Leng Yujia, Yang Yaolong, Ren Deyong, Huang Lichao, Dai Liping, Wang Yuqiong, Chen Long, Tu Zhengjun, Gao Yihong, Li Xueyong, Zhu Li, Hu Jiang, Zhang Guangheng, Gao Zhenyu, Guo Longbiao, Kong Zhaosheng, Lin Yongjun, Qian Qian, Zeng Dali
State Key Lab for Rice Biology, China National Rice Research Institute, Hangzhou 310006, China (Yu.L., Y.Y., D.R., L.H., L.D., Y.W., L.C., Z.T., Y.G., L.Z., J.H., G.Z., Z.G., L.G., Q.Q., D.Z.).
National Key Laboratory of Crop Genetic Improvement and National Centre of Plant Gene Research, Huazhong Agricultural University, Wuhan 430070, China (Yu.L., L.D., L.C., Yo.L.).
Plant Physiol. 2017 Jun;174(2):1151-1166. doi: 10.1104/pp.16.01625. Epub 2017 Apr 28.
To better understand the molecular mechanisms behind plant growth and leaf senescence in monocot plants, we identified a mutant exhibiting dwarfism and an early-senescence leaf phenotype, termed (). Histological analysis showed that the abnormal growth was caused by a reduction in cell number. Further investigation revealed that the decline in cell number in was affected by the cell cycle. Physiological analysis, transmission electron microscopy, and TUNEL assays showed that leaf senescence was triggered by the accumulation of reactive oxygen species. The gene was cloned using a map-based approach. It was shown to encode a pectate lyase (PEL) precursor that contains a PelC domain. contains all the conserved residues of PEL and has strong similarity with plant PelC. is expressed in all tissues but predominantly in elongating tissues. Functional analysis revealed that mutation of decreased the total PEL enzymatic activity, increased the degree of methylesterified homogalacturonan, and altered the cell wall composition and structure. In addition, transcriptome assay revealed that a set of cell wall function- and senescence-related gene expression was altered in plants. Our research indicates that is involved in both the maintenance of normal cell division and the induction of leaf senescence. These findings reveal a new molecular mechanism for plant growth and leaf senescence mediated by genes.
为了更好地理解单子叶植物生长和叶片衰老背后的分子机制，我们鉴定出一个表现出矮化和叶片早衰表型的突变体，命名为（）。组织学分析表明，异常生长是由细胞数量减少引起的。进一步研究发现，该突变体中细胞数量的减少受细胞周期影响。生理分析、透射电子显微镜和TUNEL分析表明，活性氧的积累触发了叶片衰老。利用图位克隆法克隆了该基因。结果表明，它编码一种含有PelC结构域的果胶酸裂解酶（PEL）前体。该突变体包含PEL的所有保守残基，并且与植物PelC具有高度相似性。该基因在所有组织中均有表达，但在伸长组织中表达量最高。功能分析表明，该基因的突变降低了总PEL酶活性，增加了甲酯化同型半乳糖醛酸的程度，并改变了细胞壁的组成和结构。此外，转录组分析表明，该突变体植株中一组与细胞壁功能和衰老相关的基因表达发生了改变。我们的研究表明，该基因参与了正常细胞分裂的维持和叶片衰老的诱导。这些发现揭示了由该基因介导的植物生长和叶片衰老的新分子机制。
