Wang Qun, Wang Mingmin, Chen Jian, Qi Weiwei, Lai Jinsheng, Ma Zeyang, Song Rentao
State Key Laboratory of Plant Physiology and Biochemistry, National Maize Improvement Center, Beijing Key Laboratory of Crop Genetic Improvement, Joint International Research Laboratory of Crop Molecular Breeding, College of Agronomy and Biotechnology, China Agricultural University, Beijing 100193, China.
Shanghai Key Laboratory of Bio-Energy Crops, Plant Science Center, School of Life Sciences, Shanghai University, Shanghai 200444, China.
Plant Cell. 2022 Mar 4;34(3):1054-1074. doi: 10.1093/plcell/koab312.
Development of the endosperm is strikingly different in monocots and dicots: it often manifests as a persistent tissue in the former and transient tissue in the latter. Little is known about the controlling mechanisms responsible for these different outcomes. Here we characterized a maize (Zea mays) mutant, endosperm breakdown1 (enb1), in which the typically persistent endosperm (PE) was drastically degraded during kernel development. ENB1 encodes a cellulose synthase 5 that is predominantly expressed in the basal endosperm transfer layer (BETL) of endosperm cells. Loss of ENB1 function caused a drastic reduction in formation of flange cell wall ingrowths (ingrowths) in BETL cells. Defective ingrowths impair nutrient uptake, leading to premature utilization of endosperm starch to nourish the embryo. Similarly, developing wild-type kernels cultured in vitro with a low level of sucrose manifested early endosperm breakdown. ENB1 expression is induced by sucrose via the BETL-specific Myb-Related Protein1 transcription factor. Overexpression of ENB1 enhanced development of flange ingrowths, facilitating sucrose transport into BETL cells and increasing kernel weight. The results demonstrated that ENB1 enhances sucrose supply to the endosperm and contributes to a PE in the kernel.
在前者中它通常表现为持久组织,而在后者中则为短暂组织。对于导致这些不同结果的控制机制,人们了解甚少。在此,我们对一个玉米(Zea mays)突变体——胚乳分解1(enb1)进行了表征,在该突变体中,典型的持久胚乳(PE)在籽粒发育过程中急剧降解。ENB1编码一种纤维素合酶5,其主要在胚乳细胞的基部胚乳转移层(BETL)中表达。ENB1功能的丧失导致BETL细胞中边缘细胞壁内突(内突)的形成大幅减少。有缺陷的内突会损害养分吸收,导致过早利用胚乳淀粉来滋养胚胎。同样,在体外以低水平蔗糖培养的野生型发育籽粒也表现出早期胚乳分解。ENB1的表达由蔗糖通过BETL特异性的Myb相关蛋白1转录因子诱导。ENB1的过表达增强了边缘内突的发育,促进蔗糖转运到BETL细胞中并增加籽粒重量。结果表明,ENB1增强了向胚乳的蔗糖供应,并有助于籽粒中持久胚乳的形成。