# Are Vestigial Organs the result of Random Mutations? **URL:** \ **Category:** Great Debates\ **Created:** [April 13, 2001, 6:30am UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796 "2001-04-13T06:30:07Z")\ **Posts on this page:** 20\ **Page:** 1
**Author:** ![jorolat](https://avatars.discourse-cdn.com/v4/letter/j/ed655f/32.png) [@jorolat](https://boards.straightdope.com/u/jorolat)\ **Post date:** [April 13, 2001, 6:30am UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/1 "2001-04-13T06:30:07Z")
The following developed out of “[**Lamarck’s Law of Use and Disuse**](http://boards.straightdope.com/sdmb/showthread.php?postid=1251853#post1251853)” which was first posted on the General Questions board and has now been moved here (Great Debates). One of the original questions asked was “ **How does current theory account for vestigial organs?** ” and various scenarios were described whereby “random mutations” were made responsible for the beginning of degradation. It was then mentioned that the eye of the mole developes normally until a certain stage is reached and then it stops. A contributor to the thread responded by referring to an article (“[**Cave Fish Grow Eyes**](http://www.abcnews.go.com/sections/science/DailyNews/cavefish_000728.html)”) which begins: > [@](#): > > **"Researchers announced on Thursday that they were successful in growing eyes in fish that have been blind for aeons — simply by inserting a lens from sighted fish"** > > and goes on to say: > > **"They implanted a lens… (and) after two months, the cave fish had grown a large eye with a distinct pupil, cornea and iris, they said. The retina of the eye had photoreceptor cells known as rods".** This appears to be identical with what happens in the mole, ie vestigial organs appear to be have been “selected for” as a **unit** with degeneration beginning from the “top down”. Could there be another mechanism at work here? after all, if random mutations were responsible, then why don’t they affect _other_ genes within (for these examples) the eye?. Furthermore, is “top down” degeneration true for all vestigial organs? Jorolat ---
**Author:** ![ssj\_man2k](https://avatars.discourse-cdn.com/v4/letter/s/e9bcb4/32.png) [@ssj\_man2k](https://boards.straightdope.com/u/ssj_man2k)\ **Post date:** [April 13, 2001, 6:41am UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/2 "2001-04-13T06:41:05Z")
Well, for that to work, everyone would have to have random mutations. All vestigial organs once had a purpose, that’s why everyone has them. They would not have stayed in the gene pool if they didn’t have a use, or if only one person or two had the organ. ---
**Author:** ![DrFidelius](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/drfidelius/32/3447_2.png) [@DrFidelius](https://boards.straightdope.com/u/DrFidelius)\ **Post date:** [April 13, 2001, 1:17pm UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/3 "2001-04-13T13:17:19Z")
It would appear to me that a single mutation which prevents the “coming together” of all the parts of an organ, such as one which stops the production of a regulatory protein needed at a certain stage of development, is more likely to occur and be preserved in the appropriate environment than a mutation “deeper” in the development process. The prevention of the start of development of an organ or a system could have a serious impact on the development of related organs or systems. For instance, to prevent an eye from starting to form in a vetebrate would require changing the timing of a number of neurological features. Any fiddling with basic development is likely to produce non-viable organisms. If a relatively simple mutation produces the result favourable to survival in a given environment there is no mecahnism known which would remove the more basic genes. They have become invisible to selection. ---
**Author:** ![Brian\_Bunnyhurt](https://avatars.discourse-cdn.com/v4/letter/b/9d8465/32.png) [@Brian\_Bunnyhurt](https://boards.straightdope.com/u/Brian_Bunnyhurt)\ **Post date:** [April 13, 2001, 3:51pm UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/4 "2001-04-13T15:51:31Z")
What is a vestigial organ? I know what it means, but do they really, truly exist? I recall in the fifties many doctors recommended the radiation shrinkage (for no apparent medical reason) of the gland behind the breastbone with disasterous results (I will remember what it is called two seconds after I post this). Anyway, even the appendix and tonsils are now known to be more useful than their lowpoint in the 1960’s when they were demonized. Even in other animals, we can’t be sure to know something is purely vestigial, since nature often determines entire species to be “vestigial.” ---
**Author:** ![jorolat](https://avatars.discourse-cdn.com/v4/letter/j/ed655f/32.png) [@jorolat](https://boards.straightdope.com/u/jorolat)\ **Post date:** [April 13, 2001, 4:57pm UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/5 "2001-04-13T16:57:26Z")
> [@](#): > > \*Originally posted by DrFidelius \* > **It would appear to me that a single mutation which prevents the “coming together” of all the parts of an organ, such as one which stops the production of a regulatory protein needed at a certain stage of development, is more likely to occur and be preserved in the appropriate environment than a mutation “deeper” in the development process. The prevention of the start of development of an organ or a system could have a serious impact on the development of related organs or systems.** Hi DrFidelius, In between the start and end of development of an organ a whole host of “random mutations” can be present which will still result in the birth of a viable organism. Human beings can have, as examples, the following eye defects at birth: Anophthalmos (absence of eyes} Congenital cataract (eye cataracts at birth) Coloboma of eye (eye parts missing) Aniridia (absence of the iris) (taken from: “[**BIRTH DEFECTS --PART 1**](http://www.monitor.net/rachel/r410.html)”) If the start of degeneration in a vestigial eye was due to randon mutation(s) then surely, in those environments where the eye is no longer “selected for”, similar birth defects to the above should be occurring on an _equal_ frequency to that of the _whole_ eye?. If such a distribution isn’t found then doesn’t that imply randomness isn’t involved and it is the _organ_ that has been “selected” against?. > [@](#): > > \*\*If a relatively simple mutation produces the result favourable to survival in a given environment there is no mecahnism known which would remove the more basic genes. They have become invisible to selection. \*\* Even after degeneration has begun these genes are still visible to random mutations. I’m not aware of any mechanism that could arbitrarily remove the more basic genes either. Jorolat ---
**Author:** ![jorolat](https://avatars.discourse-cdn.com/v4/letter/j/ed655f/32.png) [@jorolat](https://boards.straightdope.com/u/jorolat)\ **Post date:** [April 13, 2001, 5:26pm UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/6 "2001-04-13T17:26:10Z")
> [@](#): > > \*Originally posted by Brian Bunnyhurt \* > \*\*What is a vestigial organ? … Anyway, even the appendix and tonsils are now known to be more useful than their lowpoint in the 1960’s when they were demonized… Even in other animals, we can’t be sure to know something is purely “vestigial…” \*\* Hi Brian, A dictionary definition of a vestigial organ is given as: “Any part of an organism that has diminished in size during its evolution because the function it served decreased in importance or became totally unnecessary. Examples are the human appendix and the wings of the ostrich.” (taken from **A Dictionary of Biology, Oxford University Press, © Market House Books Ltd 2000** at [http://w2.xrefer.com/entry/464033](http://w2.xrefer.com/entry/464033) I agree with much of what you say but unless someone comes up with a better idea, and in order to continue this discussion, can we consider a vestigial organ to be one whose most _obvious_ function has degenerated from what it once was? Jorolat ---
**Author:** ![PosterChild](https://avatars.discourse-cdn.com/v4/letter/p/e274bd/32.png) [@PosterChild](https://boards.straightdope.com/u/PosterChild)\ **Post date:** [April 13, 2001, 6:21pm UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/7 "2001-04-13T18:21:46Z")
> [@](#): > > \*Originally posted by jorolat \* > “[**Lamarck’s Law of Use and Disuse**](http://boards.straightdope.com/sdmb/showthread.php?postid=1251853#post1251853)” Hi Jorolat, as you have spent more effort on supporting Lamark’s Laws than the rest of us, I would really like to hear your responses to the questions in your (now GD) thread. I think they would go a long way to helping some of us understand Lamarkian evolution. > [@](#): > > **"They implanted a lens… (and) after two months, the cave fish had grown a large eye with a distinct pupil, cornea and iris, they said. The retina of the eye had photoreceptor cells known as rods".** This appears to be identical with what happens in the mole, ie vestigial organs appear to be have been “selected for” as a **unit** with degeneration beginning from the “top down”. Could there be another mechanism at work here? after all, if random mutations were responsible, then why don’t they affect _other_ genes within (for these examples) the eye?. Furthermore, is “top down” degeneration true for all vestigial organs? Jorolat [/QUOTE] Developement of they eye (as well as a whole host of other organs) occurs through interdependent feedback. Having the lens in place allows the positioning and coordination of the tissue around it. So many of the genes for the eye don’t express in a vacuum, but require the cells to interact with other cells around them, so they all develop together. {Have you studied basic embryology? I think you’d find it very helpful.) A **random** mutation in a gene necessary for lens development would therefore prevent full development of the organ. the development that doesn’t rely on the lens would still occur, leaving what we would call a “vestigal” organ. 99.some% of the bases in the genome have no apparent function. In fact, the introns in genes are commonly mutated or removed in the lab during transgenic research. (In fact, transposons may be partially responsible for the intron/exon form of some genes.) Most mutations would therefore have no effect (which is why there can be so many coding differences between individuals of a species without as much phenotypic variation- it’s how genetic trees work). I find your “top level” comment confusing. Don’t both Lamarkian & Darwinian evolution find that it’s the “top level” function that determines selection? PC P.S.- Please don’t let your GD thread die. I’d really like to hear the answers.b ---
**Author:** ![DrFidelius](https://sea3.discourse-cdn.com/straightdope/user_avatar/boards.straightdope.com/drfidelius/32/3447_2.png) [@DrFidelius](https://boards.straightdope.com/u/DrFidelius)\ **Post date:** [April 13, 2001, 7:30pm UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/8 "2001-04-13T19:30:16Z")
> [@](#): > > If the start of degeneration in a vestigial eye was due to randon mutation(s) then surely, in those environments where the eye is no longer “selected for”, similar birth defects to the above should be occurring on an equal frequency to that of the whole eye?. and > [@](#): > > Even after degeneration has begun these genes are still visible to random mutations. I am certain if you were to implant lenses into the proto-eyes of a number of blind cave fish, a given percentage of them would fail to develop a full eye due to any one of the “birth defects” you had listed; that percentage being approximately equal to (or slightly higher than) the percentage of these abnormalities which appear in a sighted population. So? Also, I am certain that all the “eye support” genes in a population of blind cave fish would exhibit a random genetic drift from the state of the original sighted population. This would be exactly congruent to the selection-neutral drift we see in other sections of “junk” or non-expressed DNA. Again, so? Sounds like you have the makings of two doctoral dissertations here. Do you need help applying for grant money? I am sure the results would be interesting. ---
