Why do cave fish evolve to become blind?

As you almost certainly know, animals from many groups have colonized caves, and more often than not they evolve to lose or reduce their eyes in the Stygian environment. But why? It’s hard to tell, for losing eyes takes thousands of generations, and we’re not around long enough to do experiments. I seem to recall an experiment in which Drosophila workers kept flies in the dark for years and observed no reduction of eye size, but they didn’t test their vision (this can now be done). At any rate, that experiment wasn’t long enough.

A new paper in The American Biology Teacher by Mike U. Smith, a Professor of Medical Education at Mercer University School of Medicine (Macon, Georgia), goes over the various theories for eye loss, with the piece aimed at biology teachers, suggesting how this subject should be taught and how to avoid misconceptions. (Reference below; access is free.) Smith gives three theories, but I think he gets it a bit wrong, and I wanted to give my take. I’ll ignore the stuff about teaching, as I want to concentrate on the biology.

First,  an example: Smith’s is the classic case of Astyanax mexicanusthe Mexican tetra or “blind cave fish” found in caves in the southwest U.S. and northern Mexico.  It is in fact considered the same species as its surface-dwelling form. Here are photos of each form and the range of the blind fish (from the paper). There are 26 known populations of the blind variant, representing at least five independent cases of evolutionary eye loss. Breeding experiments show that the cave and surface forms are interfertile, and that the loss of eyes in the cave form involves several genes, not just one:

 

The cave form eats mostly the bacteria film on the water that results from the breakdown of bat and cricket feces. The eyes are still there as vestigial remnants below the surface of the skin, but begin development as normal eyes and then regress as the fish grows up. (That itself is evidence for evolution.) Fish from at least one cave have an ability to detect light, but others have no such ability; this probably reflects different evolutionary stages of eye loss (or perhaps differential light levels in the caves). The fish find their way around via vibrations detected in their lateral lines. As Smith notes, “In fact, scientists capture these fish simply by putting a net in the water and vibrating it.”

Here are Smith’s three ideas for the evolution of eye loss. His words are indented (my emphasis). I maintain that two of the hypotheses are conflated, one is largely incorrect, and he’s neglecting another hypothesis.

According to the first hypothesis, eye loss is indeed caused by direct natural selection because there is an advantage to being eyeless in the dark. Studies have shown that maintaining eye tissue, especially the retina, and the related neural tissue comes at a high metabolic cost (Moran et al., 2015; Protas et al., 2007). Therefore, cavefish without eyes are at an advantage in this environment where energy sources (food) are scarce, because blind fish do not waste energy on these useless structures.

This is a reasonable hypothesis, and one my students used to always think of first when I asked them. It applies to the disappearance of any non-used structure, like the tiny nubbins that are the vestigial “wings” of the kiwi. The “not wasting energy”, of course, implies that that energy be directed towards other structures or functions that enhance reproduction, for that’s implicit in saying that reduces eyes give cave fish an advantage via natural selection.

A second hypothesis employs the phenomenon of pleiotropy, that is, cases in which multiple phenotypic effects are caused by the same mutation in a single gene. There is, for example, evidence that one of the genes responsible for eye loss in cavefish also increases the number of taste buds on the ventral surface of the head, which helps cavefish find food more effectively (Gross, 2012). Natural selection for this increase in taste buds would, therefore, also promote blindness.

I would argue that this second hypothesis isn’t substantively different from the first. After all, if resources are redirected from inactivated eye genes to other structures or functions that enhance reproduction, those other features would reflect pleiotropic effects of the mutations that reduced the eyes. I don’t see a material difference between a). An eye-reducing gene increasing the number of taste buds (the “pleiotropic” theory) or b). An eye-reducing mutation making more nourishment available for other structures by reducing the energy requirement for building an eye. In both cases, the mutation reducing eye formation has beneficial effects on other aspects of development. Those are both instances of “pleiotropy”.

