The strain's longevity seemed connected with a group of genes whose role was to shut down other genes. But in the longer lived yeast, the sir complex left its usual position and migrated to the cell's nucleus, to a subcompartment called the nucleolus where the ribosomes, the cell's protein-making factories, are assembled. The arrival of the sir complex in the longer-lived yeast strain repressed the genes from which the circles were generated and delayed aging. At this point an intriguing but diversionary hint turned up in the form of the discovery of the human gene for a striking hereditary disease known as Werner's syndrome. Werner's patients generally die in their teens with symptoms of old age such as gray hair, wrinkled skin and cataracts.
Yeast cells possess a helicase- making gene with a similar structure to the human gene.
Dr. Guarente and his colleagues showed that when the yeast helicase gene is disrupted, the yeast cells become more sensitive to the waste circles and age prematurely. But just as everything seemed to be hanging together for establishing a universal mechanism of aging, two of the elements fell apart. No waste circles could be seen building up in the nucleolus of animal cells. And the yeast counterpart to the Werner's syndrome gene does not seem to be central to aging because adding extra copies of it does not enhance life span. Nevertheless, Dr. Guarente felt sure that the silencing of genes was a profound enough process that it was likely to tie in somehow with the equally profound process of aging, and that in higher organisms the failure of silencing might lead to some less visible damage than the waste circle build-up seen in yeast.