**Author:** ![choosybeggar](https://avatars.discourse-cdn.com/v4/letter/c/8c91f0/32.png) [@choosybeggar](https://boards.straightdope.com/u/choosybeggar)\ **Post date:** [April 13, 2001, 8:43pm UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/9 "2001-04-13T20:43:23Z")
> [@](#): > > \*Originally posted by Brian Bunnyhurt \* > \*\*What is a vestigial organ? I know what it means, but do they really, truly exist? I recall in the fifties many doctors recommended the radiation shrinkage (for no apparent medical reason) of the gland behind the breastbone with disasterous results (I will remember what it is called two seconds after I post this). > \*\* It’s called the thymus gland. It’s it not a gland, though, it’s name notwithstanding. It is the place where T cell development/maturation takes place (in fact the T cells get their name by virtue of their development there). I can imagine why irradiating the thymus was **a bad thing.[sup]TM[/sup]** The T cells that develop here are responsible for coordinating and effecting immune responses against a host of nasties. Do you remember why they thought irradiating the thymus was **a good thing[sup]TM[/sup]**? > [@](#): > > _Originally posted by Jorolat_ > \*\*This appears to be identical with what happens in the mole, ie vestigial organs appear to be have been “selected for” as a unit with degeneration beginning from the “top down”. > > Could there be another mechanism at work here? after all, if random mutations were responsible, then why don’t they affect other genes within (for these examples) the eye?. \*\* I believe there are three factors to consider here: 1. Mutations occur at a very low frequency. Therefore one wouldn’t be surprised to find a lack of multiple fatal hits in the group of genes essential for the development of a single organ. 2. Most mutations are neutral. Many land in non-coding regions. Mutations in coding regions can be silent (they change a codon without changing the encoded amino acid). Mutations can also change amino acids without affecting the function of the encoded protein. Furthermore, mutations resulting in a non-functional gene product may lack a phenotype due to functional redundancy (ie. another related gene can perform the missing function) 3. Destruction is inherently easier than creation. How long did it take the Allies to destroy Dresden? To make an eye from scratch is an almost impossibly difficult proposition. To destroy an eye, you just need 1 critical base substitution (mutation) in one critical gene. Or a few moments of carelessness ([mom voice] Stop that now or you’ll put someone’s eye out[/mom voice]) The “top down” model you propose is false from the perspective of genetics. You are only considering the fatal mutation that disrupts eye development. You ignore the larger number of neutral mutations which doubtlessly occur both in the gene that eventually takes the fatal hit as well as in other genes essential for eye development. Based on the higher frequency of neutral mutations, it is likely that many neutral mutations in the genes necessary for eye development have occurred **before** the fatal hit takes place. If one considers only an organism’s phenotype, however, one is blind (🙂 ) to silent mutations. I find it interesting, in light of your obliviousness to phenotypically silent changes in DNA, that you are a psychologist by trade. A ways back, didn’t the strict behaviorists have their way when they asserted that the study of internal states of the mind was fruitless due to the(necessarily) subjective nature of this line of inquiry? We in genetics are not similarly handicapped. We can study (and always consider) silent changes in the medium of inheritance and trait expression. In fact, one can study mutation in the absence of selection by intentionally rigging an experimental system. In psychology, this is the equilvalent of the objective examinination of an internal mental state without consideration of behavior. I find such methodologies to be very elegant and think you would too if you deepened your understanding of modern genetics. Hopefully, **Joro** , at least you’ll be satisfied that conventional genetics can explain the origin of vestigial organs quite neatly. ---
**Author:** ![jorolat](https://avatars.discourse-cdn.com/v4/letter/j/ed655f/32.png) [@jorolat](https://boards.straightdope.com/u/jorolat)\ **Post date:** [April 13, 2001, 11:38pm UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/10 "2001-04-13T23:38:57Z")
> [@](#): > > \*Originally posted by PosterChild \* > \*\* > > > [@](#): > > > > \*Originally posted by jorolat \* > > “[**Lamarck’s Law of Use and Disuse**](http://boards.straightdope.com/sdmb/showthread.php?postid=1251853#post1251853)” > > Hi Jorolat, as you have spent more effort on supporting Lamark’s Laws than the rest of us, I would really like to hear your responses to the questions in your (now GD) thread. I think they would go a long way to helping some of us understand Lamarkian evolution.\*\* Hi PosterChild, How many _times_ have I told you that I don’t support or believe in Lamarckianism?? ‘mega theatrical sigh’ ( 🙂 ). My personal interest is more related to the _indirectedness_ of “[The Baldwin Effect](http://members.aol.com/jorolat/baldwin2.html)”. There have been no replies to my last posts in the other thread so I guess people have lost interest ☹ > [@](#): > > **Developement of they eye (as well as a whole host of other organs) occurs through interdependent feedback. Having the lens in place allows the positioning and coordination of the tissue around it. So many of the genes for the eye don’t express in a vacuum, but require the cells to interact with other cells around them, so they all develop together. {Have you studied basic embryology? I think you’d find it very helpful.)** I’m pushed for time, can see other replies from DrFidelius & Choosybeggar (which I’ll have to leave for now), so I’ll have to be brief: The explanation sounds very reasonable and a further quote from [**Cave Fish Grow Eyes**](http://www.abcnews.go.com/sections/science/DailyNews/cavefish_000728.html) says: > [@](#): > > “This offers clues about what sort of molecules are involved in eye growth of any vertebrate, and it shows the growth of an eye is controlled in a large part by the lens,” Jeffery said in a statement. Interestingly another source (taken from **Investigative Ophthalmology and Visual Science, April, 1999** and available [**here**](http://www.nervenet.org/papers/Eye1.html) says: > [@](#): > > Our understanding of the molecular processes responsible for the maturation of the vertebrate eye is progressing rapidly (Graw, 1996; Freund et al., 1996). Nonetheless, _little is known_ about the critical set of genes that modulate rates and duration of normal eye growth (Williams et al., 1998). These _unidentified genes_ make a key contribution to vision by ensuring a near perfect match between developmental changes in the refractive power of the cornea and lens, the size and shape of the eye, and the position of the retina. (my italics) The unknown genes give me the impression they achieve _equilibrium_ between the “component parts”. (also: embryology - wassat? 