The following developed out of “Lamarck’s Law of Use and Disuse” 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”) which begins:
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?
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.
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.
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.”
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)
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?.
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.
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.”
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?
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.
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
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.
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]?
I believe there are three factors to consider here:
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.
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)
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.
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”.
There have been no replies to my last posts in the other thread so I guess people have lost interest
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 says:
Interestingly another source (taken from Investigative Ophthalmology and Visual Science, April, 1999 and available here says:
The unknown genes give me the impression they achieve equilibrium between the “component parts”. (also: embryology - wassat?
The Cave Fish Grow Eyes article indicates how much is dependent on the lens but your answer doesn’t address the point made in the first reply to DrFidelius:
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.
The Cave Fish Grow Eyes article indicates how much is dependent on the lens but your answer doesn’t address the point made in the first reply to DrFidelius:
**
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:
Each of the eye conditions in humans would result in a complete (or near complete) loss of sight anyway
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).
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?
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.
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.
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.
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.
And are supposed to be random.
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.
I would like to think I’m not either
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.
At the moment I don’t think it does though I do appreciate this correspondence.
(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.
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’…)
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.
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.
If you are really interested I would have thought that the web site would tell you that.
I can see evidence for it in bacteria yet alone caterpillars.
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) are also relevant:
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
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) gives a simple overview:
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), however, only seems to decrease the possibility of random mutations being responsible for these specific instances of vestigial organs:
On his experiment where he transplanted a lens into a blind cavefish Jeffrey commented (EyeNet):
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)) isn’t the most appropriate for cavefish but has been included to give an added evolutionary context:
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?)
) to silent mutations.