The third hypothesis is based on neutral mutation and genetic drift. All too often textbooks use the terms “evolution” and “natural selection” interchangeably, ignoring the importance of genetic drift. Genetic drift is “the process of change in the genetic composition of a population due to chance or random events rather than to natural selection, resulting in changes in allele frequencies over time” (Biology Online, 2008). Genetic drift differs from natural selection because observed changes in allele frequency are completely at random, not the result of natural selection for a trait. Genetic drift can have a relatively larger impact on smaller populations such as a typical population of cavefish. According to the neutral mutation and genetic drift hypothesis, therefore, normal mutation processes in a small population of cavefish sometimes produce neutral mutations (mutations that lead to phenotypic changes that natural selection does not act on), and in the absence of natural selection, totally random events can sometimes result in the increased frequency of such mutations over time. Such changes could include eye degeneration.

This discussion is confusing. Even if the eye-reducing genes were neutral, and didn’t give eyeless fish a reproductive advantage, genetic drift (the random fluctuation of eyeless and eyed forms couldn’t by itself contribute to pervasive eye loss in caves, for the caves contain only fish without eyes. Drift would produce a “random” effect: varying mixtures of eyed and eyeless fishes in different caves. We don’t see that.

Now drift may play a slight role in eye loss (slightly deleterious mutations are more likely to persist in small populations), but I think what Smith is neglecting here is a non-random phenomenon: directional mutation. By that I don’t mean that somehow there is an increased frequency in the caves of mutations that inactivate eyes compared to the surface populations—that would be a Lamarckian or teleological process—but that random mutation applies to both cave and surface populations.  In surface populations those mutations that reduce or inactivate the eyes are weeded out by selection, and these mutations are more numerous than those creating better eyes. Remember that in the genes for eye formation, as in all genes, a random hit in a complex and evolved DNA sequence is more likely to damage the gene than improve its effect on reproduction.

Therefore, with a rain of mutations affecting eyes in both populations, and in general degenerating the eyes, the more numerous “bad” mutations will be selected out of the surface populations, but, with no selection against them in the cave populations, will tend to accumulate—perhaps aided by natural selection (hypotheses 1 and 2 above). Look at it this way: if you have a fleet of cars that are never driven, and people randomly adjust the engines of those cars without knowing anything about them, all the non-used cars will eventually lose their ability to run. That’s because a random adjustment of an engine is more likely to hurt it than to improve its function.  The engines are the eyes of cave fish, and the adjustments are mutations. The adjustments accumulate because the cars don’t need to run. I think this is a more plausible explanation than simple genetic drift, which seems implausible anyway because eye-reducing mutations aren’t likely to be “neutral”, for reasons given above but also because of what I say just in my fourth hypothesis below.

Smith says this:

. . . studies of the sequences of other genes related to the cavefish eye show high frequencies of substitutions in both coding and noncoding regions, which would support the genetic drift hypothesis (Retaux & Casane, 2013).

But that seems to be wrong for several reasons.  First a high frequency of substitutions in coding regions can be due to any of the forms of natural selection discussed above. Second, non-coding regions (parts of the DNA that do not code for proteins) can sometimes affect gene expression and regulation. More important, I couldn’t find any data in the Retaux and Casane paper suggesting an increased frequency of truly neutral non-coding mutations in these cavefish. (I may have missed it, but it doesn’t seem to be there.) What I see is this paragraph (note: this is for evolutionary geneticists)

The reports cited above only concern the evolution of the coding sequences. However, phenotypic evolution (including the loss of structures) can also occur through changes in non-coding, cis-regulatory sequences. Famous examples include the loss of the pelvic spine in freshwater sticklebacks through deletion of a Pitx1 enhancer [98, 99], or gain or loss of pigmentation patterns in Drosophilae through co-option or mutation of regulatory elements in the pigmentation gene yellow [100]. Although the exact mechanism is unknown, this happened for crystallin αA in cave Astyanax [55, 101]. This chaperone and anti-apoptotic crystallin whose coding sequence is almost identical in surface fish and cavefish (one amino-acid difference only) is strongly downregulated in the cavefish lens during development and was suggested as a potential major player in the onset of cavefish lens apoptosis. In the naked mole rat Heterocephalus glaber, gamma-crystallins are turned off after birth [46]. In the mole rat Spalax ehrenbergi, the αB-crystallin promoter and intergenic regions have selectively lost lens activity after 13.5 days of embryogenesis [102, 103]. These examples show that changes in regulatory sequences also occurred in cave and other underground animals.