🙂 > [@](#): > > A **random** mutation in a gene necessary for lens development would therefore prevent full development of the organ. the development that doesn’t rely on the lens would still occur, leaving what we would call a “vestigal” organ. The [**Cave Fish Grow Eyes**](http://www.abcnews.go.com/sections/science/DailyNews/cavefish_000728.html) article indicates how much is dependent on the lens but your answer doesn’t address the point made in the first reply to DrFidelius: > [@](#): > > Human beings can have, as examples, the following eye defects at birth: > > Anophthalmos (absence of eyes} > Congenital cataract (eye cataracts at birth) > Coloboma of eye (eye parts missing) > Aniridia (absence of the iris) > > (taken from: “BIRTH DEFECTS --PART 1”) > > If the start of degeneration in a vestigial eye was due to randon mutation(s) then surely, in those environments where the eye is no longer “selected for”, similar birth defects to the above should be occurring on an equal frequency to that of the whole eye?. > [@](#): > > I find your “top level” comment confusing. Don’t both Lamarkian & Darwinian evolution find that it’s the “top level” function that determines selection? > \*\* Part of my interests is the possibility, that for vestigial organs, “random mutations” may be only occurrring at the top level (the “unidentified genes”?) in which case they may not be random. Jorolat ---
**Author:** ![choosybeggar](https://avatars.discourse-cdn.com/v4/letter/c/8c91f0/32.png) [@choosybeggar](https://boards.straightdope.com/u/choosybeggar)\ **Post date:** [April 14, 2001, 1:55am UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/11 "2001-04-14T01:55:12Z")
[QUOTE] \*Originally posted by jorolat \* The [**Cave Fish Grow Eyes**](http://www.abcnews.go.com/sections/science/DailyNews/cavefish_000728.html) article indicates how much is dependent on the lens but your answer doesn’t address the point made in the first reply to DrFidelius: > [@](#): > > Human beings can have, as examples, the following eye defects at birth: > > Anophthalmos (absence of eyes} > Congenital cataract (eye cataracts at birth) > Coloboma of eye (eye parts missing) > Aniridia (absence of the iris) > > (taken from: “BIRTH DEFECTS --PART 1”) > > If the start of degeneration in a vestigial eye was due to randon mutation(s) then surely, in those environments where the eye is no longer “selected for”, similar birth defects to the above should be occurring on an equal frequency to that of the whole eye?. \*\* Wow, I get your point:) The notion here is that the dark-dwelling cave fish requilibrates therefore loses the eye in one fell swoop whereas in us daytripping monkeybrains, there are degrees of partial eye loss, presumably the result of random mutations. There are certainly some hairs here to split, but nothing that I’d object to so much if I agreed that the proposed mechanism was plausible. The two strongest objections to your conclusions are: 1. Each of the eye conditions in humans would result in a complete (or near complete) loss of sight anyway 2. I doubt we’ve accumulated as much data on eye pathology in cave fish as we have in humans: there may be some eye variants within the fish population. What’s so damned frustrating here is that there’s no reason we need to guess, really. The facts are eminently knowable. Take the cave fish and it closest sighted relative, sequence (or at least map) genomes and determine whether the transition to eyeless was sloppy (random) or clean (directed). One quickie for you, **Joro**. Do you have a list of traits that are potentially AONE-modifiable? Even if it’s incomplete, please give us some idea of the criteria you use to determine if we’re dealing with a potential AONE modifiable trait. IIRC, you mentioned skin pigmentation, balance, vestibular input (shaking eyes in rats) and some caterpillar thingie (do you know that caterpillars lack the neural structures you suggest maintain the equilibrium in higher animals (no cerebellum, hypothalamus or limbic system, really not much brain at all). ---
**Author:** ![Jois](https://avatars.discourse-cdn.com/v4/letter/j/ea666f/32.png) [@Jois](https://boards.straightdope.com/u/Jois)\ **Post date:** [April 14, 2001, 2:32am UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/12 "2001-04-14T02:32:38Z")
> [@](#): > > \*Originally posted by DrFidelius \* > \*\*It would appear to me that a single mutation which prevents the “coming together” of all the parts of an organ, such as one which stops the production of a regulatory protein needed at a certain stage of development, is more likely to occur and be preserved in the appropriate environment than a mutation “deeper” in the development process. The prevention of the start of development of an organ or a system could have a serious impact on the development of related organs or systems. > > For instance, to prevent an eye from starting to form in a vetebrate would require changing the timing of a number of neurological features. Any fiddling with basic development is likely to produce non-viable organisms. > > If a relatively simple mutation produces the result favourable to survival in a given environment there is no mecahnism known which would remove the more basic genes. They have become invisible to selection. \*\* I’ve tried to follow this thread closely but am getting confused. This litle blurb may fit here: Research News Release: 12 April 2001 Science One gene found to command many others to build a wing Some genes are born to lead. Others, apparently, are born to follow. That scenario, where a single gene orchestrates the construction of a fruit fly wing by commanding a network of many other genes, is described in the Friday, April 13 edition of the journal Science by a team of researchers at the Howard Hughes Medical Institute, University of Wisconsin-Madison. Contact: Terry Devitt trdevitt@facstaff.wisc.edu 608-262-8282 University of Wisconsin-Madison Maybe something like the formation of a wing or an eye would be drawn out to look like a tree and the effect of the mutation would depend on where in the tree the mutation occurred? Jois ---
