In being unable to grasp the concept described on the homepage you appear to have associated it with Lamarckianism as “the next best thing” and then constructed a post based almost entirely on this misconception. Having said that there are many concepts that I can’t grasp either
But there are some points in your post I would like to comment on:
At one time people believed the earth to be flat. When they learned that it was round they then believed the sun revolved around the earth.
The real problem in both of the above beliefs is that they are egocentric: “if the sun rises here and sets over there every day then it must revolve around ME” (etc.).
There have been many discoveries since Galileo’s day but have we really “come a long way”?.
Using an historically recent example, rather than one people might have strong feelings about, consider the case of Truby King who was a child-rearing expert from early in the 20th century:
In order for children to start learning to meet the demands of “society” King recommended that infants should only be fed at fixed intervals and all crying, etc., should be ignored. Many parents saw the logical sense of his arguments and followed the advice.
An infant waking up feeling hungry midway between the fixed feeding times would, of course, begin to cry. Existing entirely in the Present Moment, and with the new brain still being “wired in”, such an infant would have no awareness of the future or that they would ever be fed again.
The experience is one of being starved to death, and with no other means of communication, the cries become increasingly angry thus heightening the risk of an “overload” occurring that disrupts inner integrity and causes a trauma. Much like breaking a horse but saying “look, no hands!”.
King’s conditioning meant he only had an egocentric view of natural life, and though I’m sure he collected a number of pointless accolades and prizes along the way, this example does demonstrate how remote the conditioned mind can be from the natural reality it believes itself to be interested in.
Evolution is about natural and non-intelligent life too. I feel that anyone who can relate to the infant in the above example (ie be non-egocentric) should, perhaps after some reflection, be able to grasp the concept of the proposed homeostatic mechanism. Lotsa people do but then still insist on arguing against it
A further point:
Geneticists may be interested in a particular “aspect” of an organism, developmental biologists another, and ethologists yet a third, etc., etc…
"Another reason for the lack of attention (to the Baldwin Effect), according to these authors, is that evolutionary biologists feel "behavior and learning are the province not of biology but of psychology and ethology."
These divisions do not exist outside of the human intellect, every organism is an integrated whole, and additionally, is not in the least bit scientific either.
I’ve only briefly looked at the “intelligent design” theory but have the impression that behind the logical arguments of “irreducible complexity” lies an awareness of natural integration. From my perspective its a shame that egocentricity still appears to be involved: it has to be intelligent. It is not intelligence, after all, that keeps us alive as we sleep.
Lamarck v. Darwin
Basically I see this as little more than cultism - much like following a particular football team and with the added oddity of neither participant being able to contribute because they are no longer alive.
Its a new day and there are new players on the field. Being continually held up by the dead hand of history (ie in how it manifests itself in the conditioned mind at the least supposed provocation) must be quite frustrating for those scientists who are occasionally guided by their inherited instincts to do something intuitive. Even Darwin had his moments of “insight” and of course many other people do too, though few wonder what it actually is…
It is tempting to reply to your post in more detail (for example: “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.” is that the same as saying “If we haven’t already found it then it can’t exist?”) but you might misconstrue this as arguing for “Lamarckianism” which would be a waste of time for both of us. In fact I’m only interested in the possibility of a non-theoretical and testable natural reality.
God’s gonna get it right in the ear because I don’t have the resources to perform my own experiments.
You have provided a lot of words to this debate (about Galileo, Albert Einstein, yank kids named Eleanor, and obscure child-rearing methodologies), but I have yet to really see you stab at the heart of the matter.
Given that my interest is in biology (more specifically molecular genetics), let us engage in a thought experiment.
You have proposed a model:
“learned behavior and characteristics at the level of individuals can significantly affect evolution at the level of the species”
--from [Genes, Phenes, and the Baldwin Effect](http://www.google.com/search?q=cache:www.fapse.ulg.ac.be/Lab/cogsci/rfrench/baldwin.pdf+phenotypic+plasticity+baldwin+effect&hl=en)
In science, we propose models all the time. We state them as hypotheses. The next step, of course, is to design experiments to test the hypothesis.
This particular model should be easily demonstratable in a population-based fashion. It should also be demonstratable on a molecular level.
