Lamarck's Law of Use and Disuse

Great Debates
1

Can anyone help with a couple of questions concerning the following ?(taken from http://www.ucmp.berkeley.edu/history/lamarck.html):

**"…“Lamarckism” or “Lamarckianism” is now often used in a rather derogatory sense to refer to the theory that acquired traits can be inherited. What Lamarck actually believed was more complex: organisms are not passively altered by their environment, as his colleague Geoffroy Saint-Hilaire thought. Instead, a change in the environment causes changes in the needs of organisms living in that environment, which in turn causes changes in their behavior. Altered behavior leads to greater or lesser use of a given structure or organ…

…It is even more interesting to note that, although Darwin tried to refute the Lamarckian mechanism of inheritance, he later admitted that the heritable effects of use and disuse might be important in evolution. In the Origin of Species he wrote that the vestigial eyes of moles and of cave-dwelling animals are “probably due to gradual reduction from disuse, but aided perhaps by natural selection.” Lamarckian inheritance, at least in the sense Lamarck intended, is in conflict with the findings of genetics and has now been largely abandoned …**

What I would like to know is:

  1. How does current theory account for vestigial organs?.

  2. How is Lamarckian inheritance in conflict with the findings of genetics?

Jorolat

2

Question 1: Do you mean why according to Darwinian theory, are unselected traits slowly lost in a population?

Question 2: A major conflict between Lamarkianism and genetics is that Lamarkianism implies a bidirectional flow of information with respect to the genome.

While we understand how information encoded by the genome becomes a phenotypic trait, there exists no known mechanism for the “reverse translation” of a trait into a DNA coding sequence.

Consider the complexity of the mechanisms which translate the genome into proteins (which ultimately dictate what a cell is, and what we are). Then consider that to inherit an acquired trait, we need a distinct set of machinery to detect the trait and encode it for packaging into the genome. I’ve never seen such a mechanism formulated by a Lamarkianist.

Also, if such “back translation” commonly took place, you’d have to explain how information that is lost during the DNA-protein transition, is re-created during “reverse translation.” The lost information is due to the degenerate coding of amino acids by DNA. For example, the amino acid proline can be encoded any one of four codons CCT,CCC,CCA or CCG). Back translating a proline residue into DNA should produce a pattern of inheritence of this codon that doesn’t conserve the third base. However, such inheritence patterns are not observed.

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Hi Choosybeggar,

Thank you for replying.

In question 1 I was specifically asking about organs rather than traits.

My understanding of Lamarckianism is also that “it implies a bi-directional flow, etc., etc…”.

The Weismann Barrier says that there is no way information “learned” by somatic cells cannot be transmitted to germ cells.

What I find interesting about this statement is that it appears to presume a one to one correspondence between somatic and germ cells whereas, in fact, somatic cells are only part of an integrated organism. Any “feedback” is likely to be, therefore, indirect - a la “The Baldwin Effect”.

Thank you again for such an informative post.

Jorolat

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As for vestigial organs: OK, first you have a functioning organ evolve, for whatever reason… Let’s use eyes as an example. For an above-ground, diurnal creature, eyes are a big advantage. Now, a population of such creatures moves into caves, and never sees light. Eyes are now not doing them any good. Now, the issue is complexity: Any added structure, whatsoever, will have a slight disadvantage to an organism, because that’s one more thing that has to develop and be maintained. Usually, this is more than offset by the advantages the structure confers, but sometimes not. Now, let’s look at two populations of, say, scorpions, one above ground, and the other in caves. When, by chance, an above-ground scorpion is hatched without functioning eyes, it’s pretty much a goner. When a cave scorpion is born blind, however, it suffers no particular disadvantage, and may even get some advantages. Maybe it’s blind because its exoskeleton grew over where its eyes should be. OK, now it doesn’t have a weak spot in its exoskeleton, now. Maybe scorpions occasionally get eye cancer, and this one won’t, now. Maybe there’s absolutely no advantage or disadvantage, this time.

The other big factor here is that it’s a lot easier to lose sight than it is to gain it. There’s plenty of things which need to work just right, and if any of them fails, the whole system fails.

