the genes. The fish with better eyes survive, presumably because they use them to find food and avoid predators. What I am getting at is. Do we know if the genes that the fish carries can be effected while the fish is alive... Is a dominant trait that is there to begin with (at birth) all there is to work with? DK
the theory that I remembered was that natural selection selected for blindness because an eye in such an environment would be more of a liability when damaged ari-freedom
ari-freedom I'm not quite sure what you mean to say. Natural selection is largely if not totally a conservative force. It works to maintain the status quo by killing off mutants that wander too far off the reservation. If vision is not required for anything then natural selection stops culling the mutants whose vision is compromised. It's very effective in this conservative role. Beneficial mutations are statistically rare and at best (with very rare exceptions like antibiotic resistance aquired through one or a few point mutations) only very slightly beneficial. On the other hand deleterious mutations are quite often so serious the organism dies long before it can reproduce and the great majority of the rest of the mutations are either neutral or very slightly deleterious. Because of this situation natural selection is ineffective at isolating and propagating any beneficial mutations. The beneficial mutations are overwhelmed by the accumulation of slightly deleterious mutations which occur so frequently. When a beneficial mutation occurs it must be accepted along with the deleterious mutations. Reproduction is an all or nothing process. Natural selection acts on the whole organism not individual pieces of it - it can't take the good without taking the bad at the same time. I recommend John Sanford's book "Genetic Entropy" for a more in depth treatment on this dilemma which IMO makes RM+NS incapable of long term progressive evolution. DaveScot
DK The first is almost certainly correct - visioned fish would lose their eyesight if bred in the dark long enough. The second - would partially visioned fish constantly find improved vision if bred in the light - is questionable. Almost certainly they would if amongst the entire population a complete set of functional vision genes already existed. This would be akin to front loading - the potential is already there. If in the entire population there was not a complete set of functional genes for eyesight a neo-darwinist would say that RM+NS would eventually restore vision regardless of the state of disrepair whereas an IDist would likely say, dependent on the scope of the "repairs" necessary, RM+NS is not sufficient with any reasonably finite number of opportunities to effect progressive positive change. DaveScot
I thought the blindness was a result of natural selection (since it was considered "beneficial" for a post hoc reason). Now you're saying this is an example of natural selection in action for everything else, since they don't change. ari-freedom
If the 1/2 of the 40% that gained sight were isolated and bred in the dark would they lose sight again due to the lack of need for sight? If the other 1/2 of the 40% was bred in the light would their eyesight improve? DK
jerry: "Something was operative in the cave environment to create blind fish. I understand how a mutation can create blindness but why would that mutation then become dominant. I can think of some reasons but they are just speculations." I would disagree. I think it is a much more passive thing. Blind offspring from sighted parents likely occur equally as often for fish not in caves as for fish in caves, but for fish in caves this is not a disadvantage, so they are not eliminated. The genetic entropy increases without limit w.r.t. visual systems until it is impaired to the point of non-functionality. SCheesman
Read the fine print. The picture captions & title are misleading. Some yellow journalism there. Normal sight was not restored but rather partial sight at best, sight that quickly deteriorated no less, in a fraction of the offspring. I question what controls were used in this experiment but don't have access to the original article.
in the most successful pairing, 40% of hybrid fry could see.
...
They then tracked eye movements while the fish were presented with a rotating pinstripe pattern. A number of the hybrids could track the pattern with their eyes — at least for a while. The young fishes' vision deteriorated with age.
