Fundamental reproductive changes and variability

Darwin said, in Origin of Species: This got me to thinking. Has any research been carried out in this area?I know Darwin didn't know about DNA and so on, but my thinking is as follows: We know that the conditions in vitro can affect an embryos development; could a mutation (or accumulation of mutations) cause the 'female harbouring area' (womb, pouch, egg, whatever) to alter its conditions enough so as to provide a benefitial change in an embryos development?Could this change be strong enough to affect fundamental elements of morphology (for example, muscle growth)?Example: A human mother has a novel mutation which alters the ambient womb temperature (you can bet that not only was that pun intended, but part of the reason I wrote this thread was because that little jest popped into my head when I was considering this) enough to make the child have increased flexibility in their tendons?Example: A human mother has a novel mutation that creates a new or unusual hormone that affects the development of the child in potentially dramatic fashion.Naturally the mother would probably pass on this mutation, and if she had a girl she might also carry it, so her child is also affected....This is broad generalisation I know, but it was a thought I was playing with and could not find easily any papers that discuss it. Anyone have any ideas?Biological evolution seems the appropriate locationSupid typosThis message has been edited by Modulous, Sun, 02-October-2005 01:30 AM

Thread moved here from the Proposed New Topics forum.

There's a theory I read on changes in morphology which are "inherited" but not genetic.I'm paraphrasing because I went over this stuff maybe 10 years ago, but here's what it was about.Say you have a population of average size humans. They are isolated from other groups and living on an island, so limited resources, no trade.If there is a famine, the generation of children raised at that time would be under nourished and therefore shorter.The next generations size may be restricted by the fact that this generation's females are smaller in stature.And vice-versa.As I recall it was being used to explain the rapid size changes in isolated animals (dwarf mammoths for example)It's not a permenant change either, since it's not genetic. For example, since WWII the Japanese diet has changed a great deal, and with it their average height has increased quite a bit in just a few generations

An example similar to your first one: If a mutation were to somehow change the insulation of a reptile's eggs, then in most species it would be more likely to hatch a certain sex of offspring, which could definitely be beneficial in times of rapid climate change. Also, I've heard that incubation temperature can have a huge affect on the morphology of certain kinds of skinks.

How else would we explain the evolution of wombs, pouches, eggs, whatever? If we find this proposition in the least bit surprising or challenging, it may be because we have become so infatuated with the tremendous explanatory power of genetics that we are blinded to the fact that it cannot explain everything. Individual cells have individual histories. These histories are inherited along with the genetic information, and are as important a factor in the development of an organism as anything in the genome.

I'm confused by what you are saying here. I propose that the normal discussed method of evolution is DNA replication error. However, some mutations may have a such an effect on the female reproductive element so as to result in further change in the offspring of the 'mutated' organism.Naturally, we start to get into knots when we suppose that the reproductive element in the embryo is the element altered by the mutated organisms altered reproductive element. Though, an interesting feedback scenario could be postulated.

Maybe I am the one who is confused. Are you talking about somatic mutations?

No I'm not.Sue is born with a genetic mutation. This mutation has an effect on her womb. When she gets pregnant, the conditions in the womb are different than is normal, perhaps an unusual hormone is released, which leads to a different development in the embryo. The embryo is then born different since. Her name is Karen. Karen has, I don't know, the ability to see into the infrared. Karen has inherited Sue's womb mutation so when she has two children, Mike and Sarah, they both can see infrared.

So we'd be seeing a germ-line mutation which influenced the way genes were expressed in the developing embryo. Selection could act on the gene causing the change in hormonal levels which resulted in expression of the genes for infrared vision, and on the gene(s) for infrared vision itself.

Yeah, the key thing I am driving at is that the mutation is not in the embryo (well it is, but that it plays no role on the development of the embryo), but in the mother.

It gets even more interesting when we consider the extent to which the mother's normal functions are influenced by hormonal secretions by the embryo, such as the persistence of the corpus luteum due to the hormone chorionic gonadotrophin being produced by the trophoblast cells. So we could get maternal germ-line mutations that affected hormonal secretions by the embryo, which in turn influenced maternal hormonal activity... It could almost get too interesting.

This article on Pharygula talks a bit about gastrulation and maternal investment. Although not directly realted to what you are talking about, it shows how the maternal "environment" is part of selection.

That's a great article, but I think it's going to take a few reads of it before I'm going to really understand it.

Hi modulous,I thought your question was interesting. I just want to give some general comments. Well of course that is true, even though Darwin had no knowledge of genetics. Genetic variability originates in mutations to the germline. The variability arises from copying errors made during cell division. This is why all of your sperm have slightly different genetic sequences. The mutations are occuring during division of cells that give rise to sperm (or to eggs). They generally aren't occuring in the embryo itself.If a mutation occurs when sperm and egg unite, obviously this will end up in the germline of that organism. But if a mutation occurs after the first cell division in the zygote, there's only a 50% chance it ends up in the germline. After the second cell division, only a 25%, and so on; it is an exponential reduction in the probability that a mutation ends up in the germline. The probability of getting a heritable mutation occuring in a zygote or embryo becomes vanishingly small within a few minutes of the first cell division taking place. It must be exceedingly rare for even a single heritable mutation to arise after fertilization has taken place.Consider your sperm, on the other hand. The average healthy human male is producing 100 million spermatazoa every day. Even though mutations occur at a low rate, all of them end up in the germ line (if that sperm is successful in fertilizing an egg; and of course if they aren't successful, they are of no evoultionary significance). So it's clear that the VAST majority of FIXED mutations occur during gamete formation rather than during development of the embryo. This is the answer to the question first posed by Darwin.This has some interesting consequences. First, most evolution must be driven by mutations that occur in males (simply because of MUCH higher sperm production than egg production, and much more numerous opportunities for mutation to occur in the male germline than in the female). For example, a recent Nature article suggests that males contribute 5.25 mutations to the zygote for every one contributed by the female. Given that each human has something like 35 new mutations, that means about 30 of them are from the father and 5 from the mother. My numbers aren't dead accurate, but you get the idea. articleYes. The only reason this seems curious is that there is a gap of one generation before the mutation's effects make themselves felt. The mutation has occured in (say) the egg that was fertilized in order to give rise to the MOTHER. It is only expressed when the mother reaches maturity and gives birth to offspring. This is kind of neat but is not different in any way to the standard view of evolution. It's just that mutations make themselves felt at different points in the life cycle.For example, we could imagine "a gene for being a good grandmother". This gene arises by mutation in an ovum. It only makes itself felt, and is only subject to natural selection, after two generations. That's right, a mutation that is only subject to natural selection after a gap of one generation. The focal child develops in an unusual manner because of a mutation that occured in the ovaries of its grandmother! No different to the standard feedback scenarios that operate in areas other than reproductive biology. For example, say you get a mutation in one of your sperms, that affects the biding site of a hormone to its receptor. The mutation makes the hormone receptor less likely to bind to its substrate. Your offspring suffer from reduced reactivity to normal levels of the hormone. All of your offspring will be subject to positive selection on any mutation IN THE HORMONE that makes it better match the receptor's binding site. The example given by Cal (chorionic gonadotropin) is just a special case in which the receptor is active in the mother and the hormone is active in the fetus. But there's no theoretical difference to the case in which hormone and receptor are active in a single individual.Hope this helps!Mickin edit:I added the word "fixed" the paragraph beginning "Consider your sperm". I capitalized the word. I think that's an important factual clarification. Obviously many mutations occur outside the germline.This message has been edited by mick, 10-22-2005 08:36 PMThis message has been edited by mick, 10-22-2005 08:40 PM

If there are "mutations" associated with follicle attachment in the ovary it seems to me that indeed biologists might have missed something. I often think about this in Mendel's use of the sign "/" when comparing eggs and pollen. The fact that genetics did not attend perspicuously to Mendel's so-called "developmental binomial" I still think theory might be able to ferret out a specific empirical catgegory to further look into the issue you raised. I have not given this a lot of thought recently as it really involves dealing with Mayr's citations of Schamallhausen against population genetics. I wish, but I am not doing a thesis on that.