黄瓜
生物
毛状体
凝集素
植物
细胞生物学
表皮(毛发)
生物化学
遗传学
作者
Duo Lv,Haifan Wen,Gang Wang,Juan Liu,Chunli Guo,Jingxian Sun,Keyan Zhang,Chao-han Li,Jiaqi You,Min‐Hsiung Pan,Huanle He,Run Cai,Junsong Pan
摘要
Abstract Cucumber (Cucumis sativus) fruit spines are a classic material for researching the development of multicellular trichomes. Some key genes that influence trichome development have been confirmed to be associated with cuticle biosynthesis and secondary metabolism. However, the biological mechanisms underlying trichome development, cuticle biosynthesis, and secondary metabolism in cucumber remain poorly understood. Cucumber (Cucumis sativus) fruit spines are classic material for researching the development of multicellular trichomes. Some key genes that influence trichome development have been confirmed to be associated with cuticle biosynthesis and secondary metabolism. However, the biological mechanisms underlying trichome development, cuticle biosynthesis, and secondary metabolism in cucumber remain poorly understood. CsTs, a C-type lectin receptor-like kinase gene, reportedly causes a tender trichome phenotype in cucumber when it mutates. In this study, the role of CsTs in cucumber fruit spine morphogenesis was confirmed using gene editing technology. Sectioning technology and cell wall component detection were used to analyze the main causes of tender fruit spines in the ts mutant. Subsequently, transcriptome data and a series of molecular biology experiments were used to further investigate the relationship between CsTs and cytoskeletal homeostasis in cucumber. CsTs overexpression partially compensated for the abnormal trichome phenotype of an Arabidopsis homolog mutant. Genetic hybridization and metabolic analysis indicated that CsTs and CsMcit can affect trichome development and cuticle biosynthesis using the same pathway. Our findings provide important background information for future research on the molecular mechanism underlying cucumber trichome development and contribute to understanding the biological function of C-type lectin receptor-like kinases.
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