Proteomics

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Global proteome remodeling during ER stress involves Hac1-driven expression of long undecoded transcript isoforms


ABSTRACT: Cellular stress responses often require transcription-based activation of gene expression to promote cellular adaptation. Whether general mechanisms exist for stress-responsive gene down-regulation is less clear. A recently defined mechanism enables both up- and down-regulation of protein levels for distinct gene sets by the same transcription factor (TF) via coordinated induction of canonical mRNAs and long undecoded transcript isoforms (LUTIs). We analyzed parallel gene expression datasets to determine whether this mechanism contributes to the conserved Hac1-driven branch of the unfolded protein response (UPRER), indeed observing Hac1-dependent protein down-regulation accompanying the up-regulation of ER-related proteins that typifies UPRER activation. Proteins down-regulated by Hac1-driven LUTIs include those with electron transport chain (ETC) function. Abrogated ETC function improves the fitness of UPRER-activated cells, suggesting functional importance to this regulation. We conclude that the UPRER drives large-scale proteome remodeling, including coordinated up- and down-regulation of distinct protein classes, which is partly mediated by Hac1-induced LUTIs.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Saccharomyces Cerevisiae (ncbitaxon:4932)

SUBMITTER: Marko Jovanovic  

PROVIDER: MSV000082454 | MassIVE | Tue Jun 12 17:13:00 BST 2018

REPOSITORIES: MassIVE

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Publications

Global Proteome Remodeling during ER Stress Involves Hac1-Driven Expression of Long Undecoded Transcript Isoforms.

Van Dalfsen Kelsey Marie KM   Hodapp Stefanie S   Keskin Abdurrahman A   Otto George Maxwell GM   Berdan Charles Andrew CA   Higdon Andrea A   Cheunkarndee Tia T   Nomura Daniel Koji DK   Jovanovic Marko M   Brar Gloria Ann GA  

Developmental cell 20180701 2


Cellular stress responses often require transcription-based activation of gene expression to promote cellular adaptation. Whether general mechanisms exist for stress-responsive gene downregulation is less clear. A recently defined mechanism enables both up- and downregulation of protein levels for distinct gene sets by the same transcription factor via coordinated induction of canonical mRNAs and long undecoded transcript isoforms (LUTIs). We analyzed parallel gene expression datasets to determi  ...[more]

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