The role of callose in guard-cell wall differentiation and stomatal pore formation in the fern Asplenium nidus
The role of callose in guard-cell wall differentiation and stomatal pore formation in the fern Asplenium nidus
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DOI：
10.1093/aob/mcp255
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发表时间：
2009-12-01
期刊：
影响因子：
4.2
通讯作者：
Galatis, B.
中科院分区：
文献类型：
--
作者：
Apostolakos, P.;Livanos, P.;Galatis, B.
为了研究愈伤组织多糖在保卫细胞（GC）壁分化和气孔形成中的作用，采用苯胺蓝染色法和（1 -> 3）-β-D-葡聚糖抗体免疫标记法对蕨类铁角蕨气孔发育过程中愈伤组织多糖的沉积模式进行了研究。本研究在未处理材料以及用抑制胼胝质合成的2-脱氧-D-葡萄糖（2-DDG）或衣霉素、香豆素或2，6-二氯苯腈处理的材料的气孔中进行（3）环匹阿尼酸（cyclopiazonic acid，CPA），其干扰细胞质Ca 2+稳态;（d）细胞松弛素B或安磺灵，它们分别分解肌动蛋白丝和微管。胼胝质然后开始从腹面壁的中间区域向其外围降解，这一过程与由伴侣质膜的局部分离形成的“内部气孔孔”保持同步。在分化GC中，胼胝质始终定位于发育中的细胞壁增厚。在2-DDG，衣霉素和CPA影响的气孔，胼胝质沉积和气孔内孔的形成受到抑制。受影响的腹壁和GC壁增厚含有膜元件。经上述处理恢复的气孔形成气孔的机制与未处理的气孔不同。香豆素或除草醚处理后，胼胝质保留在新生的腹面壁的时间比对照气孔，而内部气孔形成受阻。肌动蛋白丝的解体抑制气孔内孔的形成，但对胼胝质的沉积没有任何影响。胼胝质的沉积和降解的时间和方式对气孔内孔的形成起着重要的作用，胼胝质参与了GC壁增厚的沉积。
The pattern of callose deposition was followed in developing stomata of the fern Asplenium nidus to investigate the role of this polysaccharide in guard cell (GC) wall differentiation and stomatal pore formation.Callose was localized by aniline blue staining and immunolabelling using an antibody against (1 -> 3)-beta-d-glucan. The study was carried out in stomata of untreated material as well as of material treated with: (1) 2-deoxy-d-glucose (2-DDG) or tunicamycin, which inhibit callose synthesis; (2) coumarin or 2,6-dichlorobenzonitrile (dichlobenil), which block cellulose synthesis; (3) cyclopiazonic acid (CPA), which disturbs cytoplasmic Ca2+ homeostasis; and (d) cytochalasin B or oryzalin, which disintegrate actin filaments and microtubules, respectively.In post-cytokinetic stomata significant amounts of callose persisted in the nascent ventral wall. Callose then began degrading from the mid-region of the ventral wall towards its periphery, a process which kept pace with the formation of an 'internal stomatal pore' by local separation of the partner plasmalemmata. In differentiating GCs, callose was consistently localized in the developing cell-wall thickenings. In 2-DDG-, tunicamycin- and CPA-affected stomata, callose deposition and internal stomatal pore formation were inhibited. The affected ventral walls and GC wall thickenings contained membranous elements. Stomata recovering from the above treatments formed a stomatal pore by a mechanism different from that in untreated stomata. After coumarin or dichlobenil treatment, callose was retained in the nascent ventral wall for longer than in control stomata, while internal stomatal pore formation was blocked. Actin filament disintegration inhibited internal stomatal pore formation, without any effect on callose deposition.In A. nidus stomata the time and pattern of callose deposition and degradation play an essential role in internal stomatal pore formation, and callose participates in deposition of the local GC wall thickenings.