Cotton CSLD3 restores cell elongation and cell wall integrity mainly by enhancing primary cellulose production in the Arabidopsis cesa6 mutant

Cotton CSLD3 restores cell elongation and cell wall integrity mainly by enhancing primary cellulose production in the Arabidopsis cesa6 mutant
复制标题

棉花CSLD3主要通过增强拟南芥cesa6突变体中初级纤维素的产生来恢复细胞伸长和细胞壁完整性

DOI:
10.1007/s11103-019-00910-1
复制
发表时间:
2019-11-01
影响因子:
5.1
通讯作者:
Peng, Liangcai
Peng, Liangcai
中科院分区:
生物学2区
文献类型:
--
作者:
Hu, Huizhen;Zhang, Ran;Peng, Liangcai

文献摘要

被引文献

相似文献

过量表达棉花纤维素合成酶样D3(GhCSLD 3)基因部分地挽救了atcesa 6突变体的生长缺陷,主要通过提高初生纤维素产量来恢复细胞伸长和细胞壁完整性。在纤维素合酶样(CSL)家族蛋白中,CSLDs与纤维素合酶(CESA)蛋白具有最高的序列相似性。虽然CSLD蛋白参与了碳水化合物聚合物(纤维素、果胶和半纤维素)的合成,因此参与了植物细胞壁的形成,但CSLD蛋白的确切生物化学功能仍存在争议,其他物种中其余CSLD基因的功能尚未确定。在这项研究中,我们试图通过在atcesa 6突变体中过表达拟南芥AtCSLD 2、-3、-5和棉花GhCSLD 3基因来说明CSLD蛋白的功能,该突变体的背景是拟南芥初生细胞壁纤维素合成缺陷。我们发现GhCSLD 3过表达部分挽救了atcesa 6突变体在早期营养生长过程中的生长缺陷。尽管atcare 6突变体具有显著降低的纤维素含量、缺陷的细胞壁和较低的干质量,但GhCSLD 3过表达在很大程度上恢复了细胞壁完整性(CWI)并提高了生物量产量。我们的研究结果表明,GhCSLD蛋白的过表达增强了初生细胞壁的合成,并补偿了纤维素生产所需的CESA的损失,从而挽救了细胞伸长和CWI的缺陷。
Overexpression of cotton cellulose synthase like D3 (GhCSLD3) gene partially rescued growth defect of atcesa6 mutant with restored cell elongation and cell wall integrity mainly by enhancing primary cellulose production. Among cellulose synthase like (CSL) family proteins, CSLDs share the highest sequence similarity to cellulose synthase (CESA) proteins. Although CSLD proteins have been implicated to participate in the synthesis of carbohydrate-based polymers (cellulose, pectins and hemicelluloses), and therefore plant cell wall formation, the exact biochemical function of CSLD proteins remains controversial and the function of the remaining CSLD genes in other species have not been determined. In this study, we attempted to illustrate the function of CSLD proteins by overexpressing Arabidopsis AtCSLD2, -3, -5 and cotton GhCSLD3 genes in the atcesa6 mutant, which has a background that is defective for primary cell wall cellulose synthesis in Arabidopsis. We found that GhCSLD3 overexpression partially rescued the growth defect of the atcesa6 mutant during early vegetative growth. Despite the atceas6 mutant having significantly reduced cellulose contents, the defected cell walls and lower dry mass, GhCSLD3 overexpression largely restored cell wall integrity (CWI) and improved the biomass yield. Our result suggests that overexpression of the GhCSLD protein enhances primary cell wall synthesis and compensates for the loss of CESAs, which is required for cellulose production, therefore rescuing defects in cell elongation and CWI.