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TORC1‐signalling is down‐regulated in Saccharomyces cerevisiae hsp30Δ cells by SNF1‐dependent mechanisms

Hsp30 is a plasma membrane localized heat shock protein in Saccharomyces cerevisiae whose expression is induced by numerous environmental stressors. Elucidation of its mechanism of action has remained elusive primarily because hsp30Δ cells do not show a strong phenotype. To identify cellular functions associated with Hsp30, we thus compared the transcriptome of BY4741hsp30Δ with that of its wild type counterpart. Our studies indicate down‐regulation of the target of rapamycin complex 1 (TORC1)‐dependent gene‐expression programme in hsp30Δ cells. We further show that TORC1‐signalling through its effectors (Sch9 and Tap42) was down‐regulated in the deletion strain. Specifically, (a) phosphorylation levels of Sch9 were lower and nuclear exclusion of Rim15 (Sch9‐downstream function) was overridden in hsp30Δ cells, (b) membrane association of Tor1 and Tap42 was lower in hsp30Δ cells, and (c) Tap42‐downstream functions were abrogated in the deletion strain. Furthermore, transcription factors Rtg1, Rtg3, Gat1, and Gln3 were localized in the nucleus of the hsp30Δ as observed upon inactivation of TORC1. Studies aimed at determining how TORC1‐signalling is down‐regulated in hsp30Δ cells indicated that total reducing sugar levels were lower and ADP:ATP ratio was higher in hsp30Δ cells —conditions known to activate the Snf1 kinase and consequently to the inactivation of TORC1. We thus determined if TORC1‐signalling could be restored in hsp30Δ cells upon the deletion of SNF1. Sch9 phosphorylation levels (TORC1‐signalling) was restored to wild type levels in hsp30Δsnf1Δ cells. TORC1‐signalling is thus down‐regulated in hsp30Δ cells by SNF1‐dependent mechanisms. A probable role for Hsp30 is discussed.