You have done the appropriate background reading. Propose a hypothesis. Can you propose experiments to support your hypothesis? Can you predict results and the interpretation of such results? Have the experiments been done already? What were their results, and how are they interpreted, both in a Baldwinian (since you shy from Lamarckian) and in a Darwinian fashion?
These are the questions that we scientists ask ourselves before we embark upon any course of research. These things are required in all grant and research proposals: background, model, hypothesis, specific aims, and goals.
I have access to some of the best lab facilities in the world. I work with fruit flies, which can learn and can be trained, and are also amenable to population-based study. I have all of the molecular tools to analyze genetic change and expression change. If you come up with something and are able to convince me that it is reasonable I may just be tempted to carry out the experiments. I promise that I will keep an open mind – I am just a student of science. But, you have to give me arguments good enough for me to convince my boss (a PhD). I’d bet he’d even stick you on the paper.
Seriously, choosybeggar: we raise flies in the dark all the time. We never see eyeless flies just popping up – that would require two hits on the same gene in eye development. There are 6 or 7 genes I can name off the top of my head which cause a recessive eyeless phenotype – you would have to pick up spontaneous mutations in both copies of one locus in one generation. It never happens.
Thanks, though. I try hard to be both a cool mofo and a science dweeb. It is a thin line to walk, but I just go out there every day and try to do my job as best as I know how.
There is similarity between Darwin’s notions and the law of effect.
The law of effect is that behavior that is rewarded is likely to increase or be “stamped in” and that behavior that is punished is less likely to occur.
But this occurs in specific organisms and does not result in genetic change. Lamarck was incorrect.
Expanding on what PosterChild quoted from another thread:
Initially it was like having an answer but not being sure what the question was. Along with the above I also began looking at:
How the proposed model could account for various areas that some considered problematical in current theory
To what degree psychology was involved in the perception of evolution (at the bottom level this consisted of the context in which certain words and phrases were used such as “niche” “stress” “pressure” “junk dna” “natural selection does this” “evolution does that” etc etc)
At that point in time, and in terms of widely recognised phenomena/concepts, the proposal could only be related to homeostasis. Then I came across stationary phase mutations and from my perspective those results perceived to be “directed” are a subset of those perceived to be “due to the non-specificstresses of starvation”.
On the assumption that bacteria are representative of the single cell common ancestor stationary phase mutations are exactly the kind of phenomena I would hope to find: In principle the proposed model appears to be able to account for them in the same way that it can account for changes in more evolved organisms (ie it “works” in the same way at either end of the evolutionary scale).
Next came “The Baldwin Effect” which, as a known concept, “anchors” the proposed model at the current end of the evolutionary scale. This is the framework within which, when time permits and depending on where my interest takes me, I potter around.
Before I begin replying to your post in a more direct fashion I would like to say I have no intention of arguing the case for the proposal any more than is necessary. These discussions (and those yet to come :)) are useful but, with no easy access to resources, whatever is learned will be used to finish the web pages before moving on to other areas of psychology.
Re your post:
A provisional method of testing was devised quite early on and from time to time I’ve tried (unsuccessfully) to find the primary sources of two experiments that I subsequently found (“Evolution: Two Intriguing Lamarckian Experiments”) but for no other reason than they were the first I came across (there are others which were earmarked but as I only spend occasional amounts of time on this the “retrieval system” has become unreliable).
These two experiments were briefly decribed in “The Great Evolution Mystery” by Gordon Rattray Taylor (Secker & Warburg, London) but no references were given.
Both experiments were performed “some time ago” and in the first a chap called Frederick Griffiths performed an experiment on rats whereby they were placed on slowly revolving turntables for periods of up to 18 months or so.
When the rats were removed from the turntables their heads continued to flick in the direction of rotation and so did their eyes. This automatic flickering then appeared in their offspring.
The secondary source doesn’t give much more than the above. Taking it at face value for the moment, and arguing from the perspective of the AONE, it is not the kind of experiment I would have thought of devising - it’s too vague, too “hit or miss”.
There are two points to the upset of the AONE that are relevant. First, maintaining equilibrium from the time of the single cell common ancestor to the present day rat wasn’t achieved (obviously) in such a permanent environment. Secondly, and because of this, going round in “slow circles” would have upset the AONE a little at first but the persistence of the experience would then have made the effects accumulative.
It is strongly inferred in the secondary source that the offspring were born with both head and eyes flickering - indicative of co-ordinated changes. If the experiment had been continued for a “sufficiently” long period of time I can see the potential for gross physical changes occurring similar to those found in flatfish.
The AONE is described as a “localized” area. To put the above into perspective:
There are a number of things that could be said about these experiments the most important of which is that in concentrating on “learning” too highly evolved areas of the brain were engaged. Again its hit or miss, or in other words, its not upsetting the AONE enough - largely going over the top so to speak.
At the other extreme there is Weismanns experiment of chopping the tails off of succeeding generations of rats. This overloads the AONE from a specific area but is “non-sensical” from a homeostatic perspective. I ought to think about this some more but its something along the lines of physical trauma being a linear event across an integrated function.
None of the above experiments were devised with a specific internal model in mind.
The other experiment Taylor described is more to my liking:
This is the easiest way to target the AONE and to prove whether it exists or not: Wait for a moment in the life cycle where hereditary behaviour is both dependent upon external parameters and also necessary for maintaining continuity of Being (aka “survival”). It’s difficult to be more exact because all organisms are different but on the other hand more reflection will probably result in something less vague!
Then all you have to do is change one (or more) of the parameters in a way that will (hopefully!) produce results within a predictable range - like indirectly altering the coloured pieces of glass in a kaliedoscope and thus producing an observable shift in the patterns generated.
There is bound to be trial and error. In the above experiment, for example, the “phenotypic plasticity” of another type of caterpillar might enable it to use the sides of the leaves without any difficulty. A third type might (theoretically) find it too difficult and die.
I’m sure you’ll know if there are any points in the life cycle of fruit flies where the AONE might be triggered in this way. There would be little point in my learning sufficient about fruit flies in order to devise an experiment for them if there was no possibility of it being carried out, besides there’s probably enough in the above for anyone with the resources to be able to do it themselves. This presupposes they would be interested enough to do so!
If you have any comments or questions then I would be happy to read them with two provisos:
Owing to the origin of the proposed mechanism I’m not keen on discussing evolution on purely theoretical grounds.
I would argue that my personal lack of knowledge in any one area (ok, lots of areas :)) doesn’t detract from the proposal itself.
Compound eyes of flies are arranged in an orderly grid of 700-750 unit eyes (or ommatidia). No spirals. The development of the fly eye is the primary focus of my PhD.
Bacteria are the endpoint of evolution, as are we. They are supremely adapted to their particular environment. While as you know, we do share some common features with bacteria, they are as evolutionarily different from our last shared precursor as we are. We are not “more evolved” than bacteria.
Among common aspects, we do not share stationary phase mutation, as yet discovered. Stationary phase mutation is not directed.
I have access to PDFs of most articles published in most major journals since 1997 or so. Some online journals have PDFs going back to the early 1990s. I can provide you with any material you want, provided you delete it after you read it (copyright laws and all). All in the name of science.
The main problem I have with this is that there is no control listed. It would be a simple, powerful experiment if you made 4 groups:
Experimental group : parents with no tips of leaves, progeny with no tips of leaves.
Control 1 : parents with no tips of leaves, progeny with leaf tips.
Control 2 : parents with tips of leaves, progeny with no leaf tips.
Control 3 : parents with tips of leaves, progeny with tips of leaves.
If you can convince me that Group 1 has a significant difference from the other 3 groups, then I would be impressed.
The problem that you run into again and again with these types of experiments is that the experimental condition cannot be a lethal selection. Basically, killing all of the animals which do not meet the criteria will induce a Darwinian selection. You cannot tell if there is a Lamarckian advantage in the progeny because you have to comparison group. If you induce a selection which kills 999,999 out of 1,000,000, then you are probably just selecting a sporadic mutant in the one survivor.
So, you need a nonlethal selection and then look for a phenotype in the progeny. My initial suggestion is this:
Flies, being cold-blooded, age half as slowly at 18 degrees C versus 25C. We usually raise flies at 25C, and their generation time is 9.5 days. At 18C, it is closer to 20 days. We could take a population of flies raised at 25C and one raised at 18C and divide their progeny into 4 groups:
18C flies -> 18C progeny
18C flies -> 25C progeny
25C flies -> 18C progeny
25C flies -> 25C progeny
We could look for significant differences among the progeny:
a) do the 18C progeny age faster than the 25C progeny?
i) is this conserved at 18C and at 25C?
ii) is this conserved for more than one generation?
-I would do this by raising populations of wild-type Canton S flies at 18C and at 25C. Probably something like 12 virgins and 5 males in each vial. I would remove the parents and collect the progeny after a set amount of time. I would then divide into groups 1-4 and examine when progeny begins to come out.
b) are the 18C progeny any more cold-resistant than the 25C progeny?
-Among the collected progeny from the above groups, I would take 5 males from each group 1-4 and cold shock them at 0C or 4C.
c) are the 25C progeny more heat-resistant than the 18C progeny?
-Among the collected progeny from the above groups, I would take 5 males from each group 1-4 and heat shock them at 40C.
The only problem is that I don’t know if the 18C/25C criterion is enough to upset your AONE. It meets my criterion that it has to be a non-lethal selection.
What do you think? These experiments would be trivial – they would take a few months to run to completion, but the time investment would be nominal.
I’m going to be quite busy for the next two days, would like some time to think about your post, and will reply sometime on wednesday at the very latest
I do actually know that - I tend to view bacteria as representative of the single cell common ancestors and even then only from the perspective of the proposed mechanism. I’ll try and do better!
The idea is that when life became multi-cellular then so did the mechanism. Stationary-phase mutations discovered outside of bacteria would be a secondary phenomena.
(Deletes "Oh boy - lemme at 'em!) I am grateful for the offer and also appreciate the interest you’ve shown in this discussion. If the need arises I’ll make sure any requests are directly related to this topic
It would be good to find the primary source of this experiment to evaluate just what its potential is.
On the other hand, more background reading (when I have the time) might uncover others that are equally promising and also generate some ideas for devising new.
I agree. From my perspective targetting the AONE requires a certain degree of finesse - part of the reason why I mentioned that Weismann’s experiment was going too far.
When I looked at a method of testing some time ago I felt that using hereditary behaviour at a specific moment in time would be the easiest way to test for the mechanism and then haven’t given it much consideration since.
Consequently I’ve had to give some thought to the approach you’ve suggested and so far I’ve only had time to concentrate on the first part of the proposed experiment - ie before the heat/cold shocks:
The AONE would definitely be upset, and in a “negative” direction (see Model), because you are selecting a single point of the temperature range within which it can currently exist.
The general questions I would think about for an experiment are:
Would any proposed upset be enough to cross existing thresholds (part of the “inertia” of a wanting-to-stay-the-same mechanism) and thus trigger changes in a direction restoring equilibrium?
If the upset is sufficient then how long would it be before the changes are initiated?
How many generations would it take for the changes to “ripple” down through the genome until equilibrium is re-established?
I’ve only included 2) to cover all possibilities and it can really be considered as part of 3).
This last point, however, is quite important because if the heat/cold shocks, for this example, were applied too early in the restoration phase then the results could very well be inconclusive or there might be no discernible difference at all.
For the proposed experiment everything (obviously) will depend on the answer to 1) and the best case I can imagine is there would be a reduction of the temperature range within which the flies are viable.
Supporting this possibility is the following (taken from here):
(a search of the Bionet archives shows that no replies were posted)
I can’t think of any reason (which is not to say that one doesn’t exist :)) why an equivalent result couldn’t be achieved at the 18C point - which would then be reflected in any results from the heat/cold shock tests. Does this seem reasonable?. NB: I haven’t read much on heat/cold shock tests yet (a headache avoidance strategy) and so have no idea of what may be obtained from them.
I’m looking forward to hearing what you think, at the moment I’m intrigued by the possibilities that the above appears to offer (not least the “gap” that might be achieved between selected temperatures).
As a final point, would you be interested in helping define a possible experiment even if the time/resources required are more than you are able to consider? If so I could write it up and just leave it on the website.
I’m nearly out of time but as a final comment: I would presume that Hirsch’s flies could be accounted for by random mutations & selection etc…
If, as an example, several populations were maintained at 18C (or any other, or combinations of others, etc.) and they all changed at the same rate would this be enough to eliminate randomness and indicate that there was some kind of mechanism at work? or could another conventional explanation be given that I’m currently not aware of?
How can we measure these three points? You must have some ideas/guesses about answers. If you can use these to formulate a working hypothesis, it would make life easier for me (to understand this model). The generation time of a fruitfly at 25 deg C is 10 days. At 18 deg C, it is closer to 18-20.
There are a number of reasons I think this may have occurred. We have Canton S stocks as our lab wild type, which have been maintained at 25 deg C and at 18 deg C for many years.
All Drosophila labs have Canton S stocks. Many maintain their stocks at constant temperatures for years on end. This phenomenom has not been noted before. The easiest explanation is that Hirsch has picked up something in his population – perhaps mites (parasites that we diligently work to get rid of) or perhaps some random genetic hits. This is especially true if he has isogenized any of the Canton S chromosomes or if he started from a small population (founder effect). He should get a new stock from Bloomington, though.
It depends on my upcoming schedule. I have a busy summer (hopefully), but email me some information (or we can debate it here) and I will respond as well as I can.
This would be a good control to do – since this would involve population analysis, you would want to start with a large group of flies. These would be in several different vials in different incubators and they would be aged differently to eliminate things like food consistency, incubator fluctuations, and general weirdness. All experiments would draw from data across the population. The size of the population we would need would depend on the amount of difference you need to see. A 20 vial experiment, with 10 at each temperature and around 400 flies per vial would amount to 4000 flies at each data point. This would be relatively trivial to carry out (vials cost about $0.10 apiece). They would need to be flipped every generation, which for 10 vials would take all of 4 minutes every 14 days for the 25 deg C ones and 28 days for the 18 deg C ones.
I’m going to be busier this week than anticipated and would like to follow up some unfinished stuff from last week (related to this thread) before replying to your last post.
I haven’t heard anything further from Hirsch and now that I’ve stopped crying, put all the pins in a voodoo doll called “Helmut” that were warranted, I guess its time to move on.
As I said before I would need to know a lot more about drosophilia before guesses became even half-educated. From my perspective your offer, assuming it still stands, is the first opportunity to test for the mechanism and for that I would want to be doing more than just guessing.
Part of my hesitation in doing the necessary work is uncertainty about how interested you are.
Referring back to your last post I was interested in your comments about population analysis. A chap I know (though I haven’t seen him in about a year) performed the following variation on an experiment that is apparently done all the time by students:
Presuming the routine explanation for the above would be “random mutations followed by selection” (er, I hope I’ve got that right!) do you think, in principle, that an experiment could be devised (using multiple populations) that could determine whether the above phenomena was random or not?
I do have some thoughts on the matter but at this moment in time I’m not sure if you’re even there!
I’ve heard from Hirsch (er, an’ taken all the pins out red faced) but am unsure whether that’s the path to take. I would like to hear from you if you’re still interested.
I am extremely busy trying to get things organized for a trip to Siberia. Interest of mine is not a problem – it will be fairly trivial to get the thing started (stick a couple of vials of Canton S wild type flies at both 18 deg C 25 deg C, which will take a minute or two).
If you still wish to pursue this course, I would be glad to start. Since it will take many generations, though, most of the time will be spent waiting.
All I need from you is some legitimate testing criteria : How do we measure “thermal sensitivity?” How does that support the Baldwin Effect? Are there any other explanations for such an effect?
You excerpt of ciliates was interesting but again left me struggling to see how the Baldwin Effect plays in on it. All organisms have some level of phenotypic plasticity. The sea water experiment sounds like a Darwinian selection for those members of a population who have plasticity in a salt containing environment. Death, survival and repopulation on both arms of the experiment.
Anyway, sorry for being so tardy. Things are really busy for me.
Ok, I’m sorry for being impatient and I hope you have an enjoyable experience in Siberia. If my type appears green its because Straightdope are experimenting with new features rather than cos of any jealousy on my part. You might watch out for a similar colour in the MammothBurgers they sell at McDonaldski’s though.
Now that I feel reassured you’re still interested I’ll start looking for a characteristic in drosophilia that I recognize and that can be used - it doesn’t have to be thermal fragility but I’ll look at that first. Unfortunately I’ve just volunteered myself for another, albeit small, project and I’ll have to do both in parallel for a week or two.
Perhaps the ciliates could be left for now (or I might open another thread sometime) but if I do post anything here regarding them I’ll understand if you don’t have the time to reply
