On BioScience and Life and Such

On ScienceBlogs 27/-1-08: Quick-Change Evolution

In Uncategorized on January 27, 2008 at 9:46 pm

I have so much to learn, and I’m looking so much forward to learning it. This time around it’s in evolution theory, and I’m going to make some bold statements while learning.

Some recent posts here on SciPhu has been on Hsp90 and rapid morphologic evolution. On ScienceBlogs the topic of the day is Quick-Change Evolution. The background is a blogpost by Olivia Judson stating the return of the hopeful monster. The hopeful monster theory says that extensive morphologic changes in one individual offspring (a monster – an individual organism looking radically different from the rest of its species), sometimes creates beneficial features enabling the monster to create further offspring with similar features. In this way one can achieve rapid evolution (as short as one generation) into the beginning of a new species. The theory is a controversial one and is also called punctuated equilibrium. I however, am apparently at odds with most science bloggers and evolutionary biologists, since the hopeful monster theory sounds plausible to me. How is this linked to Hsp90 you may wonder. Well…

Knocking down Hsp90 creates rapid morphological changes from one generation to the next (for details see references in my previous posts Evolution too fast for our genes to follow, On Hsp90 and morphological evolution and The rate of evolution/mutation/adaptation and future posts to come). Hsp90 does so by masking mutations under normal conditions and then revealing them under stressful conditions. Just to repeat myself, – this concept suddenly made evolution comprehensible to me, and I do not understand why other scientists haven’t embraced the masking concept as a revolutionary concept, expanding darwinian evolution theory.

Now it’s dawning on me why…….Such masking of mutations to produce a pool of potentially crucial mutations gives support to the hopeful monster theory.

One of the main criticisms of this theory, as far as I can understand, is the improbability of a single mutation to give rise to radical morphological changes, and further that this change, if it happens, is most likely deleterious, and if it against all odds is beneficial, its even more improbable that this individual is able to produce offspring with the same trait(s). But…..

Extensive morphological change has been shown to happen due to single mutations, and…

With Hsp90 as a player in the game, it need not be a single mutation, but rather a pool of mutations already present and waiting to be exposed under stress. That increases the chances of achieving multiple changes in multiple individuals. Consequently the chance(s) of producing one or more beneficial trait(s) is(are) increased.

In addition, if such stress appears and mutations are revealed, then many individual offspring will have extensive changes, and the chances for two such individuals to mate increase dramatically.

Thus, I cannot see why a combination of the hopeful monster theory and the actions of Hsp90 (and possibly other mutation masking proteins) under stressful conditions, is a perfectly credible extension to darwinian evolution. An extension that can explain some of the rapid changes that has occured during evolution of species.

  1. Good try Sciphu (blog #126 NY Times 28 Jan)! Yes, the mutations could accumulate but they would be silent (non-expressed) and normally functioning HSP90 would keep them so. Then, with a mutation in the gene for HSP90, the latter’s function could be impaired and a strange new phenotype (“monster”) could appear.
    Some problems with this include: 1. The phenotype would be conditional, depending on coinheritance with the HSP90 mutation. Another process (some call it “genetic assimilation”) would be needed to disengage the family of mutations from dependence on the HSP90 mutation (since, in the long run HSP90 mutations should prove deleterious). 2. Even if this occurred, the monsters would not be reproductively isolated from the main group. In fact, they would be more likely to meet a member of the main group of the opposite sex than one of their fellow monsters of the opposite sex. So, in a short time their family of mutations would become shuffled with the normal genes and the monster phenotype would be lost (blending inheritance).

  2. Thank you for the comment, good to see that I have inspired someone with knowledge in this field. My background is biochemist turned molecular biologist and my knowledge in genetics of evolution is somewhat limited. But, yes I am trying. Luckily I am not the only one, better people than me has written about this (see the reference and do pubmed searches on Hsp90 and evolution). To respond to your objections: Mutations in Hsp90 is not needed to expose these morphological traits. Hsp90 is functioning normally, but there is less protein (or protein activity to be precise). This is explained in more detail in the Susan Lindquist paper and in a review in Cell research from 2006 (Cell Research (2006) 16: 742–749. doi: 10.1038/sj.cr.7310090; published online 29 Aug 2006). What happens is that normal Hsp90 is titrated away during stress and differences in the “mutated” protein is exposed. Consequently, no need for coinheritance taking away your objection #1. When it comes to your point two, I would say that your argument is only true if the “monster” traits do not confer increased fitness in the stressful environment. If the “monster” is more likely to reproduce (a significant number of normal individuals is dying off) you have evolution into new (monster) traits. Also they could be reproductively isolated, – in the case of the the fruitflies, some of the morphologic changes occur in the wings and if flying ability is decreased/increased then you could imagine that you get geographical separation between the normal group and the “monster” group, – …..reproductive isolation.

  3. OK. We will allow HSP90 not to be mutated. At a time of stress we will postulate that HSP90 is used up quicker than it can be synthesized so there is not enough available to keep your postulated family of mutations quiet.
    Let the monster phenotype required dominant mutations in genes 1-5. Since mutations are rare events, they will take some generations to accumulate. But during each generation an individual is subjected to stresses on many occasions. So mutation in gene 1 has to be non-lethal for sufficient generations for mutation 2 to appear. Then mutations 1 and 2 have to be non-lethal for sufficient generations for mutation 3 to appear … etc. Another individual of the opposite sex has to go through the same process, although not necessarily mutate genes in the same order – say 4, 2, 1 , 5, 3. Now the two monsters exist and, if they can find each other, can reproduce together. This is but one of a variety of scenarios that to many appear quite improbable. For example, you could argue that the mutations are all recessive and only when all are present together does dominance emerge (epistasis). As for improbability, you could argue that, consistent with this, speciation itself is a rare event.
    Now for reproductive isolation (necessary to prevent mixing of genes with the parental type). The postulate that some form of geographical isolation will allow the pair to reproduce their kind has been the mainstay of classical Darwinism. Given that, and given the (unlikely) possibility of some advantage over the parental types, then certainly your monsters could thrive.
    But Goldschmidt doubted that geographical isolation has been the most usual form of reproductive isolation. He proposed in his 1940 book (Judson’s source) that silent mutations accumulate in genomes to an extent that there is a change in “reaction system.” Only individuals with the same reactions systems can reproduce with each other. They are reproductively isolated from other members of their species and thus, by definition, are a new species (even if displaying no anatomical or functional differences from the parent species). This isolation is as secure as if they were separated geographically, but a beneficial mutation occurring in the new species, be it micro or macro (i.e. a monster), will allow members of the new species to preferentially survive.
    Judson and others are confused because Goldschmidt refers to a change in reaction system itself as a macromutation. Goldschmidt’s macromutation is a profound dispersed change in genotype, not phenotype. By virtue of this macromutation (genotypic mutation), Judson’s hopeful monsters (phenotypic mutations) could survive.
    Along your line of thought you might care to consider Goldschmidt’s “phenocopy” phenomenon. Certain genes are required only during short developmental time-windows. A stress during pregnancy (Goldschmidt’s heatshock) could deplete HSP90 to such an extent that there was insufficient available to tidy up a critical gene affecting development. A mutant organism would emerge. However, even if crossed with a similar mutant organism, the mutant type would not reappear (i.e. their offspring would be normal) because there had been no change in genotype. Only stress during the critical time-window would produce the phenocopy.

  4. The whole “hopeful monster” and “punctuated equilibrium” discussions show how far off track evolutionary theory is. Do the arithmetic. 650 million years since cambrian explosion. About 20,000 extra genes in an advanced species. Individual genes do little – they function as part of genetic mechanisms each of which has several genes. So a thousand or two extra genetic mechanisms. Genetic mechanisms have to be complete to function. Most genetic mechanisms such as thise involved in colour vision and blood clotting leave no trace in the fossil record. Some genetic mechanisms do, expecially if they affect the size, musculature, or surface. So a few hundred genetic mechanisms that might leave a trace when they come on-line during 650 million years. One every few million years or so. Looks remarkably like what the fossil record shows to me. A clear demonstration of the fatuity of attempting to describe evolution at a level of inheritance lower than the genetic mechanism. After all, there are genetic mechanisms that will, under the appropriate conditions, create novel genetic mechanisms but there are no genes or alleles that under any conditions generate new genes.

  5. I assume there is information out there regarding this, but I have been thinking about this idea for some time:
    It seems to me that punctuated equilibrium is speeded-up temporally in brief spurts due to the fact that mutations (and perhaps the transposition of genes/chromosomes) rarely have one effect, but multiple effects. For survivorship, the overall effect of all the changes must be a net positive, even if several other effects may, in fact, be otherwise. For example, a person with Down Syndrome shows a whole range of traits due to one genetic change. Now, if Down Syndrome were positively selected for, would not evolution begin to work on not only the mental change, but also on the other secondary signs of Down Syndrome, such as increased flexibility, larger tongue, etc… Any one of these secondary traits could turn out to be as important or more than other traits in adapting to a new niche. Thus, suddenly we have an explosion of new traits to be selected for, leading to a relatively rapid period of increased evolutionary scrutiny until once again stasis is reached, hence the fits and starts theorized by punctuated equilibrium.

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out /  Change )

Facebook photo

You are commenting using your Facebook account. Log Out /  Change )

Connecting to %s

%d bloggers like this: