细胞分裂素信号通路转录因子LpARR11调控多年生黑麦草衰老及叶绿素降解的分子机制

叶片衰老是影响饲草产量和品质的重要因素。细胞分裂素（CTK）是抑制叶片衰老和叶绿素降解的关键激素，但分子机制尚不清楚。以重要的冷季型牧草多年生黑麦草为材料，申请人发现，过量表达CTK通路转录因子LpARR11能够延缓叶片衰老，并间接抑制叶绿素降解基因的表达。进一步实验证明，LpARR11能够与叶绿素降解促进转录因子LpABF3互作。在此基础上，我们提出假说：CTK通路转录因子LpARR11与LpABF3协同叶绿素降解等代谢途径，进而影响叶片衰老进程。本项目拟通过以下研究验证该假设：①在黑麦草中敲除及过表达LpARR11，以明确其基因功能；②明晰LpARR11是否影响LpABF3的蛋白稳定性和转录激活活性；③分析共表达LpARR11和LpABF3转基因株系的表型，揭示其互作调控叶绿素降解及叶片衰老的生物学效应。本项目的实施，将为高产优质多年生黑麦草的遗传育种奠定理论基础和提供基因资源。

Leaf senescence is an important factor affecting the biomass yield and quality of forage grass. Cytokinin (CTK) plays a key role in the inhibition of leaf senescence and chlorophyll degradation. However, its underlying mechanism is still unclear. Our previous results indicate that overexpression of a CTK signaling transcription factor LpARR11 from perennial ryegrass, an important forage grass, delayed the progression of leaf senescence and indirectly suppressed the expression of chlorophyll catabolic genes. In addition, LpARR11 showed interaction with LpABF3, a transcription factor that can promote chlorophyll degradation. Based on the above results, we hypothesize that LpARR11 and LpABF3 co-regulate chlorophyll degradation and further affect leaf senescence process. The following experiments will be carried out to prove the hypothesis: ①suppression and overexpression of LpARR11 in perennial ryegrass to clarify its function; ②understanding the effects of LpARR11 on protein activity and transcriptional activity of LpABF3; ③testing the phenotype of transgenic plants with both LpARR11 and LpABF3 co-overexpressed to uncover the biological effects of the interaction between LpARR11 and LpABF3. The implementation of this project will laid a theoretical foundation and provide crucial genetic resources for the improvement breeding of perennial ryegrass.