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Background  Autophagy and molecular chaperones both regulate protein homeostasis and maintain important physiological functions.  Atg7  ( autophagy-related gene 7 ) and  Hsp27  ( heat shock protein 27 ) are involved in the regulation of neurodegeneration and aging. However, the genetic connection between  Atg7  and  Hsp27  is not known.    Methods  The appearances of the fly eyes from the different genetic interactions with or without polyglutamine toxicity were examined by light microscopy and scanning electronic microscopy. Immunofluorescence was used to check the effect of  Atg7  and  Hsp27  knockdown on the formation of autophagosomes. The lifespan of altered expression of  Hsp27  or  Atg7  and that of the combination of the two different gene expression were measured.    Results  We used the  Drosophila  eye as a model system to examine the epistatic relationship between  Hsp27  and  Atg7 . We found that both genes are involved in normal eye development, and that overexpression of  Atg7  could eliminate the need for  Hsp27  but  Hsp27  could not rescue  Atg7  deficient phenotypes. Using a polyglutamine toxicity assay (41Q) to model neurodegeneration, we showed that both  Atg7  and  Hsp27  can suppress weak, toxic effect by 41Q, and that overexpression of  Atg7  improves the worsened mosaic eyes by the knockdown of  Hsp27  under 41Q. We also showed that overexpression of  Atg7  extends lifespan and the knockdown of  Atg7  or  Hsp27  by RNAi reduces lifespan. RNAi-knockdown of  Atg7  expression can block the extended lifespan phenotype by  Hsp27  overexpression, and overexpression of  Atg7  can extend lifespan even under  Hsp27  knockdown by RNAi.    Conclusions  We propose that  Atg7  acts downstream of  Hsp27  in the regulation of eye morphology, polyglutamine toxicity, and lifespan in  Drosophila .

journal of biomedical science

Autophagy-related gene 7 is downstream of heat shock protein 27 in the regulation of eye morphology, polyglutamine toxicity, and lifespan in Drosophila