Complexity_ A Guided Tour - Melanie Mitchell [134]
In the 1980s and 1990s, this view became widely challenged. As I noted above, DNA sequencing had revealed the extensive similarities in DNA among many different species. Advances in genetics also produced a detailed understanding of the mechanisms of gene expression in cells during embryonic and fetal development. These mechanisms turned out to be quite different from what was generally expected. Embryologists discovered that, in all complex animals under study, there is a small set of “master genes” that regulate the formation and morphology of many of the animal’s body parts. Even more surprising, these master genes were found to share many of the same sequences of DNA across many species with extreme morphological differences, ranging from fruit flies to humans.
Given that their developmental processes are governed by the same genes, how is it that these different animals develop such different body parts? Proponents of Evo-Devo propose that morphological diversity among species is, for the most part, not due to differences in genes but in genetic switches that are used to turn genes on and off. These switches are sequences of DNA—often several hundred base pairs in length—that do not code for any protein. Rather they are part of what used to be called “junk DNA,” but now have been found to be used in gene regulation.
Figure 18.1 illustrates how switches work. A switch is a sequence of non-coding DNA that resides nearby a particular gene. This sequence of molecules typically contains on the order of a dozen signature subsequences, each of which chemically binds with a particular protein, that is, the protein attaches to the DNA string. Whether or not the nearby gene gets transcribed, and how quickly, depends on the combination of proteins attached to these subsequences. Proteins that allow transcription create strong binding sites for RNA molecules that will do the transcribing; proteins that prevent transcription block these same RNA molecules from binding to the DNA. Some of these proteins can negate the effects of others.
FIGURE 18.1. Illustration of genetic “switches.” (a) A DNA sequence, containing a switch with two signature subsequences, a functional gene turned on by that switch, and two regulatory master genes. The regulatory master genes give rise to regulatory proteins. (b) The regulatory proteins bind to the signature subsequences, switching on the functional gene—that is, allowing it to be transcribed.
Where do these special regulator proteins come from? Like all proteins, they come from genes, in this case regulatory genes that encode such proteins in order to turn other genes on or off, depending on the current state of the cell. How do these regulatory genes determine the current state of the cell? By the presence or absence of proteins that signal the state of the cell by binding to the regulatory genes’ own switches. Such proteins are often encoded by other regulatory genes, and so forth.
In summary, genetic regulatory networks are made up of several different kinds of entities, including functional genes that encode proteins (and sometimes noncoding RNA) for cellular maintenance or building, and regulatory genes that encode proteins (and sometimes noncoding RNA) that turn other genes on or off by binding to DNA “switches” near to the gene in question.
I can now give Evo-Devo’s answers to the three questions posed at the beginning of this section. Humans (and other animals) can be more complex than their number of genes would suggest for many reasons, some listed above in the “What Is a Gene” section. But a primary reason is that genetic regulatory networks allow a huge number of possibilities for gene expression patterns, since there are so many possible ways in which proteins can be attached to switches.
The reason