As I said elsewhere this is not surprising at all and can be easily explained by Mendel's 6 principles of inheritance coupled with RM+NS and bit of observation subsequent to Mendel. It shouldn't be surprising at all that something as complex as the eye has a complex gene network behind it that can be catastrophically damaged anywhere in a large number of genes. Random mutation introduced errors in some genes in visual cascade. In the separate populations different genes were damaged but the result was the same - total loss of vision. Because there is no need at all for vision in total darkness natural selection didn't act to cull the mutants. It explains why the fish became blind in the first place - genetic entropy on steroids so to speak. Mendel didn't know any of the above. As Mendel discovered, genes (he called them particles because they didn't tend to blend like a fluid as Darwin believed) travel in pairs in diploid organisms. Germ cells have the pairs split apart. When sexual recombination occurs one gene from each parent recombine to form a new pair. If the genes aren't identical one of the pair may be dominant while the other is recessive in the offspring. In the blind fish experiment the parents had some undamaged, or at least not catastrophically damaged, genes in the set of genes needed for visual function. The two populations had different sets of undamaged genes but neither had a complete set of undamaged genes. In the hybrid offspring there would be gene pairs in the visual array with one damaged and one undamaged gene (heterozygous for the damage) where in the parents the gene pair was two damaged genes (homozygous for the damage). As learned through observation subsequent to Mendel a damaged gene is usually a recessive gene or, conversely, an undamaged gene is usually dominant. So in the hybrids some of the visual system was restored in the first generation because where the damage was homozygous in the parent it became heterozygous in the offspring with the undamaged gene in the pair being preferentially dominant. What would be an interesting follow-up experiment is to selectively breed hybrids with partial vision to see if vision was eventually completely restored which would be conclusive evidence that a complete set of functional vision-related genes could be cobbled together from the two isolated populations' genomes. However it's only mildly interesting because complete or incomplete would not be surprising in any significant way nor would it add to our general knowledge of genetics. It would add only to knowledge about the two specific populations of blind fish. As Jerry said this doesn't really speak to ID one way or another. The neo-darwinian theory of evolution is essentially correct when applied in the short term - "microevolution" if you will. It's only when the theory is extrapolated to the long term (macroevolution) that it becomes incredible - i.e. the hypothesis that macroevolution is just a whole lot of microevolution over deep time. Processes usually don't scale to infinity in a linear manner which is something that engineers are acutely aware of but biologists tend to ignore in the case of RM+NS. What they are doing is like concluding that you can pile rocks high enough to reach the moon based upon the observation that you can pile rocks high enough to reach the clouds (a mountain). The process of rock piling doesn't scale that far in a linear manner before the underlying principle becomes non-linear. In another example, transistors can be linearly scaled down in size through quite a range and this is well explained by classical mechanics but there is a point where quantum mechanical effects overwhelm the classical and the size no longer scales down linearly due to it. Biologists are making an unjustified presumption that RM+NS scales linearly from microevolution to macroevolution when in fact the empirical evidence points to a much narrower bound where the scale remains linear. DaveScot
Is this similar to the hairless chiuaua or finch beaks? That is, once you take the hairless chiuaua or the finch out of the environment that was placing a tax on the system, the organism reverts back to its original form. ajl
Something was operative in the cave environment to create blind fish. I understand how a mutation can create blindness but why would that mutation then become dominant. I can think of some reasons but they are just speculations. I have heard about blind fish before in caves but no details. Is it just one cave or are there several caves independent of each other that have blind fish? Are there caves that have fish with eyesight? Examples like this are why I believe ID should include the modern synthesis as part of its basic approach to evolution. NDE clearly makes some changes to genomes and many of these changes help the organism to adapt and persist. However, it is limited. It is why I consider this type of research as ID research because it is part of the paradigm that Behe is preaching. Namely, the modern synthesis works but is limited as pointed out in the Edge of Evolution. So any research that shows that NDE does not produce any novelty over time is ID research whether the researcher says it is or not. jerry
Note that they became blind in the first place because natural selection was NOT operative in the cave environment w.r.t. blind individuals, so the harmful mutations were able to survive when normally they would have been eliminated -- demonstrating that the true and limited role of natural selection is to preserve information from loss by harmful mutation, not create it. SCheesman
idnet.com.au: "This is the type of thing that RM and NS can do. I would say that they lose different genes to become blind, not use different genes." I think you are quite correct; Likely both lines of blind fish became blind due to the harmful mutation and loss of separate, but vital parts of the same system responsible for the production of sight. Breeding combined and restored the "missing" genes to allow the original system to function as designed. Net gain in information from the original situation? Zero. SCheesman

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