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Pichia angusta DL1 strain: Control+ER stress vs. hac1+ER stress

ABSTRACT: Transcriptional profiling of Control and hac1 deletion mutant in ER stress condition on P. angusta DL1 strain.

ORGANISM(S): Ogataea angusta

PROVIDER: GSE68217 | GEO | 2015/07/22

SECONDARY ACCESSION(S): PRJNA282040

REPOSITORIES: GEO

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Pichia angusta DL1 strain: Control+ER stress vs. hac1+ER stress

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

Project description:Cellular stress response pathways often require transcription-based activation of gene expression to promote cellular adaptation. However, whether general mechanisms exist for stress-responsive gene down-regulation is less clear. A recently defined gene regulatory 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 deep, parallel gene expression datasets to determine whether this mechanism contributes to the conserved Hac1-driven branch of the unfolded protein response (UPRER). Indeed, we found Hac1-dependent protein down-regulation that accompanied the well-characterized 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. Aerobic respiration also appears dampened during the UPRER, and abrogated ETC function improves the fitness of UPRER-activated cells, suggesting functional importance of LUTI regulation during the UPRER. We conclude that the UPRER involves large-scale proteome remodeling, mediated in part by Hac1-induced LUTIs, and that this mechanism enables coordination of up- and down-regulation of gene expression during this stress response.

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