Posts Tagged ‘adaptation’

Darwin in the first chapter of his treatise “On the Origin of Species By Means of Natural Selection” talks about variation in domestic animals. He starts the chapter by saying:

When we look to the individuals of the same variety or sub-variety of our [….] animals, one of the first points which strikes us, is, that they generally differ much more from each other, than do the individuals of any one species [….] in a state of nature.”

Read it once more, YES!!! he said that there is more variation (breeds or varieties) among domesticated “species” like dog, cat, coconut palms etc., when compared to wild animals (or plants) like Lion (which has no breeds or varieties). He says (recognizes) that it is due to selective breeding. But how did this variety occur? He provide clues a few sentences later in the same chapter.

But I am strongly inclined to suspect that the most frequent cause of variability may be attributed to the male and female reproductive elements having been affected prior to the act of conception.”

Remember that no one knew about genes, and alleles as the basis of heridity at Darwin’s time. So his was a new observation, that guided us later. So is there any one out there fascinated about the variety among domestic animals those reproductive elements? You have a really great paper to read which shows the mechanism of evolution, the process of fixation of a variation and passing over of that variation by Schoenebeck and others. These kind of studies, does, not only study how a breed evolved but also shows us the greater picture of how evolution occurs. In a meticulously worked out paper, which should be a hard read for non-experts, they study dog breed skull shape variations.

The paper starts saying that “dog breed skull shape diversity is a largely human created phenomenon (paraphrased)”, through artificial selective breeding.

What does the paper say about this skull shape variation? It says many things but importantly provide fascinating details about how a single mutation could lead to a prominent change in skull shapes. There are more details and it is not just about a mutation, although.

They looked at two extremes of skull shapes one with flat snouts and the second with long snouts. In essence they analyze, dog skull shapes, by grouping the Bulldogs, Boxers, Pitbulls, Pugs etc., in one extreme and the Collies, Greyhounds, Saluki etc., in the other extreme. Other breeds fell in between these extremes, for the skull shapes, of long snout (dolichocephaly) to flat snout (brachycephaly).

In a very rigorous analysis they found that the change in an amino acid (building blocks of proteins) on the 452nd position of the bone morphogenetic protein 3 (BMP3) gene of brachycephalic dogs have been the reason of their short snouts. It is easily said in a sentence, but the authors have put in a lot of details, they even show the a similar mutation when induced in the zebrafish, can make its cranio-facial morphology to go weird—similar to your pitbulls!!

Brachycephalic dogs have an amino acid named Leucine (L) at the 452nd position of the BMP3 gene, which is normally an amino acid called phynylalanine (F) in normal snouted dogs and other animals. So was it a “abracadabra” F452L that produced brachycephalic dogs? Yes and no, this mutation somehow formed in few dogs, which (dog) was seen by multiple independent breeders to develop such diverse brachycephalic breeds. Now these researchers see and present us the mutation as a story about what happened while selectively breeding such variants.

If you are not a science student, you should be exhausted by now, ok that is it remember F452L!!!! And remember next time when you play with your bulldog ask it about that Leucine!!!

For interested people read further or grab the freely download-able paper at the PloS Genetics Website.

They started analysing skull shapes of dogs, available in museums and private collections. The “shifts” in shape was examined by measuring more than 500 skulls from more than 100 different breeds of dogs. The 3D measurements were statistically analysed to explain the variation among the measurements between each breeds, and they found a sub-set of “promising” measurements that could explain the changes in skull shapes.

In the next step they used this “phenotype” data to do an association study, for the genotype data they generated. The paper explicitly says that the task was straightforward since pure-bred dogs would have a very strong visual phenotype, that would not vary, thus could be used to correlate the genotype data when generated from similar pure-bred animals. So they carried out genome-wide scans to detect any genotype association to a breed phenotype, using SNP datasets.

They found 5 promising Quantitative Trait Locii (QTL’s), for which there was strong association with the “flat snout-long snout” phenotype range. One of these QTL’s contained regions of genes BMP3 and PRKG2. They could zero down on the BMP3 gene or the bone morphogenetic protein 3 gene position 452. This position possess an amino acid called Leucine, in flat-snouted dogs, instead of another amino acid called phenylalanine which is found in normal snouted breeds.

