A Chromosome 13 locus is associated with male-specific mortality in mice

Gyekis, Joseph P.; Lang, Dean H.; Vandenbergh, David J.; Gerhard, Glenn S.; Griffith, James W.; Dodds, Jeffery W.; Shihabi, Zakaria K.; Tilley, Mera; Blizard, David A.

doi:10.1007/s40520-015-0370-z

Cited by 1 publication

(1 citation statement)

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“…Over the past four decades, 16 studies have been carried out to define QTLs for longevity in mice—a surprisingly modest number given the importance and inherent interest of this topic [79, 96, 121–122, 130, 132–133, 140–148]. The first genetic analysis by Smith and Walford [130] exploited congenic strains and very large sample sizes ( n = 120 per congenic strain) to test whether longevity is modulated by sequence variants in the major histocompatibility complex (MHC, H2 ) on Chr 17.…”

Section: Mapping Longevity Loci In Mousementioning

confidence: 99%

Genetic cartography of longevity in humans and mice: Current landscape and horizons

Hook

Roy

Williams

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Aging is a complex and highly variable process. Heritability of longevity among humans and other species is low, and this finding has given rise to the idea that it may be futile to search for DNA variants that modulate aging. We argue that the problem in mapping longevity genes is mainly one of low power and the genetic and environmental complexity of aging. In this review we highlight progress made in mapping genes and molecular networks associated with longevity, paying special attention to work in mice and humans. We summarize 40 years of linkage studies using murine cohorts and 15 years of studies in human populations that have exploited candidate gene and genome-wide association methods. A small but growing number of gene variants contribute to known longevity mechanisms, but a much larger set have unknown functions. We outline these and other challenges and suggest some possible solutions, including more intense collaboration between research communities that use model organisms and human cohorts. Once hundreds of gene variants have been linked to differences in longevity in mammals, it will become feasible to systematically explore gene-by-environmental interactions, dissect mechanisms with more assurance, and evaluate the roles of epistasis and epigenetics in aging. A deeper understanding of complex networks-genetic, cellular, physiological, and social-should position us well to improve healthspan.

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