A new branch of endoplasmic reticulum stress signaling and the osmotic signal converge on plant-specific asparagine-rich proteins to promote cell death
A new branch of endoplasmic reticulum stress signaling and the osmotic signal converge on plant-specific asparagine-rich proteins to promote cell death
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DOI：
10.1074/jbc.m802654200
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发表时间：
2008-07-18
影响因子：
4.8
通讯作者：
Fontes, Elizabeth P. B.
中科院分区：
文献类型：
--
作者：
Costa, Maximiller D. L.;Reis, Pedro A. B.;Fontes, Elizabeth P. B.
nrp（富n蛋白）被确定为一种新的适应性途径的靶标，该途径整合内质网（ER）和渗透胁迫信号，基于tunicamycin和聚乙二醇处理的协调调节和协同上调。这种整合途径在几个方面与未折叠蛋白反应（UPR）的分子伴侣诱导分支不同。虽然内质网和渗透胁迫对upr特异性靶标进行反向调控，但nrp需要这两种信号才能完全激活。此外，大豆中BiP（结合蛋白）的过表达阻止了内质网胁迫诱导剂对UPR的激活，但不影响nrp的激活。我们还发现，这一整合途径转导内质网和渗透胁迫产生的PCD信号，导致与叶片衰老相关的标记出现。在大豆原生质体中，NRPs的过表达诱导了caspase-3样活性，促进了DNA的广泛断裂。此外，NRPs在植物中的瞬时表达导致叶片变黄、叶绿素损失、丙二醛产生、乙烯进化和衰老标志基因CP1的诱导。细胞分裂素玉米素是一种有效的衰老抑制剂，可以减轻这种表型。总之，这些结果表明，内质网胁迫通过内质网胁迫反应的一个新分支，通过激活植物特异性NRPs诱导叶片衰老。
NRPs (N-rich proteins) were identified as targets of a novel adaptive pathway that integrates endoplasmic reticulum (ER) and osmotic stress signals based on coordinate regulation and synergistic up-regulation by tunicamycin and polyethylene glycol treatments. This integrated pathway diverges from the molecular chaperone-inducing branch of the unfolded protein response (UPR) in several ways. While UPR-specific targets were inversely regulated by ER and osmotic stresses, NRPs required both signals for full activation. Furthermore, BiP (binding protein) overexpression in soybean prevented activation of the UPR by ER stress inducers, but did not affect activation of NRPs. We also found that this integrated pathway transduces a PCD signal generated by ER and osmotic stresses that result in the appearance of markers associated with leaf senescence. Overexpression of NRPs in soybean protoplasts induced caspase-3-like activity and promoted extensive DNA fragmentation. Furthermore, transient expression of NRPs in planta caused leaf yellowing, chlorophyll loss, malondialdehyde production, ethylene evolution, and induction of the senescence marker gene CP1. This phenotype was alleviated by the cytokinin zeatin, a potent senescence inhibitor. Collectively, these results indicate that ER stress induces leaf senescence through activation of plant-specific NRPs via a novel branch of the ER stress response.