...
首页> 外文期刊>The Plant Cell >Rho of plant GTPase signaling regulates the behavior of Arabidopsis Kinesin-13A to establish secondary cell wall patterns.
【24h】

Rho of plant GTPase signaling regulates the behavior of Arabidopsis Kinesin-13A to establish secondary cell wall patterns.

机译:植物GTPase信号传导的Rho调节拟南芥Kinesin-13A的行为以建立次级细胞壁模式。

获取原文
获取原文并翻译 | 示例
           

摘要

Plant cortical microtubule arrays determine the cell wall deposition pattern and proper cell shape and function. Although various microtubule-associated proteins regulate the cortical microtubule array, the mechanisms underlying marked rearrangement of cortical microtubules during xylem differentiation are not fully understood. Here, we show that local Rho of Plant (ROP) GTPase signaling targets an Arabidopsis thaliana kinesin-13 protein, Kinesin-13A, to cortical microtubules to establish distinct patterns of secondary cell wall formation in xylem cells. Kinesin-13A was preferentially localized with cortical microtubules in secondary cell wall pits, areas where cortical microtubules are depolymerized to prevent cell wall deposition. This localization of Kinesin-13A required the presence of the activated ROP GTPase, MICROTUBULE DEPLETION DOMAIN1 (MIDD1) protein, and cortical microtubules. Knockdown of Kinesin-13A resulted in the formation of smaller secondary wall pits, while overexpression of Kinesin-13A enlarged their surface area. Kinesin-13A alone could depolymerize microtubules in vitro; however, both MIDD1 and Kinesin-13A were required for the depolymerization of cortical microtubules in vivo. These results indicate that Kinesin-13A regulates the formation of secondary wall pits by promoting cortical microtubule depolymerization via the ROP-MIDD1 pathway.
机译:植物皮层微管阵列决定了细胞壁的沉积模式以及适当的细胞形状和功能。虽然各种与微管相关的蛋白质调节皮层微管阵列,但木质部分化过程中皮层微管显着重排的机制尚不完全清楚。在这里,我们显示植物(ROP)GTPase信号的本地Rho靶向拟南芥kinesin-13蛋白,Kinesin-13A,到达皮层微管,以建立木质部细胞中次生细胞壁形成的独特模式。 Kinesin-13A优先在次级细胞壁凹坑中定位皮层微管,皮层微管解聚以防止细胞壁沉积。 Kinesin-13A的这种定位需要存在激活的ROP GTPase,微管消耗域1(MIDD1)蛋白和皮质微管。 Kinesin-13A的敲低导致较小的次生壁坑的形成,而Kinesin-13A的过表达扩大了其表面积。单独的Kinesin-13A可以在体外解聚微管。然而,体内皮层微管的解聚需要MIDD1和Kinesin-13A。这些结果表明,Kinesin-13A通过促进经由ROP-MIDD1途径的皮层微管解聚作用来调节次生壁坑的形成。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号