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Does the Arabidopsis proton gradient regulation5 Mutant Leak Protons from the Thylakoid Membrane?
Plant Physiology ( IF 7.4 ) Pub Date : 2020-09-01 , DOI: 10.1104/pp.20.00850
Hiroshi Yamamoto 1 , Toshiharu Shikanai 2
Affiliation  

Despite generating an obvious mutant phenotype, whether the Arabidopsis (Arabidopsis thaliana) proton gradient regulation5 (pgr5) mutation influences cyclic electron transport (CET) around PSI is a topic of debate. Results of electrochromic shift analysis show that proton conductivity across the thylakoid membrane (gH+) in the pgr5 mutant is enhanced at high light intensity. Given this observation, PGR5 was proposed to regulate ATP synthase activity rather than mediating CET. The originally reported pgr5 phenotype reflects a smaller proton motive force (pmf) and could be explained by this H+ leakage model. In this study, we genetically reexamined the high-gH+ phenotype of the pgr5 mutant. Transgenic lines in which flavodiiron protein-dependent pseudo-CET replaced PGR5-dependent CET had wild-type levels of gH+, suggesting that the high-gH+ phenotype in pgr5 plants is caused secondarily by the low pmf. The pgr1 mutant shows a similar reduction in pmf because of enhanced sensitivity of its cytochrome b6f complex to lumenal acidification. In contrast to the pgr5 mutant, gH+ was lower in the pgr1 mutant than in the wild type. In the pgr1 pgr5 double mutants, gH+ was intermediate to gH+ values of the respective single mutants. It is unlikely that gH+ is upregulated simply in response to a low pmf. We did not observe uncoupling of the thylakoid membrane in the pgr5 mutant upon monitoring the quenching of 9-aminoacridine fluorescence. We conclude that the gH+ parameter may be influenced by other factors not related to the H+ leakage through ATP synthase. It is unlikely that the pgr5 mutant leaks protons from the thylakoid membrane.



中文翻译:

拟南芥质子梯度调节5突变体是否从类囊体膜中泄漏质子?

尽管产生了明显的突变表型,拟南芥(Arabidopsis thaliana质子梯度调节5pgr5)突变是否影响PSI周围的循环电子传递(CET)仍然是一个争论的话题。电致变色位移分析结果表明, pgr5突变体中跨类囊体膜的质子电导率 ( g H + )在高光强度下增强。鉴于这一观察结果,PGR5 被认为是调节 ATP 合酶活性而不是介导 CET。最初报道的pgr5表型反映了较小的质子动力 (pmf),并且可以通过该 H +泄漏模型来解释。在本研究中,我们从遗传学角度重新检查了pgr5突变体的高g H +表型。其中黄二铁蛋白依赖性假CET取代PGR5依赖性CET的转基因品系具有野生型g H +水平,这表明pgr5植物中的高g H +表型是由低pmf继发的。pgr1突变体显示出类似的 pmf 减少,因为其细胞色素b 6 f复合物对腔酸化的敏感性增强。与pgr5突变体相比,pgr1突变体中的g H +低于野生型。在pgr1 pgr5双突变体中,g H +处于各个单突变体的g H +值的中间。g H +不太可能仅仅由于低 pmf 而上调。在监测 9-氨基吖啶荧光的猝灭后,我们没有观察到pgr5突变体中类囊体膜的解偶联。我们得出结论,g H +参数可能受到与通过 ATP 合酶的 H +泄漏无关的其他因素的影响。pgr5突变体不太可能从类囊体膜泄漏质子。

更新日期:2020-09-08
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