State Key Laboratory of Hybrid Rice, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Plant Cell Rep. 2024 Oct 9;43(11):258. doi: 10.1007/s00299-024-03350-4.
Hydrogen peroxide promoted leaf senescence by sulfenylating the magnesium chelating protease I subunit (CHLI1) in the chlorophyll synthesis pathway, and inhibited its activity to reduce chlorophyll synthesis. Leaf senescence is the final and crucial stage of plant growth and development, during which chlorophyll experiences varying degrees of destruction. It is well-known that the higher ROS accumulation is a key factor for leaf senescence, but whether and how ROS regulates chlorophyll synthesis in the process are unknown. Here, we report that HO inhibits chlorophyll synthesis during leaf senescence via the I subunit of magnesium-chelatase (CHLI1). During leaf senescence, the decrease of chlorophyll content is accompanied by the increase of HO accumulation, as well as the inhibition of catalase (CAT) genes expression. The mutant cat2-1, with increased HO shows an accelerated senescence phenotype and decreased CHLI1 activity compared with the wild type. HO inhibits CHLI1 activity by sulfenylating CHLI1 during leaf senescence. Consistent with this, the chli1 knockout mutant displays the same premature leaf senescence symptom as cat2-1, while overexpression of CHLI1 in cat2-1 can partially restore its early senescence phenotype. Taken together, these results illustrate that CAT2-mediated HO accumulation during leaf senescence represses chlorophyll synthesis through sulfenylating CHLI1, and thus inhibits its activity, providing a new insight into the pivotal role of chlorophyll synthesis as a participant in orchestrating the leaf senescence.
过氧化氢通过亚磺酰化叶绿素合成途径中的镁螯合蛋白酶 I 亚基 (CHLI1) 促进叶片衰老,并抑制其活性以减少叶绿素合成。叶片衰老是植物生长发育的最后和关键阶段,在此期间,叶绿素会经历不同程度的破坏。众所周知,较高的 ROS 积累是叶片衰老的关键因素,但 ROS 是否以及如何在这个过程中调节叶绿素合成尚不清楚。在这里,我们报告 HO 通过镁螯合酶 (CHLI1) 的 I 亚基在叶片衰老过程中抑制叶绿素合成。在叶片衰老过程中,叶绿素含量的下降伴随着 HO 积累的增加,以及过氧化氢酶 (CAT) 基因表达的抑制。HO 增加的突变体 cat2-1 与野生型相比表现出加速衰老的表型和 CHLI1 活性降低。HO 通过亚磺酰化 CHLI1 在叶片衰老过程中抑制 CHLI1 活性。与此一致,chli1 敲除突变体表现出与 cat2-1 相同的过早叶片衰老症状,而在 cat2-1 中过表达 CHLI1 可以部分恢复其早期衰老表型。总之,这些结果表明 CAT2 介导的 HO 在叶片衰老过程中的积累通过亚磺酰化 CHLI1 抑制叶绿素合成,从而抑制其活性,为叶绿素合成作为参与协调叶片衰老的参与者提供了新的见解。