Lamarck's Law of Use and Disuse

Great Debates
21

Hi Jorolat, good to see you’re back in the Lamarkian discussion.

Without implying intelligence, the maintenance of homeostasis does require a correllation between the phenotypic change and the specific genes that need to be affected (as well as the type of change required).
When the AONE detects a shift away from the equilibrium of some facet, whether it’s eye movement, loss of “need” of tail or eyes, or what have you, the AONE needs to have some connection between the effect on the trait/organ and the genes that regulate the trait/organ. Once it has restored equilibrium phenotypically, it needs to be able to mutate the appropriate genes in the appropriate manner.
The oscillating eyes of the rats grown on the turntable didn’t develop from somatic genetic modifications, but from the synaptic plasticity of the cerebellum which would then have to be transmitted to the germline.

I know I’m probably not as objective as I could be, so could you explain how the article you linked explains directed mutagenesis? I’ve read it and the Science paper it refers to, and see it as supporting Darwinian evolution. (Your link even says, “This mechanism, however, provides a relatively straightforward and powerful means for generating genomic diversity.” And generating genomic diversity is at the heart of Darwinian evolution.)

I think you mentioned bike riding as an example of how Lamarkian evolution would work. It’s been several generations now, and we still have to learn to ride bikes. The equilibrium learned in the cerebellum has not been transmitted to our germlines. The same holds true for many skills that we have to learn (like walking, snapping, whistling).

It’s nice to have a chance to learn more about Lamarkianism from someone who’s studied it.

PC

22

Sorry to post twice, but it’s heady stuff…

The hormone signaling referred to here is the same that occurs throughout the body. It, at most, regulates expression of genes, not their alteration. (The reading of the book, so to speak, not the editing of text.) We need to find an example of hormones causing intrinsic genetic changes (almost by definition, hormones cause changes in gene expression).

PC

23

From M-W.com

Notice it doesn’t say anything here about how to change DNA to make a rat’s eyes jiggle.

In order for components of a system to be “in equilibrium” there needs to be some communication, a common language, some reason why an alteration in one component produces a corresponding change in another.

Consider classical chemical equilibria: two reactive gases are combined in a vessel. There’s one mole of each. When they react, they produce three moles of products (all gases). Under arbitrary condition A, the reaction proceeds in the forward direction. Under condition B, however, when pressure in the system is increased, the equilibrium favors the reactants. The reason for this is that two moles of gas (the reactants) take up less room than three moles (products). Increasing pressure favors the equilibrium state that occupies less room, therefore we see mostly the reactants at condition B. In this example, both the reactants and products are bound a common principle (ie they’re gases and subjeact to the effects of pressure on equilibria).

If we alter the scenario, however, so that the products of the reactions are three moles of solids, then increasing the pressure no longer reverses this reaction. Solids are not subject to the effects of pressure in the same manner as gases. We have interrupted the common principle of the reactant/product universe.

Such is the case with the AONE and DNA. There’s no conceivable link between developmentally altered synaptic wiring (a disequilibrated AONE) and the genome. I don’t mean there’s no neurohormonal link between the hypothalamic/pituatary/cerebellar axis and the gonads. What I mean is that the AONE and the genome are the like gaseous reactants and solid products in the flask: they are different states; in contact with one another but incapable of “passively” transmitting information about how they are being stressed from one to the other.

Without a sentient AONE, the transfer of instructions for targeted mutagenesis is impossible.

24

???
Should this have read:

25

Oh yeah, one more thing.

IMHO, this thread is now thoroughly GD. And while this may all appear to be MPSIMS, give us a few more posts and we’ll prolly end up in The BBQ Pit

26

Hi PosterChild,

I did reply to your post in “Evolution and Mathematics: Help Needed!” (http://boards.straightdope.com/sdmb/showthread.php?threadid=65734) where I explained that the mechanism I’m interested in is indirect and more appropriate to the Baldwin Effect rather than Lamarckianism.
'pauses to allow time for said article to be read followed by exclamation of “oh!” ’ ( :slight_smile: )

Without accessing the “anomalies” (referred to in the "Evo & Maths post and which would take some time) I would expect, in effect, the degree (how far down into the genome it extends), direction (+ve or -ve), and “lateral” extent (externally observable as whether co-ordinated or not) of the disruption to equilibrium to be transmitted to the AONE of the germ cells (there is more to this).

Yes, except the connection is via the AONE of the germ cells.

The first generation rats were unable to restore equilibrium and could only attempt to do so by flcking their heads and eyes in the direction of rotation - but neither was equilibrium upset to the degree that they died.

The “upset” of equilibrium was passed to the germ cells and evolutionary changes triggered in a direction that would restore it. If the experiment had been continued I can see the potential for gross physical changes following similar to those found in flat fish.

(scowls@“directed mutagenesis” :)) The point I’m making is that it could be the AONE that is triggering the molecular mechanism. From my perspective I was more than pleased to find that any molecular mechanism capable of generating genomic diversity was already known about.

I mentioned bike riding as an example of how the Baldwin Effect could be implemented:

"If succeeding generations of human beings not only learned to ride bicycles but began doing so for greatly increased periods then any transient disruptions the activity produced in the AONE would be integrated during this time.

Once existing thresholds were exceeded…co-ordinated evolutionary changes would be triggered in a direction that would restore equilibrium. From an external viewpoint this would be perceived as a relative improvement in the ability of human beings to balance that would be independent of any specific activity."

I hope I’m not labouring the point but I hadn’t even heard of Lamarck when I began and its only a couple of weeks since I’ve had a copy of the first part of his “ZOOLOGICAL PHILOSOPHY”.

As a further aside it was pleasant to be told on another forum (rather than being ridiculed, etc…) that “except for terminology your ‘take’ on evolution is remarkably similar to that of Jean Piaget”.

I’m ordering some of his books from the library but from what I’ve found on the web it is interesting to find him referring to “equilibrium” and to the Baldwin Effect.

Jorolat

ps I’ve got a funny feeling that this thread is gonna get zapped by a moderator pretty soon, am typing quietly…

27

Yes it is sentient though I have any number of reasons for not saying much beyond that.

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".

People often use expressions like “looking back on childhood” which, of course, is not the way it happened.

If you equate, as an analogy, the area of the brain of interest in to the base of a light bulb then during development of the foetus the brain grows into the stem (old mammalian) and then expands outwards into the bulb, the neo cortex.

Additionally, most of the “wiring” of the new brain occurs during the first couple of years of life and can be likened to a dimmer switch gradually increasing the voltage to the light bulb as intelligence grows.

We are integrated organisms and it’s difficult to say where one thing ends and another begins. The area of the brain (in human beings) that is of interest, and probably towards its upper limit, includes, as an example, that part which will wake a sleeping parent when their baby cries.

The way the brain of a foetus developes also reflects the way it evolved. It would obviously be a mistake to project evolved characteristics of the human AONE onto the AONE of a “less evolved” organism though, as indicated in an earlier reply, the basic “mode of operation” is the same.

When I began looking at evolution I first discussed the “anomalies” from which the proposed mechanism stems with a particular institute of psychotherapy in London. The outcome was a decision to try and present it as a “stand alone” concept because of the “noise” that psychological conditioning can generate.

Jorolat

28

Hi PosterChild,

I tend to fall back on “its not necessary to know how the mechanism is implemented in order to test for it” and in an ideal world I would look for any associated hormone(s) after operation of the mechanism had been observed, ie by repeating the experiment. There’s obviously no reason it couldn’t be done at the same time though.

It’s also quite possible that any associated hormone(s) have functions that are already known but nobody is looking for anything more. Personally I don’t feel that the step from altering gene expression to causing genetic changes is necessarily beyond the realms of possibility.

Obviously I have picked a bad example in the one given but when I first looked at “internal implementation” (before my system crash) I only wanted to know if anything could get into the nucleus. Afterwards I just did enough internet research to establish “there is much that is still unknown” and left with the feeling that there were many possibilities.

At the moment I’m obviously aware of the inadequacies of my replies in this area and am hesitating between delving into it further, in response to this thread, or carrying on with some of the more general arguments that I want to write up.

I’m happier with more “middle ground” stuff. For example, one of the first things the mechanism was “theoretically” tested against was the lateral line in fish to see if it was a sound organ.

