植物学报 ›› 2013, Vol. 48 ›› Issue (4): 389-397.DOI: 10.3724/SP.J.1259.2013.00389

• 研究报告 • 上一篇    下一篇

拟南芥胼胝质合酶基因GSL8参与细胞壁形成和根端静止中心建立与维持

刘林1*, 全先庆1, 赵小梅1, 黄力华1, 冯尚彩2, 黄坤艳1, 周晓燕1, 粟文婷1   

  1. 1临沂大学生命科学学院, 临沂 276005;
    2临沂大学现代中药研究所, 临沂 276005
  • 收稿日期:2012-07-27 修回日期:2012-11-17 出版日期:2013-07-01 发布日期:2013-08-09
  • 通讯作者: 刘林
  • 基金资助:

    山东省自然科学基金;临沂大学科研计划项目

Arabidopsis Callose Synthase Gene GSL8 is Required for Cell Wall Formation and Establishment and Maintenance of Quiescent Center

Lin Liu1*, Xianqing Quan1, Xiaomei Zhao1, Lihua Huang1, Shangcai Feng2, Kunyan Huang1, Xiaoyan Zhou1, Wenting Su1   

  1. 1College of Life Sciences, Linyi University, Linyi 276005, China;

    2Modern TCM Institute, Linyi University, Linyi 276005, China
  • Received:2012-07-27 Revised:2012-11-17 Online:2013-07-01 Published:2013-08-09
  • Contact: Lin Liu

摘要: 用T-DNA插入和RNA干扰技术敲除拟南芥(Arabidopsis thaliana)胼胝质合酶基因GSL8, 在光学和透射电子显微镜下观察野生型和突变体种子的细胞壁和胚根结构, 比较未敲除和敲除该基因幼苗细胞壁及根端分生组织结构。结果表明, 敲除该基因可导致细胞壁发育不良, 壁上出现大小不等的缺口, 缺口处没有质膜将相邻细胞分隔。用T-DNA插入法抑制该基因表达, 发现在种子发育阶段胚根不能形成正常的静止中心。用小RNA干扰技术抑制该基因表达, 结果显示根端失去静止中心。综合以上结果, 认为该基因不仅参与细胞壁发育, 也参与根端静止中心的建立与维持。

Abstract: Callose synthase gene GSL8 in Arabidopsis thaliana was knocked out by means of T-DNA insertion or RNA interference. Cell walls and root apical organization in seeds and seedlings of the knockout lines and wild-type were compared by using light and transmission electron microscopes. Gaps of various sizes were found to occur in cell walls in all knockout lines, and there were no plasma membranes in the gap regions to separate the neighboring cells. No normal quiescent center was established in the embryonic root apices during seed development in the T-DNA mutants. Furthermore, the quiescent center was demonstrated to disappear from the root apices of seedlings as the gene GSL8 was silenced by RNA interference. Based on these observations, it is suggested that the gene GSL8 was involved in the formation of cell wall as well as the establishment and maintenance of quiescent center in the root apex.