Chen Wanzhen, Liu Lang, Wang Xiaoyu, Li Haoyu, Liu Jiao, Zhi Pengfei, Chang Cheng
College of Life Sciences, Qingdao University, Qingdao 266071, China.
Int J Mol Sci. 2024 Dec 8;25(23):13187. doi: 10.3390/ijms252313187.
Waxy cuticle covers plant aerial organs and protects plants against environmental challenges. Although improved cuticle-associated traits are aimed at the wheat breeding programs, the mechanism governing wheat cuticular wax biosynthesis remains to be elucidated. Herein, wheat WW domain-containing protein TaCFL1 is characterized as a negative regulator of wax biosynthesis. The knockdown of expression results in a 15% increase in wax accumulation and decreased leaf cuticle permeability in bread wheat. Furthermore, wheat class IV homeodomain transcription factors TaHDG1.1 and TaHDG1.2 are identified as partially redundant activators of wax biosynthesis. The silencing of or expression leads to an 11% reduction in epidermal wax accumulation and an increase in leaf cuticle permeability wax, while the co-silencing of and results in a 31% reduction in epidermal wax accumulation and a further increase in wax in the leaf cuticle permeability. Moreover, wheat 3-Ketoacyl-CoA synthase TaKCS10 is isolated as an essential component of the wax biosynthetic machinery. The silencing of expression results in a 22% reduction in wax accumulation and increased leaf cuticle permeability. In addition, we demonstrated that the expression is activated by TaHDG1.1 and TaHDG1.2, and that TaCFL1 attenuates the TaHDG1-mediated transcriptional activation of . This evidence supports that the WW domain-containing protein TaCFL1 negatively regulates wax biosynthesis via attenuating the transcriptional activation of the gene mediated by HD-ZIP IV transcription factor TaHDG1.
蜡质角质层覆盖植物地上器官,保护植物免受环境挑战。尽管改良与角质层相关的性状是小麦育种计划的目标,但小麦角质层蜡质生物合成的调控机制仍有待阐明。在此,含有WW结构域的小麦蛋白TaCFL1被鉴定为蜡质生物合成的负调控因子。面包小麦中TaCFL1表达的敲低导致蜡质积累增加15%,叶片角质层通透性降低。此外,小麦IV类同源异型域转录因子TaHDG1.1和TaHDG1.2被鉴定为蜡质生物合成的部分冗余激活因子。TaHDG1.1或TaHDG1.2表达的沉默导致表皮蜡质积累减少11%,叶片角质层蜡质通透性增加,而TaHDG1.1和TaHDG1.2的共沉默导致表皮蜡质积累减少31%,叶片角质层蜡质通透性进一步增加。此外,小麦3-酮脂酰辅酶A合酶TaKCS10被分离为蜡质生物合成机制的重要组成部分。TaKCS10表达的沉默导致蜡质积累减少22%,叶片角质层通透性增加。此外,我们证明TaKCS10的表达受TaHDG1.1和TaHDG1.2激活,并且TaCFL1减弱TaHDG1介导的TaKCS10转录激活。这一证据支持含有WW结构域的蛋白TaCFL1通过减弱HD-ZIP IV转录因子TaHDG1介导的TaKCS10基因转录激活来负调控蜡质生物合成。