5

**

Huh?

Joro, before I spend a great deal of my time on this, what’s your level of understanding of modern genetics? How much formal training have you had?

Also, can you provide a 1 paragraph summary of the Baldwin effect? I know there’s a link in your sig, but if you post the idea here, more people will actually see it.

CB

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[QUOTE]
*Originally posted by jorolat *
**

This should read: The Weismann Barrier says that there is no way information “learned” by somatic cells can be transmitted to germ cells.

Jorolat (red faced)

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Chronos:

I had a lengthy dscussion fprecsely this topic with a friend (who’s in English Lit, no less). The first explanation that came to my mind was the first one - how there might be evolutionary disadvantages to having eyes in a cave. But I didn’t buy it. It seemed extremely unlikely that there would be a significant enough disadvantage to justify the state of NOT having eyes being more successful in breeding and surviving. Things like infection via the eye, or “eye cancer” just don’t seem commn enoiugh to make a difference. My friend pointed out the more likely mechanism, which is the second one that you throw out so cavalierly. Eyes are complex structures. If mutations cause eyes that DON’T work to pop up in your theoretical cave scorpion, it makes no difference. That scorpion survives as well as the sighted one, and will pass on its non-seeing genes to future generations. (Whereas in the well-lit world outside such a mutation would not see danger, and would quickly be picked off.)Since the nonseeing scorpions breed as well as the seeing ones, their genes spread. Since the eye is, as you point out, a complex structure, any of a number o mutations wil keep the scorpions sightless, and eventually they’ll probably combine.

It sometimes seems as if “Use it or Lose it!” is an evolutionary rule, but it isn’t. The rules of natural selection are that 1.) occasional mutations occur, 2.) Mutations which can successfully exploit a niche survive, 3.) Mutations which are more successful at breeding survive. What’s surprising is how such rules as "Use it or Lose it seem to come out of the above. They do so in this case because we’ve asked the question incrrectly. It’s not “Why do ceatures that live in the dark lose their eyes?”, but should really be “Under what circumstances do creatures retain the power of vision?” It’s a humbling thought that the capabilities of creatures – sight, smell, hearing, speed, strength, even probably intelligence – are all somewhat “unstable” characteristics that can easily be lost when the conditions requiring their maintenance disappear.

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Hi Chronos,

Your comments have certainly given food for thought. I remember reading a book about moles that said the whole eye developes normally in the mole foetus until a certain stage is reached and then it stops. I’m sort of just thinking aloud but I was wondering if this were true of all vestigial organs.

Furthermore, if the original cause of the degenerative process beginning was a random mutation, ought we not to expect organisms with more deformed organs, rather than vestigial, to exist in environments where such organs no longer conferred any “selective advantage”? (er, I hope I’m using the phrase correctly!).

Jorolat

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Hi Choosybeggar,

Um, sorry about the mistake re the Weismann Barrier!

I haven’t had any formal training in modern genetics but do feel I understand those (limited) areas I’ve looked at that are more directly relevant to my area of interest.

I hope this answer doesn’t deter you though I would not expect you to waste your time. If you could give a brief indication of what it is that you might want to say then either I could do the necessary background reading (if this is a feasible possibility of course) or perhaps you could give some pointers of where to look.

This quote is taken from http://members.aol.com/jorolat/baldwin2.html:

**…“The Baldwin Effect”, as Organic Selection is now more commonly known, says that the phenotypic plasticity of an organism enables it to learn and that over succeeding generations a learned behaviour may become instinctive (i.e. hereditary: phenotypic plasticity becomes phenotypic rigidity). It is not restricted to learning in the obvious sense however; the Baldwin Effect also applies, as examples, to the abilities to tan and to form calluses…
**

Typing “Baldwin Effect” into a search engine will, of course, produce many more web articles.

Jorolat

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One more question. Are traits transmitted genetically (ie encoded by DNA in a germ cell) in this model or is some other mechanism hypohesized to do the work?