NB: I would not mind, as a reader, if they had made the abstract and the introduction a bit longer 🙂

Jeffrey J. Schoenebeck, Sarah A. Hutchinson, Alexandra Byers1, Holly C. Beale, Blake Carrington, Daniel L. Faden, Maud Rimbault, Brennan Decker, Jeffrey M. Kidd, Raman Sood, Adam R. Boyko, John W. Fondon III, Robert K. Wayne, Carlos D. Bustamante, Brian C (2012). Variation of BMP3 Contributes to Dog Breed Skull Diversity PLoS Genetics, 8 (8)

ResearchBlogging.org

Darwin built his theory of Evolution on two pillars, “heritable variations” and “survival of the fittest” by which occurs evolution by the means of natural selection. How did the heritable variations move from one generation to the next? The genes (we know that alleles) carry the variation in the parents to their offspring. Survival of the fittest, said that the organism with the most advantageous trait or character survived, at intra- and inter- population or species level. So what generates the variation and the chance of survival or adaptability?

At the molecular level we know about mutations, which are stabilized in the population or species ( then called substitutions), can be a reason for variation. We are aware about the neutral theory of evolution pertaining to the genome level or molecular level. Wherein we learned that most (deleterious) mutations are “purified”, and the variation at the genetic level is as a result of random fixation of mutations or random genetic drift. The evidence for this is that if natural selection was the reason for the genetic level variation then the key genes responsible for the functions would be evolving faster (fix more mutations/carry more substitutions since they are advantageous and are naturally selected) but this is not the case, key genes always are same between organisms say at an evolutionary scale of metazoa for example. We should not confuse that there is no positive selection or fixation of advantageous (?) mutations in key genes, it is present but to a smaller extent as opposed to the neutral (or nearly neutral) evolution, it can be episodic events in most cases for key genes.

Another set of variation at molecular level could be due to expression differences, in time (heterochrony), in cells (heterotopy) and in amount (heterometry). But are these the only source of variation? if so (so much variety) what we see, how could we explain it? We should understand that the variation in morphological traits, physiology and behaviour is guided by natural selection and that neutral theory (or nearly neutral theory) pertains only to the molecular level. Apart from these mutation and expression level variation, there are other sources as well, the epigenetic variations, the phenotypic plasticity and the symbiont variation that can be selectable and indeed heritable, which is what the paper of our interest today says.

If the symbiont or (microbiome) of the organism and its genome are in intricate connection (then they can be considered the holobiont) then evolution of the organism cannot be separated with the co-evolution and co-development of its microbiome. Nature has examples for horizontal and vertical transfer of symbionts between generations. The symbiotic association of the luminiscent Vibrio fischeri on the ventral side of the squid Euprymna scolopes is an example of horizontal transfer and association of symbiont. We know this association is crucial for the survival of the host (to avoid predators) and the symbiont benefits by getting a safe place to live in. The cases of Wolbachia in arthropods (wasps) are perfect examples of vertical transmission of symbionts wherein the eggs contain the bacteria and any egg (treated) without the bacteria perishes or fails to develop. As we look deeper, even human guts harbor these kind of symbionts without which we would not be able to survive and is transmitted vertically from mothers. So should be every case of each and every organism, but proof is lacking since investigations in that angle is just gaining momentum.

Selection (natural selection) of the symbionts associated with the host due to environmental cues are presented in the paper as well. They present the case of coral-zooxanthillae symbiosis and selection of a specific strain of the microalgae in response to elevated temperatures to form the dominant community. The temperature tolerance of desert plants (and many other plants) and the inhibition of the HSP 90 (for temperature tolerance) is provided by external cues provided by symbiotic fungi, the paper provides a strong case of selection of the holobiont in response to the environmental cues. The aphid thermal tolerance is also an interplay between its symbionts (Buchnera being prominent), and this interaction can be disrupted by mutations, showing that the interaction is really selected for.

Reading the paper enables us t0 appreciate the importance of the symbiont in the development and evolution of organisms. Evolution and development is related to the environmental conditions the ecological interactions, the opportunities in environment can lead to adaptions, symbionts fits in nicely as a co-evolving component stressing the view that organisms are not individual units but interdependent. The molecular level selection forms the micro-level, the symbiont and selection forms the intermediate level and ecological interactions and external cues forms the macro-level, of adaptation, developmental variability and eventually evolution.

References:

Scott F. Gilbert, Emily McDonald, Nicole Boyle, Nicholas Buttino, Lin Gyi, Mark Mai,Neelakantan Prakash, and James Robinson, 2010. Symbiosis as a source of selectable epigenetic variation: taking the heat for the big guy. Phil. Trans. R. Soc. B, 365:1540 671-678.