The lateral line consists of a tube with “hairs” embedded in blobs of jelly which are spaced between a number of holes that let water in. Nerve impulses from the hairs are emitted in a steady stream and (obviously) go to the brain.

The basic principle is this: A sound wave enters a hole, imparts energy to a jelly blob, and is “long gone” by the time the jelly has stopped moving. The time lag between the energy being absorbed and the jelly ceasing movement has the effect of reducing the speed of sound to a level that can be detected by the “hairs”: if the jelly pushes them one way then the clicking rate goes up, and if the jelly pushes them the other way then it goes down.

Of course the picture gets more complicated when the outputs from all the jelly blobs are considered (being affected by reflected energy etc.) but integration of such sensory inputs are what brains do.

Using the model suggests the lateral line would make a basic underwater sound organ and evolution from it into the ear is, in general terms, quite straightforward (perhaps even predictable when one takes into account the
difference in how sound travels in the two mediums).

Jorolat

29

You won’t make me cry… (‘sniffle’)

Jorolat :slight_smile:

30

Hi Choosybeggar,

I guess GD means “Great Debates” but I haven’t a clue what MPSIMS means (and I got a funny feeling that it might not be good… ‘gulp’).

I’ve been thinking of rephrasing the original post and moving it to the Great Debates forum anyway! (‘smiles nervously @ moderators’}

Jorolat :slight_smile:

31

This thread has drifted rather a bit into GD territory, so if nobody minds (heck, even if some does mind, unless they tell me within about 30 seconds), I’m moving it to GD.

By the way, jorolat, MPSIMS is Mundane Pointless Stuff I Must Share, another one of the fora here. I really don’t see how this thread would fit there, though.

32

…twenty SEVEN…twenty EIGHT…

hey! (‘waves at Chronos’) wait !

…THIRTY!!

‘sigh’ too late…

Jorolat

ps thanks for the explanation, l just knew l wasn’t gonna like it… ( :slight_smile: )

33

I am quite happy to continue discussing any aspect in this thread.

In view of how it has developed with respect to the original post, however, and particularly the link given by Jois, a new topic: “Are Vestigial Organs the result of Random Mutations?” has been started.

Jorolat

34

ok, I did miss your post about the germline AONE. :frowning:
I do think some genetics and development texts would better arm you for some of these discussions. (There are actually a very many ways that there is feedback to the nucleus- in fact, the many responses that involve a change in transcription of the genes to mRNA (the first step to regulate the making of proteins) by definition are in the nucleus.) I think you’ll find that many of us in these discussions already took as proven that there is communication to the nucleus, it’s the change to the coding that we’re having problems with.

Which brings me to the very interesting point that I apparently missed before. Would the germ cell AONE be an extra-chomosomal method of propogating traits (or changes to them)? Is the AONE encoded by genes or does the change in the germ cell AONE that matches the change in the organismal AONE propogate to its decendent cells without encoding the changes in the chromosomes?
IMHO, this is the heart of the matter. If transposons are involved at this stage, their excision and transfer (or copy) would still have to be regulated by the germ cell AONE.
(Would the rats with wiggling eyes have genetic changes that encoded for wiggling eyes?)
You might want to look at DNA repair mechanisms which are implicated in regulating DNA mutations including point mutations, deletions, repeats.
I should say that I probably misinterpreted your reference to the paper on transposons. Transposons were actually used in eary genetic engineering experiments (and their discovery by a perserverant scientist is an interesting story of its own) and I thought you were using the paper to support the idea of a mechanism by which the AONE would encode changes into the genome, instead of an example of changes occuring in the genome. (Am I being clear?) I could give you several other examples of mutations/deletions/repeats occuring, even being regulated, but not directed according to a template (like the AONE).

You’ve definitely piqued my interest with this. What was the connection to DNA. I think it would be very supportive of your points.

I think I’m also confused about what you mean by indirectedness of the Baldwin Effect. Since this is the heart of your interest, would explain what it means?

Also, do have any potential systems that could function as the AONE within a single cell? It would be an interesting problem to figure out a method in which cell that is orders of magnitude less complicated than the organism can encode for all the facets of the organism that are/will be regulated by a component in the single cell.

P.C.

P.S. Sorry to keep using Lamarkianism. I only really meant the directed adaptation of an individual’s decendents as opposed to the population selection required by Darwinian evolution.

35

Hi PosterChild,

I’m going to be busy for the next week or so and I intend to initially use any spare time to follow up an interesting development in the “Are Vestigial Organs the result of Random Mutations?” thread.

I will be back though! :slight_smile:

Jorolat

36

Hi. I must admit I haven’t read the whole thread in excruciating detail, and I have only paged through jorolat’s homepage.

I have a number of issues however:

My first grad school rotation was with Susan Rosenberg, who studies stationary phase mutation. To generate stationary phase mutations, she grows E. coli that cannot digest lactose (lac[sup]-[/sup]) to saturation, and then plates on a plate with lactose as the only carbon source. Regular bacteria can digest lactose, but these ones have a +1 frameshift in one of the genes responsible for lactose digestion.

In stationary phase, she sees a population who revert the +1 frameshift and become lac[sup]+[/sup]. The mechanism is complex, but basically deals with a global downregulation of proofreading and upregulation of error-prone polymerases which are active during DNA repair. This causes slippage and high rates of mutations at mononucleotide repeats.

A couple of things:

  1. Stationary phase mutation hasn’t been seen in anything except bacteria (see below).
  2. There is no targeting to the specific non-functioning lac gene.
  3. The bacteria become globally mutagenesis prone (mut[sup]+[/sup]).
  4. This occurs in a population and only a few out of every million bugs become lac[sup]+[/sup]. These bugs get a huge advantage over their lac[sup]-[/sup] neighbors.

So no stationary phase mutation in anything but bacteria. But, a similar phenomenon has been noticed in cancer cells and in yeast. A gene responsible for chemotherapeutic drug metabolism or transport can become amplified by tandem copying (often millions of times, creating visible chromosome structures called double minutes) in order to lend resistance. Basically, if one copy of the gene can give 1/1000 resistance, 1000 copies will give full resistance. Problems again:

  1. This occurs in a population.
  2. Cancer cells have often turned off cell cycle checkpoints that would cause an ordinary cell to commit suicide if it tried to amplify its DNA.
  3. A cell who amplifies its resistance gene twice will have a two-fold advantage over its neighbor. Such a process is kind of like a snowball – a tandem repeat can expand easier than a non-repeat, so amplification four fold from two fold is easier than from one fold to two fold.

The problem with jorolat’s model (if I understand it) is that there is no population of cells here. Amplified or stationary phase cells are clonal – all descending from one cell. This doesn’t happen in the germ line (all the kids would look the same!) or in the cerebellum. It has never been described. Also, stationary phase mutation and amplification are non-directed. While this was unknown in 1988, it is very clear now. This is not an example of the environment feeding back into the genome.

Next, there are examples of the environment feeding into genetic regulation. These are not direct, however, although they may involve inherited change. These mechanisms are epigenetic regulations like methylation, imprinting, heterochromatin structuring by histone acetylation, and many other modifications to the DNA structure. These do not (that I know of) ever change the genetic information, but may silence or enhance gene expression in generations. Certain genes are turned off by the maternal or paternal germ line cells in imprinting. This can lead to certain diseases – Angelman syndrome, Prater-Willi syndrome, Beckwidth-Wiedemann, and certain other disease which can occur in a non-Mendelian form.

If I were looking for instances of Lamarckian evolution, I would focus on epigenetic inheritance. Stationary phase mutation and amplifcation are poor candidates, IMHO.

Also, I’d read up a little about Lysenko and the havoc he wrought in the Soviet Union when he convinced Stalin that Lamarck’s theories were more Marxist and must therefore be correct.

http://www.dcu.ie/~comms/hsheehan/lysenko.htm
http://www.princeton.edu/~browning/215/readings/gould.html (from Steven Jay Gould’s book The Panda’s Thumb

37

Edwino, you will learn quickly that in the world of jorolat, undescribed phenomena are but evidence of limitless possibility. He begins from a weak phenomenology and moves to a more tenuous mechanism.

