A Gutsy Way to Extend Longevity
نویسندگان
چکیده
sis has recently emerged as an important determinant of fly life span (Biteau et al., 2010). The Drosophila midgut is maintained by multipotent ISC activity. ISCs undergo asymmetric division, giving rise to an identical daughter ISC and an immature enteroblast (EB) with differentiation potential (Micchelli and Perrimon, 2006; Ohlstein and Spradling, 2006). In old flies, ISCs hyper-proliferate, but ISC daughter cells do not differentiate, which results in the accumulation of misdifferentiated ISC daughter cells, a phenotype thought to contribute to gut aging. For instance, genetic or environmental manipulations that prevent tissue maintenance have been associated with accumulation of ISCs, irregular ISC proliferation and differentiation patterns, and shorter lifespan (Biteau et al., 2010). Likewise, genetic manipulations that preserve ISCs homeostasis extend longevity (Biteau et al., 2010). Rera et al. (2011) demonstrated that the age related decline in mitochondrial activity observed in the midgut epithelia may be a key component in the loss of ISCs homeostasis. The authors showed that increasing levels of dPGC-1, specifically in the immature cells and their progeny in the midgut is sufficient to extend longevity. The transcription factor escargot (esg) is a marker for ISCs and EBs. They used the esgGal4/dPGC-1/UAS and the 5691GeneSwitch/dPGC-1 UAS system, to drive expression of dPGC-1 in esg-positive cells. dPGC-1 overexpression in esg-positive cells resulted in preservation of mitochondrial membrane potential and increased activity of mitochondrial complexes I and II.
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عنوان ژورنال:
دوره 3 شماره
صفحات -
تاریخ انتشار 2012