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SnRK2.10 激酶通过保护光合作用机制来减轻盐度的不利影响。

The SnRK2.10 kinase mitigates the adverse effects of salinity by protecting photosynthetic machinery.

机构信息

Department of Metabolic Regulation, Institute of Biochemistry, Faculty of Biology, University of Warsaw, Miecznikowa 1, 02-096 Warsaw, Poland.

Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Pawińskiego 5a, 02-106 Warsaw, Poland.

出版信息

Plant Physiol. 2021 Dec 4;187(4):2785-2802. doi: 10.1093/plphys/kiab438.

Abstract

SNF1-Related protein kinases Type 2 (SnRK2) are plant-specific enzymes widely distributed across the plant kingdom. They are key players controlling abscisic acid (ABA)-dependent and ABA-independent signaling pathways in the plant response to osmotic stress. Here we established that SnRK2.4 and SnRK2.10, ABA-nonactivated kinases, are activated in Arabidopsis thaliana rosettes during the early response to salt stress and contribute to leaf growth retardation under prolonged salinity but act by maintaining different salt-triggered mechanisms. Under salinity, snrk2.10 insertion mutants were impaired in the reconstruction and rearrangement of damaged core and antenna protein complexes in photosystem II (PSII), which led to stronger non-photochemical quenching, lower maximal quantum yield of PSII, and lower adaptation of the photosynthetic apparatus to high light intensity. The observed effects were likely caused by disturbed accumulation and phosphorylation status of the main PSII core and antenna proteins. Finally, we found a higher accumulation of reactive oxygen species (ROS) in the snrk2.10 mutant leaves under a few-day-long exposure to salinity which also could contribute to the stronger damage of the photosynthetic apparatus and cause other deleterious effects affecting plant growth. We found that the snrk2.4 mutant plants did not display substantial changes in photosynthesis. Overall, our results indicate that SnRK2.10 is activated in leaves shortly after plant exposure to salinity and contributes to salt stress tolerance by maintaining efficient photosynthesis and preventing oxidative damage.

摘要

SNF1 相关蛋白激酶 2 型(SnRK2)是一类广泛存在于植物界的植物特异性酶。它们是植物响应渗透胁迫过程中控制脱落酸(ABA)依赖和非依赖信号通路的关键调控因子。在这里,我们发现 ABA 非激活激酶 SnRK2.4 和 SnRK2.10 在拟南芥莲座叶中,于盐胁迫早期应答过程中被激活,并通过维持不同的盐胁迫触发机制,导致叶片生长迟缓。在盐胁迫下,snrk2.10 插入突变体在受损的 PSII 核心和天线蛋白复合物的重建和重排过程中受到损伤,导致更强的非光化学猝灭、更低的 PSII 最大量子产量和对高光强的适应能力降低。观察到的效应可能是由于 PSII 核心和天线蛋白的积累和磷酸化状态受到干扰所致。最后,我们发现 snrk2.10 突变体叶片在数天长时间暴露于盐胁迫下积累了更多的活性氧(ROS),这也可能导致光合作用装置的更强损伤,并引起影响植物生长的其他有害影响。我们发现 snrk2.4 突变体植物在光合作用中没有表现出明显的变化。总的来说,我们的结果表明,SnRK2.10 在植物暴露于盐胁迫后不久在叶片中被激活,并通过维持有效的光合作用和防止氧化损伤来促进耐盐性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e500/8644180/1b64a3ecdafb/kiab438f1.jpg

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