Besides, he’s stated that he paying more attention to this thread which IMO has a more focused subject matter. Check it out if you get time.

CB

38

Hi Edwino,

Thankyou for posting, hopefully the following will clarify the issues you raised:

I’m interested in stationary phase mutation (“SPM”) experiments that have produced results generally described as “non-directed but due to the non-specific stresses of starvation”.

A search engine will give more but as an example the article “**Directed Mutations: Heredity Made to Order
**” refers to experiments where the number of revertants ranged from “orders of magnitude” to “100 million” times greater than theory could account for.

Some experiments required the reversion of double mutations and none of the descriptions I have read have ever spoken of descent from a single cell.

My instant interest in anything described as “Lamarkian”, or “Directed” etc., is in case the word(s) have been applied to phenomena that may be due to an indirect (and testable) homeostatic mechanism.

Such a mechanism would have to “operate” in the same way at either end of the evolutionary scale and stationary phase mutations in bacteria, representing single cell common ancestors, appear to fit the bill.

A couple of years ago I did read articles that speculated on SPMs being connected with cancer (etc) but have never heard of them occuring in the cerebellum.

With the exception of the article referred to below I haven’t read anything by Rosenberg though I’m intrigued by your words “…basically deals with a global downregulation of proofreading and upregulation of error-prone polymerases…”. Almost as if equilibrium were being sought… (‘pause for laughter’ no? ok, ‘sigh…’ :))

The following extract from “Directed Mutation and Galileo” refers to Rosenberg’s article “Mutation for Survival” Genetics and Developement Vol 7, No. 6 (http://www.biomednet.com/library/fulltext/JGEN.gd7613, unfortunately the link is only good if you have a subscription to Biomednet :()

The only thing I can add is that neither Lysenko, Darwin, or Lamarck, invented evolution and I don’t feel responsible for anyone’s prejudice against any of them.

Jorolat

39

Be nice! you’ll have people thinking I’m crazy…

Jorolat :slight_smile:

40

It has been brought to my attention that members of the Rosenberg lab are perhaps lurking this thread (by a weird concordance of the universe). To my satisfaction, they have informed me that I have not made any factual errors (yet).

I have read jorolat’s above quote from “Directed Mutation and Galileo” about 20 times. I think I can finally comprehend most of it. I still cannot understand most of the other stuff on the homepage though.

I haven’t read Susan’s 1997 Current Opinions in Genetics and Development article (recently or perhaps ever), but I would suspect the reason she shies away from the “directed mutation” term is because, simply put, SLAM (stressful lifestyle-associated mutation, to use her terminology) is not directed. In science we try to be as accurate in our language as possible. The terms used to describe SLAM in the past have been inaccurate – that is why they invoke ire.

It has been conclusively shown: SLAM is not directed. It may have been thought to be directed in 1988, but there is 13 years of literature after that which has changed the picture significantly.

On equilibrium: Organisms downregulate and upregulate stuff all the time. We do it constantly. Biologists are constantly trying to boil down all of life into one huge feedback loop. We change our gene expression continuously in response to countless stimuli. Besides some very specifically defined instances, most of which do not directly involve the genetic material, changes in gene expression are not inherited.

This contradicts the core nature of any Baldwin principle or pseudo-neo-quasi-Lamarckian belief.

Lastly, modern genetics wouldn’t be shattered by some unlikely discovery of a bizarrre Lamarckian scenario. It would make the cover of Nature and inspire a bunch of new experiments, and all existing theories would be modified to include it. Perhaps there would be a Lasker prize or a Nobel awarded. The simple blunt ugly truth of the matter is that nobody ever has seen such a scenario, despite 130 years of copious research on the nature of inheritance.

This is the nature of peer review and openness in science. If a bizarre result is reported, reagents are requested and experiments are repeated. If the result is not replicated, then the result is withdrawn. I would like to think that we have come a long way since Galileo, especially in the world of biology where experiments are easily reproduced. A good example of this is Prusiner’s work with prions. His hypothesis that disease could be transmitted by misfolded proteins alone (without genetic material) was not immediately accepted – this was a revolutionary idea when first presented. When other experiments verified it, and the science behind it was proven sound, he was given the Nobel.