Note that there are no data here on “high frequencies of substitutions in noncoding regions” of cavefish eyes. We see a change in gene regulation without accompanying changes in the sequence of the regulated genes, but that’s probably due to “coding” changes in other regulatory genes or substitutions in regulatory regions that are not “neutral” because they affect eye formation. (Note that Smith emphasizes “neutral” mutations in his third hypothesis.) These regulatory regions are thus subject to natural selection, and are not “neutral” changes acted on solely by genetic drift, even if they’re noncoding. We would in fact expect that selection would produce that observation: more substitutions accumulating in regulatory regions in cave fish than in surface fish! No need for drift here.

Coyne’s fourth hypothesis (not really mine but neglected by Smith). Eyes are delicate organs, easily damaged and prone to infection. If you reduce the eyes when you don’t need them, you’re less prone to this kind of environmental damage, and so the genes reducing the eyes make their bearers more likely to live and reproduce. Yes, this is a form of eye loss promoted by selection, but is conceptually different from hypotheses 1 and 2 above. I wish Smith had mentioned this idea as well.

At the end, Smith says that all his suggested processes might act together:

So, what’s the right answer? What genetic evidence is there to support each of these hypotheses? As with so much in science, the answer is probably that these explanations are not mutually exclusive; it is likely that all three partially explain cavefish blindness. To understand that statement, we must have some further background on A. mexicanus genetics.

Well, the explanations may not be mutually exclusive, but to say that it’s “likely” that all three explain cavefish blindness is unwarranted. One or two of the hypotheses may explain most of the eye loss. Just because there are several possibilities doesn’t mean they’ve all acted in concert.

While I’m trying to correct or put my own gloss on Smith’s paper, I’m not trying to say it’s a bad paper. It isn’t: it brings up a useful topic to discuss in evolution classes, and suggests a wealth of hypotheses and experiments. It also has very useful suggestions on what misconceptions students might have about this issue, and how to correct them. I just think the ideas could have been formulated and expressed more carefully. While we don’t know the precise evolutionary reason for eye loss in tetras, the fact that it has occurred several times independently, as well as in other species inhabiting caves, suggests that selection rather than drift has played the major role.

___________

Smith, M. U. 2017. How does evolution explain blindness in cavefish? 

48 Comments

  1. jaxkayaker
    Posted April 23, 2017 at 10:51 am | Permalink

    Very interesting. The so-called “directional mutation” hypothesis seems as if selection is maintaining vision in non-cave populations, but selection for sight is lacking in cave populations, with the consequence that blindness is widespread and frequent. I would call that a form of neutral drift. Thus, sight is due to selection and blindness results from the lack of selection and neutral drift.

    • Richard Bond
      Posted April 23, 2017 at 10:59 am | Permalink

      I agree; my comment #2 was posted before I saw yours.

  2. Richard Bond
    Posted April 23, 2017 at 10:55 am | Permalink

    Is it not that where eyes are unused, in completely dark caves, natural selection cannot weed out deleterious mutations?

    • busterggi
      Posted April 23, 2017 at 11:25 am | Permalink

      Interesting…

    • Posted April 24, 2017 at 2:49 am | Permalink

      THis is the obvious explanation to me and the one I learnt as a zoology undergrad. nearly forty years ago!

    • Diana MacPherson
      Posted April 25, 2017 at 9:54 pm | Permalink

      My first thought as well.

