YaeL (EcfE) activates the ς<sup>E</sup> pathway of stress response through a site-2 cleavage of anti-ς<sup>E</sup>, RseA

DOI Web Site PubMed 研究データあり 被引用文献26件 参考文献1件 オープンアクセス

この論文をさがす

説明

<jats:p><jats:italic>Escherichia coli</jats:italic> YaeL (EcfE) is a homolog of human site-2 protease (S2P), a membrane-bound zinc metalloprotease involved in regulated intramembrane proteolysis. We have shown previously that YaeL, having essential metalloprotease active site motifs in the cytoplasmic domain, is indispensable for viability. Here, we obtained<jats:italic>rpoE</jats:italic>, encoding an extracytoplasmic stress response ς factor (ς<jats:sup>E</jats:sup>), as a multicopy suppressor against the <jats:italic>yaeL</jats:italic>disruption. Whereas ς<jats:sup>E</jats:sup> is thought to be activated by regulated cleavage of RseA on the periplasmic side by the DegS protease, we found that a degradation intermediate of RseA consisting of the transmembrane and the cytoplasmic domains accumulated in the YaeL-depleted cells. This intermediate was degraded on expression of YaeL but not of its metalloprotease motif mutants. Cells depleted of YaeL were incapable of activating a ς<jats:sup>E</jats:sup>-dependent promoter in response to an envelope stress. It is suggested that ς<jats:sup>E</jats:sup>activation involves two successive proteolytic cleavages: first, at a periplasmic site by DegS; second, at a cytoplasmic or intramembrane site by YaeL. Thus, YaeL is positively required for the ς<jats:sup>E</jats:sup>extracytoplasmic stress response.</jats:p>

収録刊行物

  • Genes & Development

    Genes & Development 16 (16), 2147-2155, 2002-08-15

    Cold Spring Harbor Laboratory

被引用文献 (26)*注記

もっと見る

参考文献 (1)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