Hydrogen peroxide participates in leaf senescence by inhibiting CHLI1 activity

• Published in: Plant cell reports 2024-11, Vol.43 (11), p.258-258, Article 258
• Main Authors: Wang, Shi-Jia, Zhai, Shuang, Xu, Xin-Tong, Lu, Ying-Tang, Yuan, Ting-Ting
• Format: Article
• Language: English
• Subjects: Accumulation; Arabidopsis - drug effects; Arabidopsis - genetics; Arabidopsis - growth & development; Arabidopsis - metabolism; Arabidopsis - physiology; Arabidopsis Proteins - genetics; Arabidopsis Proteins - metabolism; Biomedical and Life Sciences; Biotechnology; CAT2 gene; CAT2 protein; Catalase; Catalase - metabolism; Cell Biology; Chelation; Chlorophyll; Chlorophyll - metabolism; Developmental stages; Gene Expression Regulation, Plant - drug effects; growth and development; Hydrogen peroxide; Hydrogen Peroxide - metabolism; Leaves; Life Sciences; Lyases; Magnesium; magnesium chelatase; Mutants; Original Article; phenotype; Phenotypes; Plant Biochemistry; Plant growth; Plant Leaves - drug effects; Plant Leaves - genetics; Plant Leaves - growth & development; Plant Leaves - metabolism; Plant Sciences; Plant Senescence - genetics; proteinases; Reactive Oxygen Species - metabolism; Senescence; Synthesis
• ISSN: 0721-7714; 1432-203X; 1432-203X
• DOI: 10.1007/s00299-024-03350-4

Key Message 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 H 2 O 2 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 H 2 O 2 accumulation, as well as the inhibition of catalase (CAT) genes expression. The mutant cat2-1 , with increased H 2 O 2 shows an accelerated senescence phenotype and decreased CHLI1 activity compared with the wild type. H 2 O 2 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 H 2 O 2 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.