  3. Thanny
    Posted April 23, 2017 at 11:04 am | Permalink

    A quibble:

    “The “not wasting energy”, of course, implies that that energy be directed towards other structures or functions that enhance reproduction, for that’s implicit in saying that reduces eyes give cave fish an advantage via natural selection.”

    This isn’t necessarily true. If it takes X mouthfuls of food to acquire enough energy to build a reproductive fish with working eyes, it takes X minus Y mouthfuls to build a reproductive fish without working eyes.

    You don’t need to consume the same amount and divert the eyes’ share towards something else for the “wasted energy” argument to work. The fish can just consume less overall to reach the same point of reproductive function without having to build eyes in the process.

    • Posted April 23, 2017 at 11:20 am | Permalink

      That’s a pleiotropic effect on the relationship between food consumption and offspring production. Think of it as this trait: amount of food needed to produce one offspring. Remember, he defines pleiotropy as “multiple phenotypic effects of a single gene”.

  4. rickflick
    Posted April 23, 2017 at 11:17 am | Permalink

    My first guess was that eye damage would drive their elimination. If a fish collides with a rock and scratches the eye, something that’s bound to happen in a dark cave, it can become infected and kill the fish. This seems to be a strong driver if there are genes for eyelessness present.

    • Posted April 23, 2017 at 12:51 pm | Permalink

      Good point. The delicacy of eyes is less of a problem when they are useful for avoiding hazards.

    • gravelinspector-Aidan
      Posted April 24, 2017 at 11:25 am | Permalink

      If a fish collides with a rock and scratches the eye, something that’s bound to happen in a dark cave,

      “bound to happen”? Hmmm, that needs some support, I think.
      Humans blundering around in caves without lights walk into walls, bang their heads etc. No dispute there. Fish, on the other hand, may be a different kettle of vertebrates. They’re in water, which is a much better conductor of sound (vibration) than air ; they’ve got lateral line organs ; and their eyes are in a head surrounded by lines of the lateral line system. I think you need to provide evidence of your contentions that (1) fish bump into the rock, and (2) that they damage their eyes in the process.
      The lateral line system is very ancient – I can’t remember if it was lost at the “reptile” or “amphibian” “level” of the terrestrial vertebrates, but it was there in the “lobe-finned” fishes. In their environments of very shallow pools, you’d expect them to spend a lot of time in very murky (sediment, mud, vegetation) water. So you’d expect collision avoidance systems to be strongly conserved.

      • rickflick
        Posted April 24, 2017 at 4:39 pm | Permalink

        “I think you need to provide evidence of your contentions.”

        Ha! Here, hold my Guinness (no sipping). Stay right here. I’ll be back.

        https://www.youtube.com/watch?v=IBCr-XBWZaQ

        • gravelinspector-Aidan
          Posted April 25, 2017 at 6:18 pm | Permalink

          Needs another thousand or two generations of culling the failures.

  5. dabertini
    Posted April 23, 2017 at 11:25 am | Permalink

    Fantastic post especially since i have difficuties understanding how genetic drift acts independently from natural selection. I am an evolution enthusiast and not an expert.

  6. Posted April 23, 2017 at 11:27 am | Permalink

    I discuss this issue in my evolution class, and there I propose two factors that are described here. They include the energy cost factor for both embryonic development and for post-embryonic life, and the other factor is that fitness is reduced if the structure were injured, so there is selection for reducing the structure since having the structure provides no benefit while also reducing fitness if it were injured.
    I had not considered the aspect of genetic pleiotropy, where another needed structure might be enlarged. To me also, this is connected to selection for frugal use of energy since it provides a means for making another structure larger without adding to the energy budget. Specifically, cells that would go into a no-longer-needed structure are instead recruited during embryonic development to enlarge the other structure that is under positive selection to get bigger.

  7. ThyroidPlanet
    Posted April 23, 2017 at 11:49 am | Permalink

    Sub

  8. Curt Nelson
    Posted April 23, 2017 at 11:51 am | Permalink

    I like a combination of the 1st and 4th hypotheses. The 4th is what occurred to me as I read the 1st and I chalked up “dealing with injuries and infections” to the energy cost of the 1st, but it is a separate thing.

