Interaction between plastid and mitochondrial retrograde signalling pathways during changes to plastid redox status
Interaction between plastid and mitochondrial retrograde signalling pathways during changes to plastid redox status
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DOI：
10.1098/rstb.2013.0231
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发表时间：
2014-04-19
影响因子：
6.3
通讯作者：
Strand, Asa
中科院分区：
文献类型：
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作者：
Blanco, Nicolas E.;Guinea-Diaz, Manuel;Strand, Asa
线粒体和叶绿体相互依赖；光合作用为线粒体呼吸提供基质，线粒体代谢是维持光合作用碳同化所必需的。此外，线粒体呼吸通过从叶绿体中消散多余的氧化还原当量来保护光合作用免受光抑制。线粒体功能的遗传缺陷导致叶绿体的过度减少和通电。因此，很明显，线粒体和质体的活动需要协调，但细胞器沟通以协调其活动的方式尚不清楚。选择性氧化酶（rao1）突变体的调节因子被分离为一个突变体，该突变体不能诱导AOX1a表达以响应线粒体细胞色素c还原酶（复合物III）抑制剂抗霉素a。rao1编码核定位的周期蛋白依赖性激酶E1 （CDKE1）。有趣的是，rao1突变体在光合作用电子传递链的氧化还原变化下也表现出基因组解耦表型。因此，CDKE1被证明在逆行信号下调节光收集复合物B （LHCB）和替代氧化酶1 （AOX1a）的表达。我们的研究结果表明，CDKE1是整合线粒体和质体逆行信号的核心核成分，在应激反应中调节能量代谢。
Mitochondria and chloroplasts depend upon each other; photosynthesis provides substrates for mitochondrial respiration and mitochondrial metabolism is essential for sustaining photosynthetic carbon assimilation. In addition, mitochondrial respiration protects photosynthesis against photoinhibition by dissipating excess redox equivalents from the chloroplasts. Genetic defects in mitochondrial function result in an excessive reduction and energization of the chloroplast. Thus, it is clear that the activities of mitochondria and plastids need to be coordinated, but the manner by which the organelles communicate to coordinate their activities is unknown. The regulator of alternative oxidase (rao1) mutant was isolated as a mutant unable to induce AOX1a expression in response to the inhibitor of the mitochondrial cytochrome c reductase (complex III), antimycin A. RAO1 encodes the nuclear localized cyclin-dependent kinase E1 (CDKE1). Interestingly, the rao1 mutant demonstrates a genome uncoupled phenotype also in response to redox changes in the photosynthetic electron transport chain. Thus, CDKE1 was shown to regulate both LIGHT HARVESTING COMPLEX B (LHCB) and ALTERNATIVE OXIDASE 1 (AOX1a) expression in response to retrograde signals. Our results suggest that CDKE1 is a central nuclear component integrating mitochondrial and plastid retrograde signals and plays a role in regulating energy metabolism during the response to stress.