New findings in gene knockout, mutant and transgenic mice.
During the past year, some novel genetic modifications were shown to alter the lifespan of mice, thus expanding the list of genes and physiological processes that influence mammalian aging. Considerable progress was also made in identifying putative mechanisms of extended longevity in previously described gene knockouts, mutants and transgenics. In addition, new leads concerning mechanisms of aging were derived from studies of gene knockout mice in which aging is accelerated. Among the important findings from the period July 2006 to July 2007: Core body temperature was shown to influence longevity in homeothermic animals; a Surf1 gene knockout extended lifespan in mice; separate studies using Little and Snell dwarf mice found stress resistance enhancements correlated with longevity gains; and mice heterozygous for deletion of insulin receptor substrate 2 (IRS-2) lived longer than normal animals, while animals with homozygous or heterozygous deletion of IRS-2 selectively in the brain exhibited comparable extension of lifespan and various symptoms of delayed aging.
Department of Internal Medicine and Physiology, Southern Illinois University School of Medicine, Springfield, IL 62794-9628, USA. abartke@siumed.edu
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Bartke
D000375:Aging / Q000235:genetics*; D000818:Animals; D001831:Body Temperature; D015870:Gene Expression; D055504:Insulin Receptor Substrate Proteins; D047908:Intracellular Signaling Peptides and Proteins / Q000235:genetics; D008136:Longevity / Q000235:genetics*; D051379:Mice; D018345:Mice, Knockout; D008817:Mice, Mutant Strains; D008822:Mice, Transgenic; D023421:Models, Animal; D010750:Phosphoproteins / Q000235:genetics
D055504:Insulin Receptor Substrate Proteins; D047908:Intracellular Signaling Peptides and Proteins; C526298:Irs2 protein, mouse; D010750:Phosphoproteins