首页> 美国卫生研究院文献>Cell Stress Chaperones >The CNGCb and CNGCd genes from Physcomitrella patens moss encode for thermosensory calcium channels responding to fluidity changes in the plasma membrane
【2h】

The CNGCb and CNGCd genes from Physcomitrella patens moss encode for thermosensory calcium channels responding to fluidity changes in the plasma membrane

机译:Physcomitrella patens moss的CNGCb和CNGCd基因编码响应质膜流动性变化的热敏钙通道

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务,本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文,但由于OA文献来源多样且变更频繁,仍可能出现获取不到、文献不完整或与标题不符等情况,如果获取不到我们将提供退款服务。请知悉。

摘要

Land plants need precise thermosensors to timely establish molecular defenses in anticipation of upcoming noxious heat waves. The plasma membrane-embedded cyclic nucleotide-gated Ca2+ channels (CNGCs) can translate mild variations of membrane fluidity into an effective heat shock response, leading to the accumulation of heat shock proteins (HSP) that prevent heat damages in labile proteins and membranes. Here, we deleted by targeted mutagenesis the CNGCd gene in two Physcomitrella patens transgenic moss lines containing either the heat-inducible HSP-GUS reporter cassette or the constitutive UBI-Aequorin cassette. The stable CNGCd knockout mutation caused a hyper-thermosensitive moss phenotype, in which the heat-induced entry of apoplastic Ca2+ and the cytosolic accumulation of GUS were triggered at lower temperatures than in wild type. The combined effects of an artificial membrane fluidizer and elevated temperatures suggested that the gene products of CNGCd and CNGCb are paralogous subunits of Ca2+channels acting as a sensitive proteolipid thermocouple. Depending on the rate of temperature increase, the duration and intensity of the heat priming preconditions, terrestrial plants may thus acquire an array of HSP-based thermotolerance mechanisms against upcoming, otherwise lethal, extreme heat waves.Electronic supplementary materialThe online version of this article (doi:10.1007/s12192-013-0436-9) contains supplementary material, which is available to authorized users.
机译:陆地植物需要精确的热传感器来及时建立分子防御能力,以预期即将到来的有害热浪。质膜嵌入的环核苷酸门控的Ca 2 + 通道(CNGC)可以将膜流动性的轻微变化转化为有效的热休克反应,从而导致热休克蛋白(HSP)积累,从而阻止不稳定蛋白质和膜的热损伤。在这里,我们通过有针对性的诱变删除了两个包含热诱导的HSP-GUS报告基因盒或组成型UBI-Aequorin基因盒的小立碗藓转基因苔藓系中的CNGCd基因。稳定的CNGCd基因敲除突变导致了一个超热敏的苔藓表型,其中在比野生型更低的温度下触发了热诱导的质外性Ca 2 + 的进入和GUS的胞质积累。人工膜流化床和高温的联合作用表明,CNGCd和CNGCb的基因产物是Ca 2 + 通道的旁系亚基,起着敏感的蛋白脂热电偶的作用。根据温度升高的速率,热启动前提条件的持续时间和强度,地面植物可能因此获得一系列基于HSP的耐热机制,以抵御即将来临的,否则致命的极端热浪。电子补充材料本文的在线版本( doi:10.1007 / s12192-013-0436-9)包含补充材料,授权用户可以使用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号