From here:

Scientists have shown in literally thousands of studies that the p53 gene deserves its reputation as "the guardian of the genome." It calls to action an army of other genes in the setting of varied cell stresses, permitting repair of damaged DNA or promoting cell death when the cell damage is too great. A key net effect of p53's action is to prevent development of cancerous cells.

Now, University of Michigan Medical School scientists provide the most thorough evidence yet that p53 also regulates a trio of genes from the realm of so-called "junk" genes "” the roughly 97 percent of a cell's genetic material whose function is only beginning to be understood.

The article ENCODE finds the human genome to be an active place, by John Timmer, is provacative. The issue it highlights serves as a useful focal point around which to contrast the predictive utility of a teleological approach with that of standard evolutionary thinking. This is particularly so since more data relevant to the junk DNA question soon will be forthcoming. From the article:

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From here:

The human and chimpanzee genomes vary by just 1.2 percent, yet there is a considerable difference in the mental and linguistic capabilities between the two species. A new study showed that a certain form of neuropsin, a protein that plays a role in learning and memory, is expressed only in the central nervous systems of humans and that it originated less than 5 million years ago. The study, which also demonstrated the molecular mechanism that creates this novel protein, will be published online in Human Mutation, the official journal of the Human Genome Variation Society. [..]

Led by Dr. Bing Su of the Chinese Academy of Sciences in Kunming, China, researchers analyzed the DNA of humans and several species of apes and monkeys. Their previous work had shown that type II neuropsin, a longer form of the protein, is not expressed in the prefrontal cortex (PFC) of lesser apes and Old World monkeys. In the current study, they tested the expression of type II in the PFC of two great ape species, chimpanzees and orangutans, and found that it was not present. Since these two species diverged most recently from human ancestors (about 5 and 14 million years ago respectively), this finding demonstrates that type II is a human-specific form that originated relatively recently, less than 5 million years ago.

Gene sequencing revealed a mutation specific to humans that triggers a change in the splicing pattern of the neuropsin gene, creating a new splicing site and a longer protein. Introducing this mutation into chimpanzee DNA resulted in the creation of type II neuropsin. "Hence, the human-specific mutation is not only necessary but also sufficient in creating the novel splice form," the authors state.

The results also showed a weakening effect of a different, type I-specific splicing site and a significant reduction in type I neuropsin expression in human and chimpanzee when compared with the rhesus macaque, an Old World monkey. This pattern suggests that before the emergence of the type II splice form in human, the weakening of the type I splicing site already existed in the common ancestor of humans and chimpanzees, implying a multi-step process that led to the dramatic change of splicing pattern in humans, the authors note. They identified a region of the chimpanzee sequence that has a weakening effect on the splicing site that also probably applies to humans. "It is likely that both the creation of novel splice form and the weakening of the constitutive splicing contribute to the splicing pattern changes during primate evolution, suggesting a multi-step process eventually leading to the origin of the type II form in human," the authors state.

I talked briefly about these little RNAs here and here. Now comes the animation that outlines the basic events associated such RNA.

The non-teleological perspective views RNA as a primitive, ancient relic of the process of abiogenesis. The teleological perspective views RNA as a sophisticated molecule that plays an essential control function within the cell and has never existed apart from its cellular context.

While RNA is crucial to all living things, I think eukaryotes have more fully exploited its ability to control the proteome (a cell's protein complement). A simple fact from cell biology explains this. In prokaryotes, the process of RNA synthesis (transcription) is coupled to the process of protein synthesis (translation). This allows bacteria to more efficiently express their genes and the bacterial cell design is all about efficiency. But eukaryotes trade efficiency for flexibility, and as such, have a nucleus where the genome is physically separated from the ribosomes. This means there is a much larger window of opportunity to process and modify protein-encoding RNA in eukaryotes, which in turn means the greater potential for control. One such control mechanism exploited by eukaryotes is alternative-splicing, where a single gene can give rise to dozens of gene products that are variations on a theme.

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