首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >A P_(iib)-type Ca~(2+)-atpase Is Essential For Stress Adaptation In Physcomitrella Patens
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A P_(iib)-type Ca~(2+)-atpase Is Essential For Stress Adaptation In Physcomitrella Patens

机译:P_(iib)型Ca〜(2 +)-atpase对小肠小肠拟南芥中的压力适应至关重要

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Transient cytosolk Ca~(2+) ([Ca~(2+)]_(cyt)) elevations are early events in plant signaling pathways including those related to abiotic stress. The restoration of [Ca~(2+)]cyt to prestimulus levels involves ATP-driven Ca~(2+) pumps, but direct evidence for an essential role of a plant Ca~(2+)-ATPase in abiotic stress adaptation is missing. Here, we report on a stress-responsive Ca~(2+)-ATPase gene (PGA1) from the moss Physcomitrella patens. Functional analysis of PCA1 in a Ca~(2+) transport-deficient yeast mutant suggests that PCA1 encodes a P_(IIB)-type Ca~(2+)-ATPase harboring an N-terminal autoinhibitory domain. In vivo localizations identified membranes of small vacuoles as the integration site for a PCA1:GFP fusion protein. PCA1 mRNA levels are up-regulated by dehydration, NaCl, and abscisic acid, and PCA1 loss-of-function mutants (△PCA1) exhibit an enhanced susceptibility to salt stress. The △PCA1 lines show sustained elevated [Ca~(2+)]_(cyt) in response to salt treatment in contrast to WT that shows transient Ca~(2+) elevations, indicating a direct role for PCA1 in the restoration of prestimulus [Ca~(2+)]_(cyt). The altered Ca~(2+) response of the △PCA1 mutant lines correlates with altered expression levels of stress-induced genes, suggesting disturbance of a stress-associated signaling pathway. We propose that PCA1 is an essential component for abiotic stress adaptation in Physcomitrella involved in the generation of a specific salt-induced Ca~(2+) signature.
机译:瞬时细胞溶质Ca〜(2+)([Ca〜(2 +)] _(cyt))升高是植物信号传导途径中的早期事件,包括与非生物胁迫相关的那些。 [Ca〜(2 +)] cyt还原到刺激水平涉及ATP驱动的Ca〜(2+)泵,但是直接证明植物Ca〜(2 +)-ATPase在非生物胁迫适应中的重要作用是失踪。在这里,我们报道了来自青苔藓小立碗藓的胁迫响应Ca〜(2 +)-ATPase基因(PGA1)。 Ca〜(2+)运输缺陷型酵母突变体中PCA1的功能分析表明,PCA1编码具有N末端自抑制域的P_(IIB)型Ca〜(2 +)-ATPase。体内定位确定小液泡膜为PCA1:GFP融合蛋白的整合位点。脱水,NaCl和脱落酸会上调PCA1 mRNA的水平,而PCA1功能丧失的突变体(△PCA1)对盐胁迫的敏感性更高。 △PCA1系显示出盐处理对[Ca〜(2 +)] _(cyt)的持续升高,而WT显示出瞬时Ca〜(2+)升高,这表明PCA1在恢复刺激前的直接作用[Ca〜(2 +)] _(cyt)。 △PCA1突变株的Ca〜(2+)响应改变与胁迫诱导基因表达水平的改变相关,提示胁迫相关信号通路的干扰。我们提出PCA1是非小生境中适应Physcomitrella中非生物应激适应的重要组成部分,该过程涉及特定盐诱导的Ca〜(2+)标记的产生。

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