Abstract
The process of plant senescence is complex and highly coordinated, and is regulated by many endogenous and environmental signals. Ethylene and jasmonic acid are well-known senescence inducers, but their molecular mechanisms for inducing leaf senescence have not been fully elucidated. Here, we studied a receptor gene downstream of an ethylene signal transduction pathway, ETHYLENE RESPONSE FACTOR F5 (SlERF.F5). The silence of SlERF.F5 causes accelerated senescence induced by age, darkness, ethylene, and jasmonic acid. However, overexpression of SlERF.F5 may delay leaf senescence. We further found that silencing of SlERF.F5 inhibited the expression of chlorophyll-related genes CHLH, CHLM, POR, CAO1, GUN4, PPH, SGR1, RBCS, and AUREA genes, and the light-responsive RBCS and LHCA1 gene. Moreover, silencing of SlERF.F5 increases the sensitivity of SlERF.F5-RNAi lines to ethylene and jasmonic acid compared to wild type. In the dark-induced aging experiment, the qRT-PCR analysis showed the expression levels of genes related to the ethylene biosynthesis pathway and the jasmonic acid signaling pathway in SlERF.F5-RNAi lines increased compared with wild type. Yeast two-hybrid experiments showed that SlERF.F5 and SlMYC2 (a transcription factor downstream of the JA receptor) can interact physically, thereby mediating the role of SlERF.F5 in jasmonic acid-induced leaf senescence. Collectively, our research provides new insights into how ethylene and jasmonic acid promote leaf senescence in tomatoes.
The apple C2H2-type zinc finger transcription factor MdZAT10 positively regulates JA-induced leaf senescence by interacting with MdBT2