**Author:** ![jorolat](https://avatars.discourse-cdn.com/v4/letter/j/ed655f/32.png) [@jorolat](https://boards.straightdope.com/u/jorolat)\ **Post date:** [April 14, 2001, 8:29am UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/13 "2001-04-14T08:29:15Z")
> [@](#): > > \*Originally posted by DrFidelius \* > **I am certain if you were to implant lenses into the proto-eyes of a number of blind cave fish, a given percentage of them would fail to develop a full eye due to any one of the “birth defects” you had listed; that percentage being approximately equal to (or slightly higher than) the percentage of these abnormalities which appear in a sighted population. So?** As far as I am yet aware, in those environments where the eye is no longer “selected for”, only vestigial eyes are found - not organisms where any one of the listed defects have spread throughout the population. This indicates the “random mutations” causing degeneration may not be random. > [@](#): > > Also, I am certain that all the “eye support” genes in a population of blind cave fish would exhibit a random genetic drift from the state of the original sighted population. This would be exactly congruent to the selection-neutral drift we see in other sections of “junk” or non-expressed DNA. Again, so? Exploration of “the unknown” often entails a parallel inner exploration. In trying to make sense of new discoveries an ongoing uncertainty owing to “loose ends” is often avoided by giving the loose ends a derisory label. I feel there is a real possibility this is why the stretches of DNA whose function is as yet unknown have been termed “junk”. I would have thought that open mindedness on this point could be easily achieved by removing all the junk DNA from a genome. If viable organisms aren’t produced then the unknown stretches can not be “junk”. I wouldn’t be surprised to find what is perceived to be “a random genetic drift” but would like to make the general observation that it’s possible to become intrigued by the patterns found in a kaleidoscope without ever being aware of the (fewer) coloured pieces of glass that have generated them. > [@](#): > > Sounds like you have the makings of two doctoral dissertations here. Do you need help applying for grant money? I am sure the results would be interesting. \*\* Both are intriguing. I’m just exploring how relevant vestigial organs may be to an interest I have and don’t intend delving into them any more than is necessary. Jorolat ---
**Author:** ![jorolat](https://avatars.discourse-cdn.com/v4/letter/j/ed655f/32.png) [@jorolat](https://boards.straightdope.com/u/jorolat)\ **Post date:** [April 14, 2001, 10:05am UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/14 "2001-04-14T10:05:34Z")
> [@](#): > > \*Originally posted by choosybeggar \* > > > [@](#): > > > > _Originally posted by Jorolat_ > > \*\*This appears to be identical with what happens in the mole, ie vestigial organs appear to be have been “selected for” as a unit with degeneration beginning from the “top down”. > > > > Could there be another mechanism at work here? after all, if random mutations were responsible, then why don’t they affect other genes within (for these examples) the eye?. \*\* > > I believe there are three factors to consider here: > > 1. Mutations occur at a very low frequency. Therefore one wouldn’t be surprised to find a lack of multiple fatal hits in the group of genes essential for the development of a single organ. The point I’m making is that the fatal hits always seem to be hitting the organ as a whole and not substructures within it. > [@](#): > > 1. Most mutations are neutral etc., etc… And are supposed to be random. > [@](#): > > I find it interesting, in light of your obliviousness to phenotypically silent changes in DNA, that you are a psychologist by trade. A ways back, didn’t the strict behaviorists have their way when they asserted that the study of internal states of the mind was fruitless due to the(necessarily) subjective nature of this line of inquiry? I have found these posts very useful, and because I wouldn’t like any future correspondence to be coloured by misconceptions and/or assumptions, I would like to point out I said (in another thread) that my interest in evolution began through “anomalies” found in psychology but not that I was a psychologist. Nor did I give any indication of the source of the anomalies (and nor are they relevant to this thread). However “subjectivity” can certainly be a problem. A few years ago, for example, a woman in her mid twenties was admitted to hospital, diagnosed with a “severe” mental illness, and at one point expected to spend the rest of her life in a vegetative state - completely unaware of the passage of time. The _reality_, on the other hand, was that she didn’t have a mental illness but had been subjected to non-stop psychological violence throughout her life. If any mistake had been made in immediately identifying the psychic structures that surfaced as the harm was reversed then she might well still be there rather than having returned to society where she has since married, borne children, etc… There was no room for theory, attitude, or opinion, and I do hope your reference to behaviorists doesn’t mean you are projecting your perception of them onto me. > [@](#): > > We in genetics are not similarly handicapped. I would like to think I’m not either 🙂 > [@](#): > > …I find such methodologies to be very elegant and think you would too if you deepened your understanding of modern genetics. Well it does need deepening but I don’t want to lose sight of the wood because of all the trees and this thread is about vestigial _organs_. This doesn’t mean that I’m conviently dismissing all that you have said about silent mutations etc (and about which I have a passing familiarity) just that it should apply to all genes _equally_: “To destroy an eye, you just need 1 critical base substitution (mutation) in one critical gene.” To destroy a substructure within an eye should require no more. > [@](#): > > Hopefully, **Joro** , at least you’ll be satisfied that conventional genetics can explain the origin of vestigial organs quite neatly. At the moment I don’t think it does though I do appreciate this correspondence. Jorolat ---
**Author:** ![jorolat](https://avatars.discourse-cdn.com/v4/letter/j/ed655f/32.png) [@jorolat](https://boards.straightdope.com/u/jorolat)\ **Post date:** [April 14, 2001, 11:29am UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/15 "2001-04-14T11:29:33Z")
> [@](#): > > \*Originally posted by choosybeggar \* > \*\* > > > [@](#): > > > > \*Originally posted by jorolat \* > > Human beings can have, as examples, the following eye defects at birth: > > > > Anophthalmos (absence of eyes} > > Congenital cataract (eye cataracts at birth) > > Coloboma of eye (eye parts missing) > > Aniridia (absence of the iris) > > > > (taken from: “BIRTH DEFECTS --PART 1”) > > > > If the start of degeneration in a vestigial eye was due to randon mutation(s) then surely, in those environments where the eye is no longer “selected for”, similar birth defects to the above should be occurring on an equal frequency to that of the whole eye?. > > \*\* > > Wow, I get your point:) The notion here is that the dark-dwelling cave fish requilibrates therefore loses the eye in one fell swoop whereas in us daytripping monkeybrains, there are degrees of partial eye loss, presumably the result of random mutations.\*\* (very funny! :)) In those environments where the eye isn’t selected for then partial eye defects should spread throughout the population as often as the “complete” vestigial eye does. > [@](#): > > The two strongest objections to your conclusions are: > > 1. Each of the eye conditions in humans would result in a complete (or near complete) loss of sight anyway > 2. I doubt we’ve accumulated as much data on eye pathology in cave fish as we have in humans: there may be some eye variants within the fish population. In answer to 1) : That’s not the point (see comment above) In answer to 2) : If a partial eye defect had spread throughout a population where the eye was no longer being selected for then I am sure it would have raised eyebrows. If such a phenomena has been reported then I haven’t heard about it or been unable to locate it so far (anyone want to show off their expertise on search engines? no? ok, ‘sigh’…) > [@](#): > > What’s so damned frustrating here is that there’s no reason we need to guess, really. The facts are eminently knowable. I think there’s a possibility that a “the sun rises in the east, sets in the west, therefore it revolves around the earth” kind of logic being applied to vestigial organs. > [@](#): > > Take the cave fish and it closest sighted relative, sequence (or at least map) genomes and determine whether the transition to eyeless was sloppy (random) or clean (directed). It would be interesting to see the results of such an exercise. I don’t think anyone is looking for a directed transition (and certainly not me) though on the other hand data can often be interpreted in a number of ways. Generally in the articles I’ve read it has either been stated, or implicitly inferred, that there has been a _progressive_ loss of functionality in the **whole** organ. > [@](#): > > One quickie for you, **Joro**. Do you have a list of traits that are potentially AONE-modifiable? Even if it’s incomplete, please give us some idea of the criteria you use to determine if we’re dealing with a potential AONE modifiable trait. If you are _really_ interested I would have thought that the web site would tell you that. > [@](#): > > (shaking eyes in rats) and some caterpillar thingie (do you know that caterpillars lack the neural structures you suggest maintain the equilibrium in higher animals (no cerebellum, hypothalamus or limbic system, really not much brain at all). \*\* I can see evidence for it in bacteria yet alone caterpillars. Jorolat ---
**Author:** ![jorolat](https://avatars.discourse-cdn.com/v4/letter/j/ed655f/32.png) [@jorolat](https://boards.straightdope.com/u/jorolat)\ **Post date:** [April 14, 2001, 2:19pm UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/16 "2001-04-14T14:19:43Z")
> [@](#): > > \*Originally posted by Jois \* > \*\*I’ve tried to follow this thread closely but am getting confused. This litle blurb may fit here: > > Research News Release: 12 April 2001 > Science > One gene found to command many others to build a wing > Some genes are born to lead. Others, apparently, are born to follow. That scenario, where a single gene orchestrates the construction of a fruit fly wing by commanding a network of many other genes, is described in the Friday, April 13 edition of the journal Science by a team of researchers at the Howard Hughes Medical Institute, University of Wisconsin-Madison. > > Contact: Terry Devitt > trdevitt@facstaff.wisc.edu > 608-262-8282 > University of Wisconsin-Madison > > Maybe something like the formation of a wing or an eye would be drawn out to look like a tree and the effect of the mutation would depend on where in the tree the mutation occurred? > > Jois \*\* Hi Jois, **Pleiotropic** genes (genes affecting more than one trait) are indicative of the internal _integration_ of an organism, a fact reinforced by the recent announcement of the number of genes found in the human genome (approx 30k). The following extracts from another recent press release ([**full article**](http://www.eurekalert.org/releases/ucsb-awi033001.html)) are also relevant: > [@](#): > > **A worm is more like a human than previously thought** > > "Rothman’s lab studies the nematode worm known as C. elegans… > > …In the C. elegans embryo, when there are only four cells, a single cell is selected to produce mesoderm and endoderm organs. “Despite the enormous differences, remarkably, it appears that the same genes operate at that stage to control that selection in both the worm and vertebrate animals,” said Rothman. > > This implies that the common ancestor from many hundreds of millions of years ago, shared by both humans and worms, used the same early regulatory machinery. The invention of groups or layers of cells that could ultimately produce heart, lungs and **other key organs** (my emphasis) which allow humans to thrive as large animals, evolved from a single event during which this regulatory switch was invented… Very interesting! 🙂 Jorolat ---