  9. Randall Schenck
    Posted April 23, 2017 at 12:03 pm | Permalink

    Question from the audience – If the cave and surface-dwelling form are truly the same species, has there been any attempt to breed the two for further research?

    • Posted April 23, 2017 at 12:59 pm | Permalink

      Follow up question from the audience. If the cave and surface forms are infertile in breeding experiments, as you say, does that not make them separate species pretty much by definition?

      • Posted April 23, 2017 at 1:05 pm | Permalink

        As far as I know; they can hybridize in the lab and produce fertile offspring. That doesn’t mean they AREN’T different species, as they could be segregated by habitat preference, but it does mean that we can’t say they’re the same species.

        • nicky
          Posted April 23, 2017 at 8:21 pm | Permalink

          What do the eyes of the offspring look like?

  10. aihardin
    Posted April 23, 2017 at 12:20 pm | Permalink

    Reed Cartwright just published a paper modeling the effects of selection vs migration in cave fish and found that selection for blindness would have to be incredibly strong to result in the homogenous blindness observed while the preferential migration of seeing fish to the surface can be rather modest and achieve the same result. https://bmcevolbiol.biomedcentral.com/articles/10.1186/s12862-017-0876-4

    • Posted April 23, 2017 at 1:11 pm | Permalink

      I think they also say that selection might well be that strong. At any rate, you need selection to account for eyelessness in the first place; it might be maintained by differential avoidance of the “wrong” habitat.

    • W.Benson
      Posted April 23, 2017 at 3:14 pm | Permalink

      Why should seeing (and imperfectly seeing) fish migrate to the surface? You would expect fish to go where the best feeding was, wouldn’t you?

      It seems possible to test among several (but not all) hypotheses using (natural) hybrid fish (from cave mouths?) and keeping fish with different degrees of eye development in pens in dark caves. If natural selection is important, you would expect to see it: eyed fish might show either more eye infections (Hypothesis 4) or smaller gonads or egg loads (Hyp 1). I doubt if molecular genetics can resolve the question as cleanly as some good, old-fashion, low-tech experiments, but you’d have to get your feet wet to do them.

  11. Eduardo
    Posted April 23, 2017 at 1:07 pm | Permalink

    Very nice.

  12. DiscoveredJoys
    Posted April 23, 2017 at 1:19 pm | Permalink

    It seems from the above that the fish start with the structure for eyes but the development doesn’t take place. I can imagine that structural changes (other than perhaps size) are quite difficult for selection to influence because there must be quite a few related genes to ‘undo’ as well.

    On the other hand if the development pathway is subjected to selection, this could be quite ‘easy’. Perhaps light is an environmental trigger which affects how the development pathway forms, and in the absence of light over many generations the development pathway could mutate and become metabolically expensive or harmful to fitness?

  13. ladyatheist
    Posted April 23, 2017 at 1:22 pm | Permalink

    This is an example of why I am a fan of science & of scientists! Someone builds on others’ works, then proposes a new direction, and someone else refines that proposed new direction. It takes a village to make a good idea great!

  14. Leigh Jackson
    Posted April 23, 2017 at 1:47 pm | Permalink

    Another fascinating topic. Lots of food for thought. Good comments too.

    Again it mystifies me how one might begin to explain ex-eyed cave fishes, other than by evolutionary mechanisms.

    The God “hypothesis”, by comparison, hits me as beyond contempt. It’s like an assault on the intellect. Intelligent design is a repudiation of human intelligence.

    Theistic evolution is no better. Evolutionary mechanisms require God’s hidden quantum mechanical guiding hand like I need a hole the size of my brain in my brain.

    • Posted April 23, 2017 at 2:47 pm | Permalink

      I had a student who explained to me that vestigial organs resulted from the biblical fall from grace.
      And that was that.

      • ladyatheist
        Posted April 23, 2017 at 6:18 pm | Permalink

        But did the animals also fall from grace?

