Huang Jia-Bao, Zou Yi, Zhang Xiaojing, Wang Mingyan, Dong Qingkun, Tao Li-Zhen
State Key Laboratory for Conservation and Utilization of Subtropical Agro-bioresources, South China Agricultural University, Guangzhou, China.
Guangdong Provincial Key Laboratory of Protein Function and Regulation in Agricultural Organisms, College of Life Sciences, South China Agricultural University, Guangzhou, China.
Front Plant Sci. 2020 Jan 8;10:1641. doi: 10.3389/fpls.2019.01641. eCollection 2019.
Cell wall biosynthesis plays essential roles in cell division and expansion and thus is fundamental to plant growth and development. In this work, we show that an mutant , isolated by a forward genetic screen, displays embryo defects and short, swelling primary root with the failure of maintenance of root apical meristem reminiscent to several cell wall-deficient mutants. Map-based cloning identified is a mutant allele of (), an enzyme involved in cellulose synthesis. Cellulose content in the mutant was dramatically decreased. Moreover, ( from hereon) caused aberrant auxin distribution, as well as defective accumulation of root master regulators PLETHORA (PLT1 and PLT2) and misexpression of auxin response factor 5 (). The abnormal auxin distribution is likely due to the reduced accumulation of auxin efflux transporters PIN-FORMED (PIN1 and PIN3). Surprisingly, we found that the orientation of actin microfilaments was severely altered in root cells, whereas the cortical microtubules stay normal. Our study provides evidence that the defects in cellulose synthesis affect polar auxin transport possibly connected with altered F-actin organization, which is critically important for vesicle trafficking, thus exerting effects on auxin distribution, signaling, and auxin-mediated plant development.
细胞壁生物合成在细胞分裂和扩展中起着至关重要的作用，因此对植物的生长和发育至关重要。在这项研究中，我们发现通过正向遗传学筛选分离出的一个突变体表现出胚胎缺陷以及短而肿胀的初生根，根尖分生组织无法维持，这与几个细胞壁缺陷突变体相似。基于图谱的克隆鉴定出该突变体是参与纤维素合成的酶（）的一个突变等位基因。突变体中的纤维素含量显著降低。此外，（从这里开始）导致生长素分布异常，以及根主控调节因子多胚基因（PLT1和PLT2）的积累缺陷和生长素响应因子5（）的错误表达。生长素分布异常可能是由于生长素外排转运蛋白PIN-FORMED（PIN1和PIN3）的积累减少所致。令人惊讶的是，我们发现在突变体根细胞中肌动蛋白微丝的方向发生了严重改变，而皮层微管保持正常。我们的研究提供了证据，表明纤维素合成缺陷影响极性生长素运输，可能与肌动蛋白丝组织的改变有关，这对囊泡运输至关重要，从而对生长素分布、信号传导以及生长素介导的植物发育产生影响。
