Scientists from the Florida campus of The Scripps Research Institute (TSRI; Florida, USA) have found in animal models that a single gene plays a surprising role in aging that can be detected early on in development. Shuji Kishi and colleagues utilized various genetic approaches to disturb Spns1 during the embryonic and/or larval stages of zebrafish—which have emerged as a powerful system to study diseases associated with development and aging. The team produced some models with a shortened life span, others that lived long lives. They showed that Spns1, in conjunction with another pair of tumor suppressor genes, beclin 1 and p53 can, influences developmental senescence through two differential mechanisms: the Spns1 defect was enhanced by Beclin 1 but suppressed by ‘basal’ p53. In addition to affecting senescence, Spns1 impedes autophagy, the process whereby cells remove unwanted or destructive proteins and balance energy needs during various life stages. The study authors report that: “Our findings thus suggest that Spns1 is critically involved in lysosomal acidification and trafficking during autophagy, and differentially acts in a pathway with Beclin 1 and p53 in the regulation of senescence.”
Gene to Combat Aging Identified
Spns1 may mediate the aging process.
Tomoyuki Sasaki, Shanshan Lian, Jie Qi, Peter E. Bayliss, Christopher E. Carr, Shuji Kishi, et al. “Aberrant Autolysosomal Regulation Is Linked to The Induction of Embryonic Senescence: Differential Roles of Beclin 1 and p53 in Vertebrate Spns1 Deficiency.” PLoS Genetics, 26 Jun 2014.
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