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Joro,
I read some of your web page stuff re:the Baldwin Effect. Here are what I find to be the major problems:

  1. From what I know about retrotransposons, they will not do the job for you. They are mobile genomic elements, and they can take adjacent sequences with them. Mobile, here, is used as a relative term. As in mobile compared to the rest of the genome which never gets off it’s fat, lazy ass to go anywhere. This article describes the properties of a type of retrotransposon (LINE-1) that comprises 15% of the mammalian genome. This one discusses how retrotransposons can introduce genetic variation. My sense is that these guys move very slowly. That like any other mutagenic process, the majority of hits are deleterious and that no mechanism has been postulated whereby mutations can be targetted.

  2. I have difficulty understanding the directedness of the potential examples of the Baldwin effect in action that you list. For example, the rats on the turntable. Lets say I believe that the AONE detects a disequilibrium, and that the necessary neural pathways exist to direct the germ cells to mutate DNA. What I don’t understand is how the AONE knows what to change? The fact that the next generation had wobbly heads implies that the AONE knew exactly what region of the genome controls such behavior (and BTW, we assume that there is a gene or set of genes that if mutated would get the job done in the absence of other deleterious effects).

Evolution, on the other hand, requires no such self-awareness at the genome level. We like evolution so much because (a) it explains well the forms we observe and (b) it is simple; random mutation coupled with selection.

Also, I don’t think the Cairns article is that relevant to your cause. While it is interesting that stressed bacteria know (roughly) what regions of their genome when randomly mutated will tend to produce more fit individauls, this is a far cry from what you (or Baldwin) propose.

There’s another great example of directed mutation in eukaryotic biology that you may be interested in. This is in my own field of B cell immunology. B cells (the antibody producing cells) mutate the antibody encoding genes they carry. The region of the genome that is mutated if quite well confined to the immunoglobulin variable region genes (the genes that encode the antigen-binding part of the antibody) You could argue that the B cell knows it should mutate this region. In a sense that is true. But the mutations introduced are random and more often than not generate garbage (frameshifts, stop codons, antibodies which lose binding to antigen, autoantibodies) but very rarely, they generate an antibody that binds better to an antigen than the parental immunoglobulin. These rare clones are selectively expanded on the basis of their affinity for antigen and grow to comprise what is termed the memory immune response (ie. you react better and faster the second time you’re exposed to an antigen).

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Hi Choosybeggar,

I’ve probably said it before but from an overall perspective it doesn’t matter whether retrotransposons (rtps) do the job or not because the proposed mechanism can be tested without knowing how it is internally achieved.

All that is needed is knowing how to disturb equilibrium to a degree (and no more, mutilations are “non-sensical”) that will induce a genetic change within a predictable range.

Should the mechanism exist it would make sense that any associated structures would be most evident in the more “evolved” organisms. Conceptually three major elements are required:

  1. A means of continously integrating about a mean somewhere within the AONE (eg three layered structures).

  2. Signalling pathways from the AONE into the nucleii of germ cells.

  3. Molecular mechanisms within those nucleii.

Examples of all of the above are known to exist though I’m not really in a position to suggest which of them may or may not be part of the proposed mechanism.

The two links you gave were too technical for me to feel sure I understood them correctly; a more “digestible” article (from my perspective) can be found here:

http://unisci.com/archives/19991/0305993.htm

Another article (which I’ve mislaid) gave two characteristics of the rtps being described that I found especially interesting:

  1. They are either only active, or mostly active, in germ cells.

  2. The activity of vertically transmitted rtps “dies away” over succeeding generations.

The rat is a fait accompli whereby equilibrium has been maintained throughout its evolutionary history.

The AONE of the rat and that of its germ cells are obviously seperate. When the thresholds of the rat AONE are exceeded/not met then the area of the upset could conceivably be transmitted to the germ cell AONE by chemical messenger.

Upsetting the germ cell AONE would trigger “molecular mechanisms” in an attempt to restore equilibrium which could take a “number” of generations to achieve. No awareness of gene function is involved, just restoration of equilibrium.

