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Turning the Clock Back: Mechanisms of Aging

Studies in evolutionary biology tell us that all living organisms originated from a common ancestor, yet lifespans vary greatly. Clearly, something in the genome accounts for such stark differences; the question is what? Why do we live as long as we do? Why do our bodies break down as we age?

On March 6, Prof. Vadim Gladyshev, medicine, Harvard, led a seminar at Cornell titled “Mechanisms of Aging and Redox Control” that attempted to answer some of these questions.

The study of the mechanisms that affect aging is one of the Gladyshev lab’s newer projects, but it is their extensive work on selenoproteins that led to an interest in the field.

Selenoproteins are any proteins that include the residue of a selenocysteine amino acid. A key component of this amino acid is selenium, an essential trace element in humans and many other life forms. Selenocysteine is interesting because it is coded by the gene bases UGA, which are also used to signal the termination of the process by which ribosomes create proteins.

Gladyshev’s initial interest was on studying how many selenoproteins existed. However, due the intense focus on the human genome project, all genes that encoded selenocysteine were interpreted as termination signals. Gladyshev’s lab was one of the first to predict that these genes could be used to code for selenocysteine. Using both the organization of RNA structures and looking at similar proteins, Gladyshev’s lab found that the human genome has genes that code 25 selenoproteins.

Selenoproteins are common in eukaryotes, cells that contain subunits enclosed in membranes. Mammals contain selenoproteins but most other organisms have a cysteine-containing protein, in which the selenium atom is replaced by one of sulfur. One gene that is functionally connected, evidenced by a similar pattern of occurrence, with the selenoprotein is MSRA, the gene that helps code a family of enzymes known as methionine sulfoxide…

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