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Translational offsetting as a mode of estrogen receptor alpha-dependent regulation of gene expression

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE120917 | GEO | 2019/09/24

REPOSITORIES: GEO

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Translational offsetting as a mode of estrogen receptor α-dependent regulation of gene expression.

Project description:Estrogen receptor alpha (ERα) activity is associated with increased cancer cell proliferation. Studies aiming to understand the impact of ERα on cancer-associated phenotypes have largely been limited to its transcriptional activity. Herein, we demonstrate that ERα coordinates its transcriptional output with selective modulation of mRNA translation. Importantly, translational perturbations caused by depletion of ERα largely manifest as "translational offsetting" of the transcriptome, whereby amounts of translated mRNAs and corresponding protein levels are maintained constant despite changes in mRNA abundance. Transcripts whose levels, but not polysome association, are reduced following ERα depletion lack features which limit translation efficiency including structured 5'UTRs and miRNA target sites. In contrast, mRNAs induced upon ERα depletion whose polysome association remains unaltered are enriched in codons requiring U34-modified tRNAs for efficient decoding. Consistently, ERα regulates levels of U34-modifying enzymes and thereby controls levels of U34-modified tRNAs. These findings unravel a hitherto unprecedented mechanism of ERα-dependent orchestration of transcriptional and translational programs that may be a pervasive mechanism of proteome maintenance in hormone-dependent cancers.

| S-EPMC6885737 | biostudies-literature

Translational offsetting as a mode of estrogen receptor ?-dependent regulation of gene expression

Project description:Estrogen receptor alpha (ER?) activity is associated with increased cancer cell proliferation. Studies aiming to understand the impact of ER? on cancer-associated phenotypes have largely been limited to its transcriptional activity. Herein, we demonstrate that ER? coordinates its transcriptional output with selective modulation of mRNA translation. Importantly, translational perturbations caused by depletion of ER? largely manifest as "translational offsetting" of the transcriptome, whereby amounts of translated mRNAs and corresponding protein levels are maintained constant despite changes in mRNA abundance. Transcripts whose levels, but not polysome-association, are reduced following ER? depletion lack features which limit translation efficiency including structured 5'UTRs and miRNA target sites. In contrast, mRNAs induced upon ER? depletion whose polysome-association remains unaltered are enriched in codons requiring U34-modified tRNAs for efficient decoding. Consistently, ER? regulates levels of U34-modifying enzymes and thereby controls levels of U34-modified tRNAs. These findings unravel a hitherto unprecedented mechanism of ER?-dependent orchestration of transcriptional and translational programs that may be a pervasive mechanism of proteome maintenance in hormone-dependent cancers.

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Translational offsetting as a mode of estrogen receptor alpha-dependent regulation of gene expression

Project description:Translational offsetting as a mode of estrogen receptor alpha-dependent regulation of gene expression

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