        Also, is falling from grace the same as descending from trees?

        • Posted April 26, 2017 at 3:50 pm | Permalink

          Snakes did fall from grace and lost their limbs, but I don’t remember fish ever sinning. In fact, Jesus and his audience apparently valued them.

  15. Gregory Kusnick
    Posted April 23, 2017 at 2:02 pm | Permalink

    I don’t see a material difference between a). An eye-reducing gene increasing the number of taste buds (the “pleiotropic” theory) or b). An eye-reducing mutation making more nourishment available for other structures by reducing the energy requirement for building an eye.

    It seems to me there is a difference. Suppose I’m remodeling my house and want to combine two small rooms into one big room. If the contractors says “It’ll be expensive, so you might have to give up something else to stay within budget,” that’s a fundamentally different sort of tradeoff than if he says “Sorry, it’s a load-bearing wall; we can’t remove it without bringing the whole house down.” In one case I have some latitude to prioritize my goals; in the other I don’t.

    I’ve always understood pleiotropy to be more like the latter sort of tradeoff (one gene with two distinct functions) than like the former (multiple genes competing for metabolic resources).

    On a minor point:

    the bacteria film on the water that results from the breakdown of bat and cricket feces

    Surely the bacteria are the agents of that breakdown, not an incidental byproduct of it.

    • Posted April 23, 2017 at 3:50 pm | Permalink

      Yes, you’re right about the bacteria; I was quoting what the authors said.

      As for pleiotropy, geneticists would consider it a pleiotropic effect of a gene if it suddenly allowed you to produce eggs with less nutrition. That’s a tradeoff in the way evolutionists look at it: a tradeoff between egg production and eye production. Given the complex nexus of development, the “function” of a gene becomes nearly meaningless. For instance, many mutants that affect eye color have a deleterious effect on viability. That’s considered to be pleiotropy though it sounds weird to say that the “function” of an eye gene is to make the fly viable. But the inactivation of a gene can have complex ramifications in development.

  16. eric
    Posted April 23, 2017 at 2:15 pm | Permalink

    It’s hard to tell, for losing eyes takes thousands of generations, and we’re not around long enough to do experiments.

    I just took my kid to the Skyline Caverns in VA a little while ago, and they do experiments on fish in caves (tehy stock the underground lakes in the cave complex, and watch what happens). Evidently, when there is literally no light around the pools, the eyes will degenerate in use in less than a generation (i.e., the original stocked fish lose their ability to see). Not genetically, obviously, but developmentally and cognitively they cease to function correctly. I suppose once that’s happened, any mutation affecting eye development in future generations is neutral and thus can be expected to propagate like a neutral mutation. Eyes in such fish aren’t giving just a lesser advantage, they’re giving no advantage – because they’ve stopped working.

    • Posted April 23, 2017 at 2:50 pm | Permalink

      That is interesting!
      I was thinking about the fruit fly experiment that Jerry mentioned, and wondered if it was ok and useful to ‘seed’ the stock with some mutant flies that have reduced eyes. There are several mutations that do that, and it might speed things up a bit.

  17. Bogi Trickovic
    Posted April 23, 2017 at 3:02 pm | Permalink

    I am a bit confused about your remark that genetic drift would produce varying mixtures of eyed and eyeless fishes in different caves. Although drift is a random process, I always thought that the effect of genetic drift (and resulting distribution of alleles or, in this case, phenotypes) depends on mutation rates and population size. So if mutation rates towards eyeless forms are higher given that it’s much easier to break than to make something, wouldn’t you expect to see more eyeless individuals within a cave? Likewise, you would expect to see more caves where eyeless mutant is fixed. Whether this is 60% or 95% of caves ultimately depends on mutation rates (i.e. rates at which these forms are introduced in the population) and population size. It’s like a drunkard’s walk, except that a drunkard has a broken leg, so he keeps staggering to one side until he reaches the trench. Am I wrong about this?

    • Posted April 23, 2017 at 3:45 pm | Permalink

      Not if the traits are neutral; it would be mutation pressure rather than drift that would explain the near complete frequency of eyelessness in cave fish.

  18. Steve Gerrard
    Posted April 23, 2017 at 3:40 pm | Permalink

    I prefer the directional mutation idea, with the nice analogy of the fleet of cars. The strong selection for these fish will be favoring positive mutations that enable survival and reproduction without vision, such as use of the lateral lines for detecting vibrations, or the surface feeding behavior. In some cases that could entail re-purposing parts of the neurological system that were previously used for vision and vision-related behavior.

    In all cases selection will be ignoring any detrimental effect on vision or vision-related behavior, since vision is useless to these fish. It seems perfectly reasonable to me that a useless organ would deteriorate over generations, and it seems likely that there could be multiple ways in which mutations shut it down. It’s more like the loss of eyes is collateral damage incurred while making the changes needed to function better in the dark.

    As a side note, it does seem to me that for vision in particular, there is often too much emphasis on the eyeball itself, and not enough on the very elaborate neural systems required to make productive use of an eyeball (or it’s precursors).

  19. Posted April 23, 2017 at 5:50 pm | Permalink

    Strikes me that there are many more ways to be eyeless than there are to have eyes. So being blind is the default position. So I suppose it’s use it or lose it.

  20. Tony Eales
    Posted April 23, 2017 at 7:05 pm | Permalink

    This reminded me of a piece I read by Ed Yong about this paper Borowsky, R. (2008). Restoring sight in blind cavefish. Current Biology, 18(1), R23-R24. Apparently cross breeding blind fish from different caves produced offspring with restored sight. https://notexactlyrocketscience.wordpress.com/2008/01/07/cross-breeding-restores-sight-to-blind-cavefish/

  21. nicky
    Posted April 23, 2017 at 8:38 pm | Permalink

    I always only considered hypothesis one, eyes and associated neuronal system, are ‘expensive’. Now it is clear there might be much more to it. Food for thought…
    The Borowski experiment is fascinating.

  22. Posted April 24, 2017 at 8:22 am | Permalink

    Cool, thanks for posting this. I had these guys (blind tetras) in my tank when I was a kid.

  23. Posted April 24, 2017 at 8:40 am | Permalink

    It seems to me you could test the ‘selective loss’ vs ‘drift’ explanation by crossing different species from different caves. If a cross between 2 eyeless species regains much of the eye that would suggest the loss of fuction mutations were in different genes and fucntional copies were complementing each other in the hybrid.
    On the other hand if the hybried had eyes indistinguishable from the parents that would suggest there are particular loss of functions that are selected because of some other unknown benefit

    • nicky
      Posted April 24, 2017 at 8:47 pm | Permalink

      See above at 20, the Borowski experiments.
      Maybe I’m a bit dense, but I fail to see how the result (they do recover functional eyes in a substantial number of cases) would suggest drift rather than selection.

  24. Posted April 24, 2017 at 10:23 am | Permalink

    I recall several years ago a certain very confused instructor of freshman biology wrote an article on these fish, claiming it was all due to pleiotropy, and entirely random to boot, and thus these fish showed how trivial is natural selection.

  25. Brian Salkas
    Posted April 24, 2017 at 10:59 am | Permalink

    The hypothesis about neutral drift seems compelling, but is it possible that that process was sped up by the fact that eyes are soft tissue and therefor vulnerable to bacterial infection? So not only are they costly in terms of energy, but they are an opening for bacteria to get in. Sorry if someone else brought this up, I have not read all the comments,

  26. Posted April 24, 2017 at 1:09 pm | Permalink

    How does one go about accumulating data to test the hypotheses?

  27. nicky
    Posted April 24, 2017 at 8:37 pm | Permalink

    Another factor not yet mentioned, is that predation in these caves must be very low or inexistent. So even pitch darkness is not a prerequisite. And if we do experiments it should be kept in mind too.


%d bloggers like this: