Requirement for Hsp90 and a CyP-40-type Cyclophilin in Negative Regulation of the Heat Shock Response

摘要: Abstract The heat shock response is a highly conserved mechanism that allows cells to withstand variety of stress conditions. Activation this characterized by increased synthesis proteins (HSPs), which protect cellular from stress-induced denaturation. Heat transcription factors (HSFs) are required for expression HSPs during conditions and can be found in complexes containing components the Hsp90 molecular chaperone machinery, raising possibility involved regulation response. To test this, we have assessed effects mutations impair activity machinery on related events inSaccharomyces cerevisiae. Mutations either reduce level protein or eliminate Cpr7, CyP-40-type cyclophilin full function, resulted HSF-dependent activities. Genetic tests also revealed Cpr7 function synergistically repress gene promoters. Conditional loss both acquisition thermotolerant phenotype. Our results reveal negative under nonstress establish specific endogenous role S.