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莱茵衣藻ATP合酶突变体的光敏感性

The light sensitivity of ATP synthase mutants of Chlamydomonas reinhardtii.

作者信息

Majeran W, Olive J, Drapier D, Vallon O, Wollman F A

机构信息

Unité Propre de Recherche-Centre National de la Recherche Scientifique 1261, Institut de Biologie Physico-Chimique, 13 rue Pierre et Marie Curie, 75005 Paris, France.

出版信息

Plant Physiol. 2001 May;126(1):421-33. doi: 10.1104/pp.126.1.421.

DOI:10.1104/pp.126.1.421
PMID:11351104
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC102315/
Abstract

Chlamydomonas reinhardtii mutants defective in the chloroplast ATP synthase are highly sensitive to light. The ac46 mutant is affected in the MDH1 gene, required for production or stability of the monocistronic atpH mRNA encoding CF(O)-III. In this and other ATP synthase mutants, we show that short-term exposure to moderate light intensities-a few minutes-induces an inhibition of electron transfer after the primary quinone acceptor of photosystem II (PSII), whereas longer exposure-several hours-leads to a progressive loss of PSII cores. An extensive swelling of thylakoids accompanies the initial inhibition of electron flow. Thylakoids deflate as PSII cores are lost. The slow process of PSII degradation involves the participation of ClpP, a chloroplast-encoded peptidase that is part of a major stromal protease Clp. In the light of the above findings, we discuss the photosensitivity of ATP synthase mutants with respect to the regular photoinhibition process that affects photosynthetic competent strains at much higher light intensities.

摘要

莱茵衣藻中叶绿体ATP合酶有缺陷的突变体对光高度敏感。ac46突变体的MDH1基因受到影响,该基因对于编码CF(O)-III的单顺反子atpH mRNA的产生或稳定性是必需的。在这个以及其他ATP合酶突变体中,我们发现,短期暴露于中等光照强度下(几分钟)会导致在光系统II(PSII)的初级醌受体之后的电子传递受到抑制,而较长时间暴露(几个小时)会导致PSII核心逐渐丧失。类囊体的广泛肿胀伴随着电子流的初始抑制。随着PSII核心的丧失,类囊体瘪缩。PSII降解的缓慢过程涉及ClpP的参与,ClpP是一种叶绿体编码的肽酶,是主要的基质蛋白酶Clp的一部分。鉴于上述发现,我们讨论了ATP合酶突变体的光敏感性与在高得多的光照强度下影响光合活性菌株的常规光抑制过程的关系。