Goals: In the previous lecture, you learned about proposed relationships between development and evolution. The patterns suggested by von Baer's law and Haekle's law were described before anyone knew anything about the genetics that underlie the developmental process; hypotheses of heterochrony were developed when people had observed more of the causes of embryogeny. Today, we know even more about the genetics of development. It turns out that there are genes that regulate the expression of other genes. Some of these have been related to the development of complex structures in animals. This will be the focus of the lecture today.
Related Textbook Material: Freeman and Herron (2001) Chapter 17
Lab Manual Questions over this material are in Lab Manual Chapter XVIII
HOM/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 HOM/Hox genes that determine the position of the structural features within individual structures of the body, such as the limbs.
The evolution of HOM/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 HOM/Hox genes.
HOM/Hox genes are arranged on chromosomes in a highly organized fashion. Features of their organization on chromosomes include:
The fact that HOM/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 HOM/Hox genes may have resulted in the potential for more structural complexity in animals. It would make sense that if HOM/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 HOM/Hox genes than earlier animals had. This was determined by mapping the number of HOM/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 HOM/Hox genes -- apparently BEFORE all the diversity of structural complexity evolved -- suggests that HOM/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 HOM/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 HOM/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.
Study Tips: