Dysregulation of cell-to-cell connectivity and stomatal patterning by loss-of-function mutation in Arabidopsis CHORUS (GLUCAN SYNTHASE-LIKE 8)
Dysregulation of cell-to-cell connectivity and stomatal patterning by loss-of-function mutation in Arabidopsis CHORUS (GLUCAN SYNTHASE-LIKE 8)
复制标题
DOI：
10.1242/dev.049197
复制
发表时间：
2010-05-15
期刊：
影响因子：
4.6
通讯作者：
Torii, Keiko U.
中科院分区：
文献类型：
--
作者：
Guseman, Jessica M.;Lee, Jin Suk;Torii, Keiko U.
植物表皮上气孔和阀门的形成需要信号成分和细胞命运决定因素的协调作用。为了了解气孔模式的调控，我们使用部分缺乏气孔信号受体的背景进行了遗传筛选。在这里，我们报道了合唱（chor）的分离和表征，它赋予了由无话可说（SPCH）介导的气孔系细胞过度增殖。chor打破了三个ERECTA家族基因之间的冗余，并强烈增强了过多口腔功能丧失引起的气孔模式缺陷。白菜幼苗也表现出不完全的细胞分裂和生长缺陷，包括根组织模式和根毛细胞形态发生的破坏。CHOR编码一种假定的胼胝质合成酶葡聚糖合成酶样8 (GLUCAN synthase - like 8, GSL8)，这是在细胞板、细胞壁和胞间连丝上沉积胼胝质所必需的。一致地，在chor中，表皮细胞之间的共plastic大分子扩散显著增加，并且通常不能在细胞间移动的蛋白质（包括荧光蛋白标记的SPCH）扩散到邻近细胞。这种表型不是由细胞分裂缺陷引起的一般性状。我们的研究结果表明，限制共塑运动可能是气孔发育过程中细胞命运决定因素适当分离的重要步骤。
Patterning of stomata, valves on the plant epidermis, requires the orchestrated actions of signaling components and cell-fate determinants. To understand the regulation of stomatal patterning, we performed a genetic screen using a background that partially lacks stomatal signaling receptors. Here, we report the isolation and characterization of chorus (chor), which confers excessive proliferation of stomatal-lineage cells mediated by SPEECHLESS (SPCH). chor breaks redundancy among three ERECTA family genes and strongly enhances stomatal patterning defects caused by loss-of-function in TOO MANY MOUTHS. chor seedlings also exhibit incomplete cytokinesis and growth defects, including disruptions in root tissue patterning and root hair cell morphogenesis. CHOR encodes a putative callose synthase, GLUCAN SYNTHASE-LIKE 8 (GSL8), that is required for callose deposition at the cell plate, cell wall and plasmodesmata. Consistently, symplastic macromolecular diffusion between epidermal cells is significantly increased in chor, and proteins that do not normally move cell-to-cell, including a fluorescent protein-tagged SPCH, diffuse to neighboring cells. Such a phenotype is not a general trait caused by cytokinesis defects. Our findings suggest that the restriction of symplastic movement might be an essential step for the proper segregation of cell-fate determinants during stomatal development.