The study focuses on Atg15, a lipase required for intravacuolar lysis of autophagic bodies and Cvt bodies. Atg15 is located in ER and transported to vacuoles for break down membranes of autophagic bodies.
The known major forms of autophagy include: macroauthophagy, microauthophagy, and chaperone-mediated autophagy. Tang08 argues for an fusion of vauoles with ER vesciles, termed secretophagy, based on Atg 15. Tang08 found that Atg15 is the only autophagy protein that is critical for CR-mediated lifespan extension (Table 1 in Tang08), in the sense that only atgD did not show CR RLS extension effect.
Tang08's table 2 listed RLS under YEPD and CR media (0.5% glucose) for BY4742 (wild type), atg17D, atg10D, vam7D, ypt7D, nyv1D, erg2D-petite (?), erg3D, erg5D, erg6D, erg28D, sur4D, lcb4D, lcb5D, atg11D, vac17D, tco89D, nvj1D.
Interestingly, CR significantly shorten RLS in ypt7D, nyv1D, and erg6D. In figure 4, Tang08 showed that CR exacerbates vacuolar defects in erg6D cells.
My own data showed that nvj1D (?need to double-check this) can extend replicative lifespan.
The pleiotropic role of lysosome-like vacuole in intracellular renewal/repairs mechanisms suggests its role on cellular robustness, which can be detected by Gompertz coefficient based on my network model of cellular aging. The robustness may also be experimentally measured by GFP, DHR, and DHE staining, cellular morphologies etc. I wonder whether the number of genes involved are good enough for regression based analysis of Gompert coefficient and other measures.
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