- BOSTON - A simple mistake in cell division can trigger signs of aging,
according to an MIT study to be published Friday.
- Two MIT scientists say the cause of aging
may be prompted by a "mistake" that causes circular bits of redundant
DNA to accumulate within cell nuclei. This buildup clogs normal cellular
- David A. Sinclair and Leonard Guarente
performed the study on brewer's yeast cells, but believe the same process
occurs in humans.
- "At the moment this is our best
candidate for what goes wrong in aging," Guarente told The Boston
Globe. He said while he and his colleagues are searching for the phenomenon
in other "diverse" species, finding proof in human tissues "may
be a long process."
- The scientists' find, published in the
journal Cell, stems from work on a rare human disorder of premature aging
called Werner's syndrome. Because of gene mutation, affected individuals
appear normal until their teens, then develop signs of accelerated aging
and die in their 30s.
- Guarente and Sinclair have been studying
the gene defect in the yeast cells and how it causes the organism to become
infertile, show signs of aging and die after a lifespan half that of normal
- The MIT scientists noticed yeast cells
- with a defect similar to the Werner's syndrome defect - had abnormalities
in a structure within their nucleus called the nucleolus.
- "Because ribosomal DNA is the most-repeated
DNA sequence in the cell, the cell has a challenge in keeping these repeated
DNA sequencing stable," Guarente said. "These repeats could be
the Achilles' heel of the cell."
- Occasionally, a circular chain of ribosomal
DNA "pops out," he said. Whenever the cell divides, these useless
circles multiply too, eventually becoming so numerous that the ribosomes
that contain them burst, accounting for abnormalities that MIT scientists
first observed in yeast cells with the premature-aging gene.
- If the MIT researchers' theory is found
to describe aging in other species, they think they may be able to find
a way to slow it down.