**Author:** ![choosybeggar](https://avatars.discourse-cdn.com/v4/letter/c/8c91f0/32.png) [@choosybeggar](https://boards.straightdope.com/u/choosybeggar)\ **Post date:** [April 14, 2001, 3:06pm UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/17 "2001-04-14T15:06:19Z")
> [@](#): > > **CB:** “To destroy an eye, you just need 1 critical base substitution (mutation) in one critical gene.” > > **J:** To destroy a substructure within an eye should require no more. > > **CB:** Hopefully, **Joro** , at least you’ll be satisfied that conventional genetics can explain the origin of vestigial organs quite neatly. > > **J:** At the moment I don’t think it does though I do appreciate this correspondence. The abstract below was referenced in the [Science article about lens transplantation:](http://www.sciencemag.org/cgi/content/full/289/5479/631?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=cave+fish&searchid=QID_NOT_SET&stored_search=&FIRSTINDEX=&fdate=10/1/1995&tdate=4/30/2001) > [@](#): > > Evolution of eye regression in the cavefish Astyanax: Apoptosis and the Pax-6 gene > Jeffery, WR;Martasian, DP > AMERICAN ZOOLOGIST > 38: (4) 685-696 SEP 1998 > > Document type: Article Language: English > > Abstract: > The eye is an extraordinary organ in terms of its development and evolution. In cave animals, the eye is sometimes reduced or eliminated as a consequence of adaptation to life in perpetual darkness. We have used the characid teleost Astyanax mexicanus as a model system to investigate the mechanisms of eye degeneration during the evolution of a cave vertebrate. Eyed surface populations of Astyanax entered caves during the Pleistocene, and their descendants lost their eyes and pigmentation. **Astyanax populations exhibiting various degrees of eye regression have been reported in 29 Mexican caves,** Surface populations with characteristics of the ancestral stock still exist in the vicinity of these caves. Thus, Astyanax represents one of the few instances in which the ancestral (surface fish) and the derived (cavefish) developmental modes are extant and available far comparative studies. The cavefish embryo develops an optic primordium consisting of a lens vesicle and optic cup but the rudimentary eye arrests in development and degenerates, Here we report that eye degeneration is accompanied by extensive apoptosis and downregulation of the Pax-6 gene in the developing lens. The results suggest that alterations in lens development are important factors in eye regression during cavefish evolution. > Addresses: > Jeffery WR, Penn State Univ, Dept Biol, 208 Mueller Lab, University Pk, PA 16802 USA. > Penn State Univ, Dept Biol, University Pk, PA 16802 USA. Bolding mine. Apparently there is diversity in the eye lesions of the cave fish and the Science article chose one variant to investigate. ---
**Author:** ![JDM](https://avatars.discourse-cdn.com/v4/letter/j/90db22/32.png) [@JDM](https://boards.straightdope.com/u/JDM)\ **Post date:** [April 14, 2001, 8:15pm UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/18 "2001-04-14T20:15:36Z")
I’m doing this from memory from a SJG book that I read 3 or 4 years ago. I don’t remember which one (maybe Eight Little Piggies?)- I got them all out of the library and read them one after the other. The thing with the mole rat is this, IIRC. On a molecular level, based on a scientist’s work whose name I don’t remember, changes in genetic material are “random, i.e. neutral.” This gave the ability to predict the degree of variation in the genetic material in one part of the mole rat’s eye, based upon no selection pressure. What was found was less variation than predicted. HOWEVER- it was also found that the mole rat retained a degree of photosensitivity, in spite of being “blind:,” its cycles of “winterization” were controlled only by amouny of daylight, and not at all by temperature. To survive, therefore, it needed something of its eye left (easier to use existing structures than create new ones, even if for a different purpose [Are you listening, Mr. Behe?]), but the remainder could vary neutrally. Thus the selection pressure controlled the degree of variation. I haven’t explained this all that clearly, perhaps, (it’s late) but when I read this I thought “Why wasn’t this on the front page of the Times?” Correlation does not prove causation, but a cheap-and-dirty way of demonstrating causation can be to vary one or the other of the correlated items. If varying the one changes the other by a similar ratio, then you’re a big step closer to proving causation. AFAIAC, this particular study proved Natural Selection. Sorry I can’t give cites-I did a search on Google for “gould mole rat eyes” and came up with one hit that I couldn’t get to (linked from World-of-Dawkins) that may have been to the paper Gould’s article discussed. It may be possible for someone in the USA to get it. JDM ---
**Author:** ![jorolat](https://avatars.discourse-cdn.com/v4/letter/j/ed655f/32.png) [@jorolat](https://boards.straightdope.com/u/jorolat)\ **Post date:** [April 15, 2001, 5:10pm UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/19 "2001-04-15T17:10:10Z")
> [@](#): > > \*Originally posted by choosybeggar \* > The abstract below was referenced in the [Science article about lens transplantation:](http://www.sciencemag.org/cgi/content/full/289/5479/631?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=&fulltext=cave+fish&searchid=QID_NOT_SET&stored_search=&FIRSTINDEX=&fdate=10/1/1995&tdate=4/30/2001) > > > [@](#): > > > > Evolution of eye regression in the cavefish Astyanax: Apoptosis and the Pax-6 gene > > Jeffery, WR;Martasian, DP > > AMERICAN ZOOLOGIST > > 38: (4) 685-696 SEP 1998 > > > > Document type: Article Language: English > > > > Abstract: > > {snip) > > **Astyanax populations exhibiting various degrees of eye regression have been reported in 29 Mexican caves** > > (snip) > > Bolding mine. Apparently there is diversity in the eye lesions of the cave fish and the Science article chose one variant to investigate. Hi ChoosyBeggar, I think it may be unintentionally misleading to speak of _diversity_ in the eye lesions and that the highlighted “degrees of regression” in your post gives a more accurate perspective. There are more detailed descriptions available but the following quote ([**Astyanax mexicanus**](http://www.lifesci.utexas.edu/courses/zoo334c/projects/1998/Chris_Elmore/Astyanax_mexicanus.html)) gives a simple overview: > [@](#): > > The eyes of these fish have a diameter that varies between 10-20% that of epigean fish (Peters and Peters, 1966). The development of the structures within the eyes is more complex in larger eyes and more rudimentary in the smaller That is not to say that there aren’t _differences_ from the “lens downwards” (so to speak) but I only have partial access to Science Online and haven’t read the full article. What Jeffrey says in the following (**[The Jeffrey Lab On The Web](http://www.life.umd.edu/labs/jeffery/index1.html)**), however, only seems to _decrease_ the possibility of random mutations being responsible for these specific instances of vestigial organs: > [@](#): > > Current studies include the molecular regulation of lens apoptosis and the antagonism between the pax6, pax2, and midline signaling genes, which appears to be responsible for the regression of eye development in cave fish. We are also studying the evolution of eye regression in different cave fish populations, **which appear to have evolved independently** (my emphasis). In these studies, we seek to understand whether parallel evolution has occurred by the same or different mechanisms. On his experiment where he transplanted a lens into a blind cavefish Jeffrey commented ([**EyeNet**](http://www.aao.org/eyenet_mag/10_00/news.html)): > [@](#): > > “I was surprised by the fact that the cave fish, despite lacking eyes as adults, retained the capacity to respond to signals generated by the lens,” said William R. Jeffery, PhD, of the study he co-authored. “Presumably, the cave fish has not received such signals since it lost its eyes, probably in late Pleistocene times.” > > Dr. Jeffery suggested that fibroblast growth factors and insulin-related growth factors are two possible candidates for the **chemical signals** (my emphasis) that triggered eye formation in the blind fish. I find it astonishing, as only a single example, that “random mutations” could give rise to the removal of the _precise_ chemical signals that will affect eye development and in that _specific_ environment! Unfortunately info on the web is seldom available in the exact form wanted but the pax genes do appear to play a leading role. The next quote ([**Isolation and developmental expression of the amphioxus Pax-6 gene (AmphiPax-6)**](http://www.biologists.com/Development/125/14/dev2286.html)) isn’t the most appropriate for cavefish but has been included to give an added evolutionary context: > [@](#): > > Pax-6 genes have been identified from a broad range of invertebrate and vertebrate animals and shown to be always involved in early eye development. Therefore, it has been proposed that the various types of eyes evolved from a single eye prototype, by a Pax-6-dependent mechanism. Here we describe the characterization of a cephalochordate (_thought to be the closest living invertebrate relatives of the vertebrates_) Pax-6 gene. > > Expression of AmphiPax-6…is also detectable in Hatschek’s left diverticulum as it forms the preoral ciliated pit, part of which gives rise to the homolog of the vertebrate anterior **pituitary** (my emphasis)… > > This zone includes cells that will differentiate into the lamellar body, a presumed homolog of the vertebrate **pineal eye** (my emphasis). The fact that cavefish aren’t truly blind ([**BLIND MEXICAN CAVE FISH (ASTYANAX HUBBSI) RESPOND TO MOVING VISUAL STIMULI**](http://www.biologists.com/serve.cgi?JEB/188/01/jeb9009.pdf) nb PDF file) is also interesting: > [@](#): > > In blind cave fish, as in other fish, extra-ocular photoreceptors have been located in the pineal organ (Herwig, 1976). Extra-pineal photoreceptors have not been identified in blind cave fish yet, but their presence and location can be inferred from studies in other fish Blind cavefish often exhibit other changes (eg loss of pigmentation, etc.) but not always as expected ([**University of Hamburg**](http://www.rrz.uni-hamburg.de/biologie/zim/eng/pathoe.htm)): > [@](#): > > We are presently analyzing the structure and function of the pineal organ in cave fish, which is a basic component of the inner clock. Although **we expected a regression** (my emphasis) of this organ in cave animals living in an almost non-rhythmic environment, we found a persisting light sensitivity and a rhythmic synthesis of melatonin in the cave fish pineal organ Jorolat ---
**Author:** ![choosybeggar](https://avatars.discourse-cdn.com/v4/letter/c/8c91f0/32.png) [@choosybeggar](https://boards.straightdope.com/u/choosybeggar)\ **Post date:** [April 16, 2001, 12:01am UTC](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796/20 "2001-04-16T00:01:34Z")
**joro** Check out [this page](http://www.life.umd.edu/labs/jeffery/genetics.html) on the [Jeffrey Lab Home page](http://www.life.umd.edu/labs/jeffery/index1.html). It demonstrates their results from breeding cavefish. > [@](#): > > Genetic crosses of cavefish and surface fish yield F1 progeny with uniformly small eyes and pigmentation. Backcrosses of the F1 progeny to the cavefish parent yield fish with eyes ranging from completely regressed to the small eyes characteristic of the F1s. This result shows that **multiple genes** are involved in eye regression. Pigmentation segregates independently of eye formation. Bolding mine. So no matter what, we’re talking about multiple genes. To me that vastly decreases the likelihood that independently evolved lines of cavefish will have lost their eyes by the same mechanisms. I’ll dig more, be back later. I’ll also address the rest of your post then. (BTW what in the hell do the last three cites of your last post have to do with the OP?) [Next page](https://boards.straightdope.com/t/are-vestigial-organs-the-result-of-random-mutations/61796.md?page=2)