Monday, January 9, 2012

Transposons May Have Played a big role in evolution

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Over the last few years, what scientists had once called “junk” DNA is not quite jusk to them anymore. Scientists have just recently had to deal with the fact that less than five percent of the human genome contains functioning genes. Of the other ninety-five percent, half is anonymous noncoding DNA. The other half is parasitic DNA known as transposons. Researchers now believe that transposons may not have been the excess baggage that people originally took them for, but one real player in evolution. These rogue bits of DNA may be what distinguish us from our closest primate kin.


In the 140’s Barbara McClintock developed the idea that DNA sequences are not always static. They sometimes move around from place to place, leaving biological peculiarities in their wake. With this idea she was able to explain why the Indian corn she was studying did not inherit the coloring in the orderly fashion of Gregor Mendel’s peas. Instead, something was causing variations to appear- more or less at random. The changes, McClintock suggested, were the handiwork of mobile genetic elements, which are today known as transposons. Unable to understand her work, other scientists were reluctant to go along with such an unorthodox idea.


By the 160’s, however, McClintock’s ideas were gaining ground. In 18 she won the Nobel prize for her transposon research. Even now, few scientists have come to terms with just how important transposons might have been during evolution.


One of the people who can truly appreciate their significance is John McDonald, a molecular biologist at the University of Georgia. According to him, “Without transposons nothing more interesting than a bacterium may have crawled out of the primordial mud.”


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McDonald believes that the unseen struggle between transposons and host was responsible for the two major events in animal evolution chromatin formation and methylation.


Methylation occurred around 500 million years ago, when vertebrates like fish, birds, and mammals began to appear. These organisms harbored more genes than any before. Their genomes were littered with molecular additions called methyl groups. Methylation is still poorly understood, but McDonald thinks it added a second layer of gene inactivation over and above that offered by chromatin. Genes lacking methyl groups tend to be available for making proteins. Genes with methyl groups do not make protein. It’s as if these molecular ornaments work like a master switch for shutting down inappropriate activity in the genome. Like chromatin formation, methylation may have arisen as a strategy to defend against transposons. Molecular biologist Adrian Bird has argued, “… that without chromatin formation and methylation complex life would have been impossible…”


Another key player in evolution is the Alu element. Alus are unique to primates, and for some unknown reason, they seem to have spread widely around 0 to 50 million years ago. Each of us has nearly a million Alus. They compose more than five percent of our DNA.


When Reynolds was studying Alus she realized they bore an uncanny resemblance to something she had seen before. She had been working with distinctive DNA sequences that act as anchors points for proteins that bind to hormones. When a hormone is bound this way, it can switch on a whole set of genes, starting a cascade of biochemical events thoughout the body.


These sequences are extremely powerful, so the discovery that they reside is all Alu elements startled Reynolds. As Alus moved during primate evolution, they would have had the power to alter which set of genes got triggered by which hormone and when.


“These Alus could have generated more diversity- but subtle diversity. We’re not talking about knocking out a gene, but just slightly elevating or reducing its expression in certain tissues, so that you could gradually change the evolution of the species. Alus were probably very important in primate evolution, because without them you may never have had the diversity from which to select the primates.”


There are three main types of transposon cut-and-paste, retrotransposon, and horizontal transmission. Cut-and-paste are the simplest, their DNA instructs the cell to make an enzyme that can seek out the transposon, pick it up by both ends, and reinsert it at a new location. A common but more sophisticated variety is the retrotransposon. The cell treats the retrotransposon just like one of its own genes and creates RNA from it. Just after the RNA is assembled, the retrotransposon makes an enzyme called a reverse transcriptase, which cunningly converts the RNA back into a DNA copy that is an exact replica of the original transposon. That duplicate then finds a new place along the genome and takes up residence.


Transposons have also managed to escape from their hosts and move to new ones, sometimes from a different species, by a mysterious process called horizontal transmission. Although no one knows exactly how it happens, the transposons probably hitch a ride on an unsuspecting virus that happens to have infected the host. The transposon jumps on board, and its free.


Entomologist Hugh Robertson of the University of Illinois found evidence for hundreds of such cases of horizontal transmission, sometimes between very different species. That strategy, he believes, may be the transposon’s only means of survival.


“Within any particular host, they will eventually die by mutation and become nonfunctional. By jumping to a new host, they get a new lease on life before dying out in the old host.”





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