Molecular Evolution: Molecular Studies of Evolutionary Processes

NOTE: These are lecture notes for Biology 391, Organic Evolution, at The University of Tennesee at Martin.  Anyone outside of UT Martin wishing to use these notes or to contact me for additional information should first read the information obtained by clicking here.

Goals: Learn how DNA studies are providing information about evolutionary processes such as adaptation, convergent evolution, origin of new genes, key innovations and adaptive radiation, and relationships between development and evolution

Related Textbook Material: Freeman and Herron (2001) Chapters 4, 17, and 18

Lab Manual Questions over this material are in Lab Manual Chapter XII


The Lecture:

Studying natural selection at the DNA level:
 
Most mutations that affect the phenotype are likely to be harmful.  At the DNA level, we say that such harmful mutations are subject to negative or purifying selection, the loss of harmful mutations through natural selection.  Sites in the DNA subject to negative (purifying) selection will show stasis: lack of evolutionary change.  In contrast, some mutations are beneficial and subject to positive selection: natural selection leading to increase and fixation of a mutation.  Sites subject to positive selection will show replacement substitutions: changes in DNA that lead to the presence of new amino acids (amino acid substitutions).
 
To study positive or negatve selection in DNA, we can compare rates of replacement substitution to rates of silent substitution.  If replacement substitution rates are much lower than silent, we have evidence of negative selection -- these traits are evolving more slowly than expected through neutrality, suggesting there is selection against traits arising at these sites.  In constrast, if replacement substitution rates are higher than silent substitution rates, we have evidence of positive selection -- such sites have evolved more rapidly than they would through drift, suggesting selection favoring them and leading to rapid evolutionary change.
 
Studying the origin of new traits:

One source of new traits is gene duplication.  Unequal crossover in meiosis can lead to duplicated genes.  Once there are two copies of a gene with the same function present on a chromosome, one copy is likely subject to negative/purifying selection to maintain the original function, but the other is freed of selection for that function and if mutations arise that give it a new, beneficial function -- a new trait -- it will be subject to positive selection.  To study this, we can look for gene duplications by seeing if there are genes, especially near each other on a chromosome, that have much common sequence, suggesting one arose as a duplicate of the other.  We can then compare the copies and look to see if one has been subject to negative, the other positive, selection.
 
Regulatory genes are genes whose protein products (that is, the proteins for which they code) affect the expression of other genes. That is, instead of coding for proteins that act directly as enzymes in the biochemical processes of cells, or that make up structures, regulatory genes code for proteins that bind to DNA and determine whether or not other genes will be transcribed.  Changes in regulatory genes can potentially lead to large scale changes in traits; the existence of regulatory genes can provide the basis for changes in other genes to lead to new traits.

Hox genes are regulatory genes that affect the development of the basic aspects of structure of an animal. These basic aspects of structure include determination of which end becomes the head, and where structures are positioned from the head end to the tail end in an organism. There are also Hox genes that determine the position of the structural features within individual structures of the body, such as the limbs.

The evolution of Hox genes has been studied phylogenetically to determine how the evolution of these genes may be related to the evolution of the structural complexity of organisms. To understand how this works, you first need to know something about Hox genes.

Hox genes are arranged on chromosomes in a highly organized fashion.  Features of their organization on chromosomes include:

The fact that Hox genes with similar function occur near each other suggests that they originated, evolutionarily, through gene duplication. Gene duplication occurs when an extra copy of a gene is made, along a chromosome, next to the original copy. This kind of mutation occurs because of errors during crossing over during meiosis; if the homologous chromosomes are not perfectly aligned it is possible for crossing over to result in the copies of a gene from both chromosomes ending up on the same chromosome (the other chromosome would be missing this gene, and would most likely result in a non-functional gamete, but the gamete getting two copies of the gene would probably be OK since it has all the genes it needs, plus an extra copy.)

Gene duplications creating more Hox genes may have resulted in the potential for more structural complexity in animals. It would make sense that if Hox genes are important in determining the organization of body structure, then the presence of more of them may allow for more complex organization and more complex structure. Phylogenetically, in the animals, it appears that the ancestor to the group that contains both the arthropods (insects and relatives) and the vertebrates evolved a higher number of Hox genes than earlier animals had. This was determined by mapping the number of Hox genes present in species onto a phylogeny of animals to determine where they originated, just as we have done to study adaptation through the phylogenetic comparative method (click here if you need to review the lecture on the phylogenetic comparative method)

The fact that the ancestor to the more structurally complex animal groups had evolved a larger number of Hox genes -- apparently BEFORE all the diversity of structural complexity evolved -- suggests that Hox genes may have been a key innovation, as discussed in the lecture on adaptive radiation and species selection. (Click here if you need to review the lecture on species selection.) That is, once a larger number of Hox genes evolved, it made the evolution of diverse structures possible, and these allowed animals to use the environment in a diversity of ways. This may have contributed to the high rate of speciation that occurred in these groups and produced the major forms of complex animal life. Your textbook refers to this time of high speciation and evolution of structural diversity as "the Cambrian Explosion."

So far, we have considered regulatory genes, specifically Hox genes, generally. Now we will consider a specific example of how the development of a structure is regulated genetically. By doing so, we can look at the possible relationship between the evolution of regulatory genes and heterochrony (remember from the previous lecture that heterochrony refers to mutational changes resulting from speeding up or slowing down the process of embryonic development.)

The example we will look at (both in this lecture and in your textbook) is the tetrapod limb -- that is, the arms and legs of the vertebrates that dwell on land. The tetrapod limb (arm or leg) develops initially as a bud of tissue. As it develops, different molecules secreted by different different developing tissue zones cause define the three spacial axes through which limbs develop: anterior-posterior (head end versus tail end), dorsal-ventral (back versus stomach sides), and proximal-distal (close to the body versus distant from the body). Hox genes are also active during development and apparently regulate cells based on how far along the limb they are.

The shape of limb that develops depends on the amount and timing of expression of the molecules that determine axes along the three axes.  Changing in timing or amount of expression could occur as a result of mutation in the genes regulating their expression -- in regulatory genes.  Such mutations would change the rate at which the limbs develop.  Remember from the previous lecture that mutations that change the rate of development are called heterochrony. Here we can see at a molecular level how heterochrony could arise through mutations in the genes that regulate timing and amount of molecules produced, and provide the basis for the evolution of the various sizes, shapes, and functions we see in the vertebrates.  So we can see that the patterns initially described by general descriptive laws such as von Baer's Law, and then explained based on heterochrony, now have been demonstrated as plausible by studies on the molecular level.

Regulatory genes and "deep homology":  homologous regulatory genes may provide the basis for independent evolution of similar traits.  For example, structurally diverse parts of the body that stick out such as echinoderm tube feet,  vertebrate limbs, arthropod limbs, "parapodia" on annelid worms, and the soft segmented legs of onychophorans ("velvet worms"; thought to be possible intermediates between annelid worms and arthropods) are all based on the presence of the same regulatory gene ("distal-less") although phylogenetic analysis indicates several of these evolved independentlyl.  So traits can have homologous regulatory genes that provided the bases for the independent evolution of similar traits based on the presence of those regulatory genes.
 
Convergent evolution, at a genetic level, is thus possible in two main different ways.  One possibility is that there are some regulatory genes or other genes that act as "switches" to turn on and off expression of traits that can lead to the same traits evolving independently -- the genetic basis for those traits was present ancestrally, but switched off and on independently.  Another possibility is that convergent evolution is really independent -- different mutations in different genes lead to the same traits in different species.
 

Questions? e-mail me at rirwin@utm.edu

Click here to return to the index of lectures