Preliminary Studies Of The Molecular Mechanism Of Snf7 In Autophagy In Saccharomyces Cerevisiae

Autophagy is an evolutionarily conserved pathway that regulates the cellular degradation process in eukaryotic cells.A basal level of autophagy occurs constitutively.Meanwhile,this process can be further induced by various types of environmental stress including starvation,hypoxia and pathogen invasion.Autophagy ensures cells to keep basal metabolic level in extreme environment for survival.Excessive or insufficient macroautophagy will cause serious damage to cells and many diseases are associated with dysregulation of macroautophagy.Exploring the molecular mechanism of autophagy is important to elucidate the biological role of autophagy and find new drug targets for disease treatment.Macroautophagy process generates a closed autophagosome,a double-membrane organelle.The maturation of autophagosome requires phagophore closure to completely engulf the cargo.However,it remains unclear how phagophore form closed autophagosome through remodeling of the double-membrane structure.It has been reported that the endosomal sorting complex required for transport(ESCRT)complex is involved in this process,but the underling molecular mechanism is still unrevealed.Here we show that Snf7,a component of ESCRT-III complex in Saccharomyces cerevisiae,is involved in macroautophagy determined by fluorescent colocalization and EGFP-Atg8 degradation assay.Intriguingly,Snf7 knockout,but not Vps20(the upstream component of Snf7 in ESCRT-III complex),severely impairs autophagy.What is more,we found an interaction between Snf7 and Atg8.In all,we suggest that Snf7 is recruited to phagophore by interacting with Atg8 thus facilitating phagophore closure.Our results preliminarily elucidated the molecular mechanism of phagophore closure regulated by Snf7,which provides a further understanding of the biogenesis process of autophagosome.