Abstract
A family of highly-conserved 70 kDa stress proteins is localized in various intracellular compartments of Saccharomyces cerevisiae. Their gene expression is specifically and/or sometimes cooperatively regulated at the transcriptional level by cis-acting elements found in their respective promoters. Here, we find that depletion of cytosolic Ssa1p induced BiP(Kar2p) in the endoplasmic reticulum at the transcriptional level. By analyzing internal deletion mutants of the KAR2 promoter, we determined that the heat shock element (HSE) is necessary for KAR2 gene induction in response to the depletion of Ssa1p. Furthermore, either the KAR2HSE or SSA1HSE is sufficient for gene activation, as assayed using HSE-CYC1-lacZ fusion reporter plasmids. Finally, temperature-sensitive ssa1 mutants transformed with an HSE-CYC1-lacZ fusion vector exhibited strong induction of beta-galactosidase activity when shifted to a restrictive temperature. These results show that loss of functional Ssa1p from the cytosol up-regulates KAR2 gene expression through an HSE-mediated pathway and also support the idea that SSA1 gene expression is autoregulated.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
