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Translational control of the cytosolic stress response by mitochondrial ribosomal protein L18.

Abstract：

:In response to stress, cells attenuate global protein synthesis but permit efficient translation of mRNAs encoding heat-shock proteins (HSPs). Although decades have passed since the first description of the heat-shock response, how cells achieve translational control of HSP synthesis remains enigmatic. Here we report an unexpected role for mitochondrial ribosomal protein L18 (MRPL18) in the mammalian cytosolic stress response. MRPL18 bears a downstream CUG start codon and generates a cytosolic isoform in a stress-dependent manner. Cytosolic MRPL18 incorporates into the 80S ribosome and facilitates ribosome engagement on mRNAs selected for translation during stress. MRPL18 knockdown has minimal effects on mitochondrial function but substantially dampens cytosolic HSP expression at the level of translation. Our results uncover a hitherto-uncharacterized stress-adaptation mechanism in mammalian cells, which involves formation of a 'hybrid' ribosome responsible for translational regulation during the cytosolic stress response.

journal_name

Nat Struct Mol Biol

journal_title

Nature structural & molecular biology

authors

Zhang X,Gao X,Coots RA,Conn CS,Liu B,Qian SB

doi

10.1038/nsmb.3010

subject

Has Abstract

pub_date

2015-05-01 00:00:00

pages

404-10

issue

5

eissn

1545-9993

issn

1545-9985

pii

nsmb.3010

journal_volume

22

pub_type

杂志文章

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