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PGR5 and NDH-1 systems do not function as protective electron acceptors but mitigate the consequences of PSI inhibition.
Biochimica et Biophysica Acta (BBA) - Bioenergetics ( IF 4.3 ) Pub Date : 2020-01-11 , DOI: 10.1016/j.bbabio.2020.148154
Sanna Rantala 1 , Tapio Lempiäinen 1 , Caterina Gerotto 1 , Arjun Tiwari 1 , Eva-Mari Aro 1 , Mikko Tikkanen 1
Affiliation  

Avoidance of photoinhibition at photosystem (PS)I is based on synchronized function of PSII, PSI, Cytochrome b6f and stromal electron acceptors. Here, we used a special light regime, PSI photoinhibition treatment (PIT), in order to specifically inhibit PSI by accumulating excess electrons at the photosystem (Tikkanen and Grebe, 2018). In the analysis, Arabidopsis thaliana WT was compared to the pgr5 and ndho mutants, deficient in one of the two main cyclic electron transfer pathways described to function as protective alternative electron acceptors of PSI. The aim was to investigate whether the PGR5 (pgr5) and the type I NADH dehydrogenase (NDH-1) (ndho) systems protect PSI from excess electron stress and whether they help plants to cope with the consequences of PSI photoinhibition. First, our data reveals that neither PGR5 nor NDH-1 system protects PSI from a sudden burst of electrons. This strongly suggests that these systems in Arabidopsis thaliana do not function as direct acceptors of electrons delivered from PSII to PSI - contrasting with the flavodiiron proteins that were found to make Physcomitrella patens PSI resistant to the PIT. Second, it is demonstrated that under light-limiting conditions, the electron transfer rate at PSII is linearly dependent on the amount of functional PSI in all genotypes, while under excess light, the PGR5-dependent control of electron flow at the Cytochrome b6f complex overrides the effect of PSI inhibition. Finally, the PIT is shown to increase the amount of PGR5 and NDH-1 as well as of PTOX, suggesting that they mitigate further damage to PSI after photoinhibition rather than protect against it.

中文翻译:

PGR5和NDH-1系统不能用作保护性电子受体,但可以减轻PSI抑制的后果。

在光系统(PS)I处避免光抑制是基于PSII,PSI,细胞色素b6f和基质电子受体的同步功能。在这里,我们使用了一种特殊的光照方案,即PSI光抑制处理(PIT),以通过在光系统中积累过量电子来特异性抑制PSI(Tikkanen and Grebe,2018)。在分析中,拟南芥野生型与pgr5和ndho突变体进行了比较,后者缺少描述为PSI保护性替代电子受体的两个主要循环电子转移途径之一。目的是研究PGR5(pgr5)和I型NADH脱氢酶(NDH-1)(ndho)系统是否能保护PSI免受过量电子胁迫的影响,以及它们是否有助于植物应对PSI光抑制的后果。第一,我们的数据表明,PGR5和NDH-1系统均不能保护PSI免受电子突然爆发的影响。这有力地表明拟南芥中的这些系统不能用作从PSII传递到PSI的电子的直接受体-与发现使Physcomitrella patens PSI抗PIT的黄素铁蛋白相反。其次,证明了在光限制条件下,PSII处的电子传输速率线性依赖于所有基因型中功能性PSI的量,而在过量光照下,细胞色素b6f复合物上电子流的PGR5依赖性控制将被超越PSI抑制作用。最后,PIT被证明可以增加PGR5和NDH-1以及PTOX的含量,
更新日期:2020-01-13
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