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COBL7 通过调控拟南芥纤维素沉积参与气孔形成。

COBL7 is required for stomatal formation via regulation of cellulose deposition in Arabidopsis.

机构信息

State Key Laboratory of Hybrid Rice, Department of Plant Sciences, College of Life Sciences, Wuhan University, Wuhan, 430072, China.

Shanghai Key Laboratory of Plant Molecular Sciences, College of Life Sciences, Shanghai Normal University, Shanghai, 200234, China.

出版信息

New Phytol. 2024 Jan;241(1):227-242. doi: 10.1111/nph.19327. Epub 2023 Oct 18.

DOI:10.1111/nph.19327
PMID:37853545
Abstract

As a key regulator of plant photosynthesis, water use efficiency and immunity, stomata are specialized cellular structures that adopt defined shapes. However, our knowledge about the genetic players of stomatal pore formation and stomatal morphogenesis remains limited. Forward genetic screening, positional cloning, confocal and electron microscopy, physiological and pharmacological assays were employed for isolation and characterization of mutants and genes. We identified a mutant, dsm1, with impaired cytokinesis and deformed stomata. DSM1 is highly expressed in guard mother cells and guard cells, and encodes COBRA-LIKE 7 (COBL7), a plant-specific glycosylphosphatidylinositol (GPI)-anchored protein. COBRA-LIKE 7 and its closest homologue, COBL8, are first enriched on the forming cell plates during cytokinesis, and then their subcellular distribution and abundance change are correlated with the progressive stages of stomatal pore formation. Both COBL7 and COBL8 possess an ability to bind cellulose. Perturbing the expression of COBL7 and COBL8 leads to a decrease in cellulose content and inhibition of stomatal pore development. Moreover, we found that COBL7, COBL8 and CSLD5 have synergistic effects on stomatal development and plant growth. Our findings reveal that COBL7 plays a predominant and functionally redundant role with COBL8 in stomatal formation through regulating cellulose deposition and ventral wall modification in Arabidopsis.

摘要

作为植物光合作用、水分利用效率和免疫的关键调节因子,气孔是专门的细胞结构,具有特定的形状。然而,我们对气孔孔形成和气孔形态发生的遗传调控因子的了解仍然有限。我们采用正向遗传学筛选、定位克隆、共聚焦和电子显微镜、生理和药理学测定等方法,对突变体和基因进行分离和鉴定。我们发现了一个突变体 dsm1,其胞质分裂受损,气孔变形。DSM1 在保卫母细胞和保卫细胞中高度表达,编码植物特异性糖基磷脂酰肌醇(GPI)锚定蛋白 COBRA-LIKE 7(COBL7)。COBRA-LIKE 7 和其最接近的同源物 COBL8,在胞质分裂过程中首先在形成的细胞板上富集,然后其亚细胞分布和丰度变化与气孔孔形成的渐进阶段相关。COBL7 和 COBL8 都具有结合纤维素的能力。干扰 COBL7 和 COBL8 的表达会导致纤维素含量降低,并抑制气孔孔的发育。此外,我们发现 COBL7、COBL8 和 CSLD5 对气孔发育和植物生长有协同作用。我们的研究结果表明,COBL7 通过调节拟南芥纤维素的沉积和腹壁的修饰,与 COBL8 在气孔形成中发挥主要的和功能冗余的作用。

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