...
首页> 外文期刊>Plant and cell physiology >Disruption of the ndhF1 gene affects Chl fluorescence through state transition in the cyanobacterium Synechocystis sp. PCC 6803, resulting in apparent high efficiency of photosynthesis.
【24h】

Disruption of the ndhF1 gene affects Chl fluorescence through state transition in the cyanobacterium Synechocystis sp. PCC 6803, resulting in apparent high efficiency of photosynthesis.

机译:ndhF1基因的破坏通过蓝藻集胞藻(Synechocystcystis sp。)中的状态转换影响Chl荧光。 PCC 6803,导致光合作用的明显高效率。

获取原文
获取原文并翻译 | 示例
   

获取外文期刊封面封底 >>

       

摘要

In Synechocystis sp. PCC 6803, the disruption of the ndhF1 gene (slr0844), which encodes a subunit of one of the NDH-1 complexes (NDH-1L complex) serving for respiratory electron transfer, causes the largest change in Chl fluorescence induction kinetics among the kinetics of 750 disruptants searched in the Fluorome, the cyanobacterial Chl fluorescence database. The cause of the explicit phenotype of the ndhF1 disruptant was examined by measurements of the photosynthetic rate, Chl fluorescence and state transition. The results demonstrate that the defects in respiratory electron transfer obviously have great impact on Chl fluorescence in cyanobacteria. The inactivation of NDH-1L complexes involving electron transfer from NDH-1 to plastoquinone (PQ) would result in the oxidation of the PQ pool, leading to the transition to State 1, where the yield of Chl fluorescence is high. Apparently, respiration, although its rate is far lower than that of photosynthesis, could affect Chl fluorescence through the state transition as leverage. The disruption of the ndhF1 gene caused lower oxygen-evolving activity but the estimated electron transport rate from Chl fluorescence measurements was faster in the mutant than in the wild-type cells. The discrepancy could be ascribed to the decreased level of non-photochemical quenching due to state transition. One must be cautious when using the Chl fluorescence parameter to estimate photosynthesis in mutants defective in state transition.
机译:在集胞藻中。 PCC 6803是ndhF1基因(slr0844)的破坏,该基因编码用于呼吸电子转移的NDH-1复合物(NDH-1L复合物)之一的亚基,导致Chl荧光诱导动力学中最大的变化是在Fluorome(蓝细菌Chl荧光数据库)中搜索了750种破坏物。通过测量光合速率,Chl荧光和状态转变来检查ndhF1破坏者显性表型的原因。结果表明,呼吸电子传递的缺陷对蓝藻中的Chl荧光有明显的影响。 NDH-1L配合物的失活涉及从NDH-1到质体醌(PQ)的电子转移,将导致PQ池的氧化,从而导致向状态1的过渡,其中Chl荧光的产量很高。显然,尽管呼吸的速率远低于光合作用的速率,但呼吸可能会通过状态转换作为杠杆作用而影响Chl荧光。 ndhF1基因的破坏导致较低的放氧活性,但突变体中Chl荧光测量的估计电子传输速率比野生型细胞快。差异可以归因于由于状态转变导致的非光化学猝灭水平降低。当使用Chl荧光参数来估计状态转换缺陷的突变体中的光合作用时,一定要谨慎。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

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