ژن RAS: یک دستگاه فرمول طول عمر ساکارومایسس سرویزیه
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|38074||1999||8 صفحه PDF||سفارش دهید||5261 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Neurobiology of Aging, Volume 20, Issue 5, September–October 1999, Pages 471–478
The genetic analysis of the yeast replicative life span has revealed the importance of metabolic control and resistance to stress. It has also illuminated the pivotal role in determining longevity that the RAS genes play by the maintenance of homeostasis. This role appears to be performed by the coordination of a variety of cellular processes. Metabolic control seems to occupy a central position among these cellular processes that include stress resistance. Some of the features of metabolic control in yeast resemble the effects of the daf pathway for adult longevity in Caenorhabditis elegans and the metabolic consequences of selection for extended longevity in Drosophila melanogaster, as well as some of the features of caloric restriction in mammals. The distinction between dividing and nondividing cells is proposed to be less important for the aging process than generally believed because these cell types are part of a metabolic continuum in which the total metabolic capacity determines life span. As a consequence, the study of yeast aging may be helpful in understanding processes occurring in the aging brain.
The metric of the yeast life span is the number of divisions (generations) that an individual cell completes or, in other words, the number of daughter cells produced  and . We call this the replicative life span. More recently, aging has also been studied as the length of time yeast cells remain viable in stationary phase . These two rather distinct ways of looking at longevity and aging in this organism may not be as disparate as it would seem. (This statement will be subjected to a critical evaluation later in this article.) Unless stated otherwise, life span will refer here to the replicative life span. Yeasts undergo many morphological and physiological changes as they progress through their replicative life span . Among the most universal age changes are the increase in generation time (the time between consecutive buddings) , increase in size , and progressive decline in mating ability  and . It is difficult to use these changes as biomarkers of aging. The increase in generation time can be uncoupled from life span, resulting in an early appearance of this senescent phenotype . This uncoupling has also been found for size increase . The decline, with age, in the ability to respond to the mating pheromone α-factor has been used to define premature or accelerated senescence in yeast  and . Mutations that give rise to such premature aging cause a redistribution of Sir-transcriptional silencing complexes  and  to either extrachromosomal ribosomal DNA  or double-stranded DNA breaks . This redistribution results in a loss of transcriptional silencing at the silent mating-type loci that is the direct cause of the loss of response to the mating pheromone. Thus, it is difficult to use loss of response to the pheromone as a measure of the global aging process. Perhaps, the loss of mating ability in yeast is the equivalent of a unimodal progeroid syndrome .