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Are human disease and senescence the result of Natural Selection?

AutorRodríguez-Pérez, Juan Antonio ; Navarro, Arcadi
Fecha de publicaciónjul-2013
CitaciónXIII Jornada de Biologia Evolutiva (2013)
ResumenThe increasing global ageing of the World’s population, has spurred the interest of research in the causes and mechanisms of ageing and senescence. The physical decay of organisms with age (senescence) has long been an unsolved problem in biology. Even if many authors have proposed solutions to the conundrum, there is no single theory that has universal acceptance or that accounts for the ultimate evolutionary purpose of senescence, if it indeed exists. From a strictly physical point of view, ageing could be seen as the mere consequence of the difficulties in keeping entropy, that is, thermodynamic instability, far from organisms. But from an evolutionary perspective, several theories have been proposed to understand the meaning of senescence. Perhaps the most popular of these theories is the pleiotropic theory of senescence, suggested by Williams in 1957. This theory states that mutations conferring risk for traits that are damaging for the organism late in life (e.g. after the fertile stage) might be maintained in a population if they are advantageous early in life, when they can result in an increased reproductive success. In humans, pleiotropy has been shown to be common in SNPs discovered by genome wide association studies (GWAS), where at least 17% of the genes and 4.6% of SNPs related to examined conditions have been found to be involved in at least 2 or more conditions. The pleiotropic theory of senescence has been shown to be consistent with evidence coming from certain genes (mTOR, from specific conditions (haemochromatosis) or from th e life-long reproductive patterns of a few animal models (swans and the fruit fly). However, an exhaustive assessment of its possible impact in the senescence of our species has not yet been carried out. Using public metadata from Genome-Wide Association Studies (GWAS) we are trying to quantify the global extent of antagonistic pleiotropy in the human species, and to test if it has had any evolutionary implications in susceptibility to disease or recent adaptations.
DescripciónTrabajo presentado en la XIII Jornada de Biologia Evolutiva, celebrada en Barcelona el 2 de julio de 2013.
Aparece en las colecciones: (IBE) Comunicaciones congresos
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