Aviv-Sharon Elinor, Sultan Laure D, Naveh Leah, Kupervaser Meital, Reich Ziv, Charuvi Dana, Adam Zach
Faculty of Agriculture, The Robert H. Smith Institute of Plant Sciences, The Hebrew University of Jerusalem, Rehovot, 76100, Israel.
Department of Biomolecular Sciences, Weizmann Institute of Science, Rehovot, 76100, Israel.
Plant J. 2025 Feb;121(4):e17263. doi: 10.1111/tpj.17263.
Non-photochemical quenching (NPQ), the dissipation of excess light energy as heat, has been long recognized as a major protective mechanism that minimizes the potential for oxidative damage to photosystem II (PSII) reaction centers. Two major positive contributors to NPQ are the carotenoid zeaxanthin, generated from violaxanthin by the enzyme violaxanthin de-epoxidase (VDE or NPQ1), and the thylakoid protein PsbS (NPQ4). The involvement of the lumenal Deg proteases in the repair of PSII from photoinhibition prompted us to further explore their possible role in other responses of Arabidopsis thaliana to high light. Here we show that upon exposure to high light, the single deg1 and the triple deg158 mutants display different levels and kinetics of NPQ, compared with the deg58 mutant and WT that behave alike. In response to high light, the two genotypes lacking Deg1 overaccumulate NPQ1 and NPQ4. After temporal inhibition of protein translation in vivo, the level of these two proteins in deg1 is higher than in WT. Together, the results suggest that Deg1 represents a new level of regulation of the NPQ process through adjusting the quantity of NPQ1 and NPQ4 proteins, probably through their proteolysis.
非光化学猝灭(NPQ),即将多余光能以热的形式耗散,长期以来一直被认为是一种主要的保护机制,可将光系统II(PSII)反应中心遭受氧化损伤的可能性降至最低。NPQ的两个主要正向贡献者是由紫黄质脱环氧化酶(VDE或NPQ1)将紫黄质转化生成的类胡萝卜素玉米黄质,以及类囊体蛋白PsbS(NPQ4)。腔内Deg蛋白酶参与PSII从光抑制中修复的过程,这促使我们进一步探索它们在拟南芥对高光的其他反应中可能发挥的作用。在此我们表明,与表现相似的deg58突变体和野生型相比,暴露于高光下时,单突变体deg1和三突变体deg158表现出不同水平和动力学的NPQ。响应高光时,缺乏Deg1的这两种基因型会过度积累NPQ1和NPQ4。在体内对蛋白质翻译进行短暂抑制后,deg1中这两种蛋白质的水平高于野生型。总之,这些结果表明Deg1可能通过蛋白水解作用调节NPQ1和NPQ4蛋白的数量,从而代表了NPQ过程调控的一个新层面。