Sterols are required for cell-fate commitment and maintenance of the stomatal lineage in Arabidopsis.
Sterols are required for cell-fate commitment and maintenance of the stomatal lineage in Arabidopsis.
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DOI：
10.1111/tpj.12190
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发表时间：
2013-06
期刊：
影响因子：
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通讯作者：
P. Qian;Bing Han;Edith C F Forestier;Zhìhóng Hú;Na Gao;Wenwen Lu;H. Schaller;Jia Li;S. Hou-S.
中科院分区：
文献类型：
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作者：
P. Qian;Bing Han;Edith C F Forestier;Zhìhóng Hú;Na Gao;Wenwen Lu;H. Schaller;Jia Li;S. Hou-S.
在植物气孔发育过程中，细胞不对称分裂对细胞增殖和命运决定具有重要的调控作用。虽然在气孔发育过程中控制不对称分裂和细胞分化的基因已经被报道，但是控制不对称分裂到细胞分化过程的调节因子仍然知之甚少。在这里，我们报道了拟南芥甾醇C-14还原酶基因FACKEL （FK）的一个弱等位基因（FK - j3158），该等位基因在叶表皮上显示出小细胞簇和气孔，这是在气孔不对称分裂缺陷的突变体中经常看到的一种常见现象。有趣的是，这些分裂的物理不对称性在fk突变体中似乎是完整的，但细胞命运的不对称性受到了极大的干扰，这表明fk途径将不对称分裂过程中的这两个关键事件联系起来。甾醇谱分析显示，fk-J3158突变阻断了下游的甾醇生产。进一步的研究表明，环丙醇异构酶1 （cpi1）、甾醇14α-去甲基化酶（cyp51A2）和hydra1 （hyd1）突变体，对应于甾醇生物合成途径同一分支的酶，表现出与fk相似的气孔发育缺陷表型。fenproimorph是拟南芥中FK甾醇C-14还原酶的抑制剂，在野生型叶片中也会引起这些异常的小细胞和气孔表型。遗传实验表明，甾醇的生物合成是正确的气孔模式所必需的，可能是通过一个尚未确定的额外信号通路。对时间推移细胞分裂模式、气孔前体细胞分裂标记和DNA倍性的详细分析表明，在气孔系细胞中，需要甾醇来适当地限制细胞增殖、不对称命运规范、细胞命运承诺和维持。这些事件发生在气孔前体细胞物理不对称分裂之后。
Asymmetric cell division is important for regulating cell proliferation and fate determination during stomatal development in plants. Although genes that control asymmetric division and cell differentiation in stomatal development have been reported, regulators controlling the process from asymmetric division to cell differentiation remain poorly understood. Here, we report a weak allele (fk-J3158) of the Arabidopsis sterol C-14 reductase gene FACKEL (FK) that shows clusters of small cells and stomata in leaf epidermis, a common phenomenon that is often seen in mutants defective in stomatal asymmetric division. Interestingly, the physical asymmetry of these divisions appeared to be intact in fk mutants, but the cell-fate asymmetry was greatly disturbed, suggesting that the FK pathway links these two crucial events in the process of asymmetric division. Sterol profile analysis revealed that the fk-J3158 mutation blocked downstream sterol production. Further investigation indicated that cyclopropylsterol isomerase1 (cpi1), sterol 14α-demethylase (cyp51A2) and hydra1 (hyd1) mutants, corresponding to enzymes in the same branch of the sterol biosynthetic pathway, displayed defective stomatal development phenotypes, similar to those observed for fk. Fenpropimorph, an inhibitor of the FK sterol C-14 reductase in Arabidopsis, also caused these abnormal small-cell and stomata phenotypes in wild-type leaves. Genetic experiments demonstrated that sterol biosynthesis is required for correct stomatal patterning, probably through an additional signaling pathway that has yet to be defined. Detailed analyses of time-lapse cell division patterns, stomatal precursor cell division markers and DNA ploidy suggest that sterols are required to properly restrict cell proliferation, asymmetric fate specification, cell-fate commitment and maintenance in the stomatal lineage cells. These events occur after physical asymmetric division of stomatal precursor cells.