The AONE would appear to always operate “top down” on the genome. An example of this could be the eye of the mole whose function has degenerated. During development of the foetus, however, the eye developes normally until a certain stage is reached and then it stops.

This could reflect the current boundary between when the eye once developed to completion and the subsequent action of the AONE. I’m wondering if this may be true of all vestigial organs - the AONE is ideally located to discriminate at the organ level.

It’s another area worth looking at, and like any of the others, it may not pan out.

There is lots of stuff still to be written up and the next logical step would be to do a comparison of how the proposed mechanism operates at the two extremes given on the web site.

The Baldwin Effect is a two stage process and it is only the second stage that involves the mechanism. I don’t have the notes to hand but there are at least five major points where operation of the mechanism is more or less identical.

Generally I’m still trying to put an overall framework on the web site within which I can work but the example you gave in B cell immunology is very interesting.

I should have time in a day or two to see what I can find on the web so maybe I can come back to you on that a bit later. Is it related to the ground covered by “Lamarck’s Signature”? (which is on my “beg, steal, or borrow” list). If it isn’t related I would still be interested to hear your opinion of the book anyway (or what you might have heard about it).

You might think the idea of an internal mechanism is crazy and that I should be locked up for my own good but I find these discussions very useful! :slight_smile:

Jorolat

Model of an Internal Evolutionary Mechanism (based on an extension to homeostasis) linking Stationary Phase Mutations to The Baldwin Effect:
http://www.geocities.com/jorolat/index.html

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**

Agreed, although a mechanism makes otherwise tenuous phenomenological data more palatable.

I’d have to see an awful lot of data to believe any one of the above three are true. Why not lay it all on the line and post your magnum opus in GD?

**

I think it’s unlikely that you or your AONE will cause your person any harm.

I’d still like to know if you believe that the AONE needs to be “informed” about the function of the genes it is mutating. This seems to me to be implicit in the mechanism you propose. I don’t know if you realize how much of a hard sell a genetically informed AONE is. Think along the lines of coercing me to swallow the rotting corpse of a burning porcupine to get an idea.:slight_smile:

14

The translucent body of an Ozark cave fish. (www.agfc.state.ar.us)
**W A S H I N G T O N, July 28 — 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.

Apparently, the lens seemed to send out signals that instructed the eyes in the blind cave fish to grow — a finding that sheds light on how eyes evolve and develop the researchers said. ** Rueters
How about the lens sending out signals instructing the eyes? Isn’t that info back to the DNA?

Jois

15

There is transmission of information back to the genome (DNA) all the time. Every one of your cells contains all of the genes necessary to make every protein in your body, but not all of them are active all the time. There is an extensive amount of signaling to achieve the activation and suppression of certain genes in certain cells. That’s why your heart doesn’t grow hair and your toes isn’t growing lungs: those genes aren’t turned on in those organs.

When an organism (such as our cave critter) loses functionality of such complicated structures as it’s eyes, it doesn’t lose all of the many hundreds of genes at once; rather only a few or a single gene becomes non-functional (through mutations that are no longer selected against in this particular environment): say, perhaps, a gene that makes a functional lens. If we come along and surgically insert a lens into one of these critters, many of the remaining eye-genes could very well still be there, patiently waiting for signals to turn on. Our new lens will cause signal proteins to activate certain regions of DNA: the old machinery will fire up again, and soon we’ll be crankin’ out all the old eye proteins. But note that the genes for these proteins were already in the genome; no changes to the DNA were made; pieces that were already there are merely switched on or off. What these researchers did was basically show that these historical genes are still present (albeit not functioning).

What is being discussed in this thread, however, is equivalent to an external stimulus causing an undetermined internal mechanism to decide things would work better if it took its molecular screwdriver and started tinkering around with bits of DNA that then get passed on to the organisms descendents. This seems unlikely, as such a mechanism would nearly have to be sentient: choosing this base to change so that that amino acid was substituted and the subsequent protein folded into this new (and better functioning) shape. So far, I’ve seen no way that this could be accomplished.

-b

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Thank you, Bryan, very neatly done!

Jois

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[QUOTE]
*Originally posted by choosybeggar *

  1. The Cerebellum could easily be associated with the mechanism.

It “controls the movements involved in the swimming of a fish, the flying of a bird and playing a musical instrument or driving a car. Once learned, complex movements such as are involved in signing our name, picking up a glass, walking, even talking, seem to be ‘programmed’ into the cerebellum, so that we can do them ‘automatically’” (Psychology, Richard D. Gross)

“The cerebellum also synthesizes all (my italics) sensory information from vision, inner ear, muscles and joints , etc., etc…” (ibid).

The relevance of the above to the Baldwin Effect is obvious. Additionally:

“Its grey matter in fact consists of three layers of cells, the middle layer of which, the purkinje cells, can link each synapse with up to 100,000 other neurons, more than any other kind of brain cell (my italics)” (same source - used cos its close to hand).

  1. Owing to a system crash I have lost my original notes when I looked at this area last year. The following extract is relevant though:

“The gonadotropin releasing hormone (GnRH) released by the hypothalamus stimulates the secretion of follicule stimulating hormone (FSH) and luteinizing hormones (LH) from the gonadotroph cells of the anterior pituitary (1-3). Receptors for FSH and LH are present on somatic Leydig and Sertoli cells, respectively, which have the function of transmitting the hormonal stimulus to the germ cells (4, 5).” (http://bioscience.org/1996/v1/d/nantel1/htmls/3.htm)

In addition, one researcher commented “there is much that is still unknown” which means there is still much to be discovered.

  1. I would again suggest the possibility of retrotransposons playing a role.

There is almost certainly a lot more relevant to all of the above that I haven’t come across yet.

There isn’t any awareness of gene functionality at all in the same way that bacteria aren’t aware of gene functionality when they replicate.

The proposed mechanism is all about maintaining equilibrium.

Regarding posting my magnum opus here: I had an original structure that I’ve been working to that is still incomplete.

In addition there are a number of areas whose potential I haven’t finished evaluating. For example, I wrote the original post in this thread with only a vague sense that “there might be something here” (ie in vestigial organs).

Now I have a far better idea, aided by the correspondence with you and others, and most recently by the link given in Jois’s post (which I’ll have to answer later), of exactly what I’m after.

It might not pan out but until I can formulate the right question I’m unlikely to get the right answer!

Jorolat

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The full article can be found at:

http://www.abcnews.go.com/sections/science/DailyNews/cavefish_000728.html

Jorolat

19

I appreciate your post is addressed to Jois but it’s posted in a public forum and other readers may feel the points you made have gone unanswered.

The mechanism being discussed is homeostatic, makes no decisions, and does no choosing.

To describe it in those terms is like saying “There’s supposed to be these little critters called bacteria, see?, and whenever they feel like it (‘giggle’) they unziiiip! their DNA, copy it, and then divide themselves into TWO!!! HAHAHA!”

When put like that bacteria seem almost magical !

The fact is bacteria *do * replicate. No more sentience is required for the mechanism than that needed to replicate, to exhibit the phenomena of stationary phase mutations, to keep you alive while your intellect sleeps, or, to use your own example, than that needed by the lens to “cause signal proteins to activate certain regions of DNA”.

No matter how much is known about the mechanics of the operation it is still amazingly “clever” of the “lens” to achieve that don’t you think?.

From the perspective of what has been discussed in this thread I find it extremely interesting, that in the case of vestigial organs such as the eye, it might be the “top level” of the organ that is always selected for.

If random mutations were responsible for the beginning of degeneration in organs no longer selected for then why don’t these mutatations affect the other genes within these organs?

Jorolat

20

They do. Random mutations are just that - they do not target any particular gene. To grossly oversimplify matters, almost all of these mutations will be deleterious and will be selected against. They therefore will not persist in subsequent generations.

A more nuanced view is that most mutations are actually “neutral”, that is, they neither benefit nor harm the individual organism. You’d expect a species to accumulate these neutral mutations through its evolutionary development. Indeed, you’ll find more similarities if you compare DNA sequences from closely related species than the DNA sequences from more distantly related species.