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质体代谢物 MEcPP 通过逆行信号调控核应激反应基因的表达。

Retrograde signaling by the plastidial metabolite MEcPP regulates expression of nuclear stress-response genes.

机构信息

Department of Plant Biology, University of California Davis, Davis, CA 95616, USA.

出版信息

Cell. 2012 Jun 22;149(7):1525-35. doi: 10.1016/j.cell.2012.04.038.

DOI:10.1016/j.cell.2012.04.038
PMID:22726439
Abstract

Plastid-derived signals are known to coordinate expression of nuclear genes encoding plastid-localized proteins in a process termed retrograde signaling. To date, the identity of retrograde-signaling molecules has remained elusive. Here, we show that methylerythritol cyclodiphosphate (MEcPP), a precursor of isoprenoids produced by the plastidial methylerythritol phosphate (MEP) pathway, elicits the expression of selected stress-responsive nuclear-encoded plastidial proteins. Genetic and pharmacological manipulations of the individual MEP pathway metabolite levels demonstrate the high specificity of MEcPP as an inducer of these targeted stress-responsive genes. We further demonstrate that abiotic stresses elevate MEcPP levels, eliciting the expression of the aforementioned genes. We propose that the MEP pathway, in addition to producing isoprenoids, functions as a stress sensor and a coordinator of expression of targeted stress-responsive nuclear genes via modulation of the levels of MEcPP, a specific and critical retrograde-signaling metabolite.

摘要

质体衍生信号被认为在一个称为逆行信号转导的过程中协调编码质体定位蛋白的核基因的表达。迄今为止,逆行信号转导分子的身份仍然难以捉摸。在这里,我们表明,甲基赤藓醇磷酸(MEcPP),一种由质体甲基赤藓醇磷酸(MEP)途径产生的异戊烯基的前体,引发选定的应激响应性核编码质体蛋白的表达。对单个 MEP 途径代谢物水平的遗传和药理学操作表明,MEcPP 作为这些靶向应激响应基因的诱导剂具有高度特异性。我们进一步证明,非生物胁迫会增加 MEcPP 的水平,从而引发上述基因的表达。我们提出,MEP 途径除了产生异戊烯基外,还通过调节 MEcPP 的水平作为一种应激传感器和靶向应激响应性核基因表达的协调者发挥作用,MEcPP 是一种特定且关键的逆行信号转导代谢物。

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