首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Ethylene-mediated cross-talk between calcium-dependent protein kinase and MAPK signaling controls stress responses in plants
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Ethylene-mediated cross-talk between calcium-dependent protein kinase and MAPK signaling controls stress responses in plants

机译:乙烯介导的钙依赖性蛋白激酶和MAPK信号传导之间的串扰控制植物的胁迫反应

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摘要

Plants are constantly exposed to environmental changes and need to integrate multiple external stress cues. Calcium-dependent protein kinases (CDPKs) are implicated as major primary Ca2+ sensors in plants. CDPK activation, like activation of mitogen-activated protein kinases (MAPKs), is triggered by biotic and abiotic stresses, although distinct stimulus-specific stress responses are induced. To investigate whether CDPKs are part of an underlying mechanism to guarantee response specificity, we identified CDPK-controlled signaling pathways. A truncated form of Nicotiana tabacum CDPK2 lacking its regulatory autoinhibitor and calcium-binding domains was ectopically expressed in Nicotiana benthamiana. Infiltrated leaves responded to an abiotic stress stimulus with the activation of biotic stress reactions. These responses included synthesis of reactive oxygen species, defense gene induction, and SGT1-dependent cell death. Furthermore, N-terminal CDPK2 signaling triggered enhanced levels of the phytohormones jasmonic acid, 12-oxo-phytodienoic acid, and ethylene but not salicylic acid. These responses, commonly only observed after challenge with a strong biotic stimulus, were prevented when the CDPK's intrinsic autoinhibitory peptide was coexpressed. Remarkably, elevated CDPK signaling compromised stress-induced MAPK activation, and this inhibition required ethylene synthesis and perception. These data indicate that CDPK and MAPK pathways do not function independently and that a concerted activation of both pathways controls response specificity to biotic and abiotic stress.
机译:植物不断受到环境变化的影响,需要整合多种外部压力提示。钙依赖蛋白激酶(CDPKs)是植物中主要的主要Ca 2 + 传感器。尽管有不同的刺激特异性应激反应,但CDPK激活与丝裂原激活的蛋白激酶(MAPKs)激活类似,是由生物和非生物应激触发的。为了调查CDPK是否是保证应答特异性的潜在机制的一部分,我们确定了CDPK控制的信号通路。缺少其调节性自动抑制剂和钙结合域的烟草的截短形式CDPK2在本生烟草中异位表达。渗入的叶子通过激活生物胁迫反应对非生物胁迫刺激作出反应。这些反应包括活性氧的合成,防御基因的诱导和SGT1依赖性细胞死亡。此外,N末端CDPK2信号触发了植物激素茉莉酸,12-氧代植物二烯酸和乙烯(但不是水杨酸)水平的升高。当共表达CDPK的内在自抑制肽时,通常只能在强烈的生物刺激后才能观察到这些反应。值得注意的是,升高的CDPK信号传导损害了应力诱导的MAPK活化,并且这种抑制作用需要乙烯的合成和感知。这些数据表明CDPK和MAPK途径并不独立起作用,并且这两种途径的一致激活控制了对生物和非生物胁迫的响应特异性。

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