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Auxin as an inducer of asymmetrical division generating the subsidiary cells in stomatal complexes of Zea mays

机译:生长素作为不对称分裂的诱导物在玉米气孔复合物中产生辅助细胞

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摘要

The data presented in this work revealed that in Zea mays the exogenously added auxins indole-3-acetic acid (IAA) and 1-napthaleneacetic acid (NAA), promoted the establishment of subsidiary cell mother cell (SMC) polarity and the subsequent subsidiary cell formation, while treatment with auxin transport inhibitors 2,3,5-triiodobenzoic acid (TIBA) and 1-napthoxyacetic acid (NOA) specifically blocked SMC polarization and asymmetrical division. Furthermore, in young guard cell mother cells (GMCs) the PIN1 auxin efflux carriers were mainly localized in the transverse GMC faces, while in the advanced GMCs they appeared both in the transverse and the lateral ones adjacent to SMCs. Considering that phosphatidyl-inositol-3-kinase (PI3K) is an active component of auxin signal transduction and that phospholipid signaling contributes in the establishment of polarity, treatments with the specific inhibitor of the PI3K were carried out. The presence of suppressed polarization of SMCs and prevented their asymmetrical division, whereas combined treatment with exogenously added NAA and restricted the promotional auxin influence on subsidiary cell formation. These findings support the view that auxin is involved in Z. mays subsidiary cell formation, probably functioning as inducer of the asymmetrical SMC division. Collectively, the results obtained from treatments with auxin transport inhibitors and the appearance of PIN1 proteins in the lateral GMC faces indicate a local transfer of auxin from GMCs to SMCs. Moreover, auxin signal transduction seems to be mediated by the catalytic function of PI3K.
机译:这项工作中提供的数据表明,在Zea中可能外源添加了生长素吲哚-3-乙酸(IAA)和1-萘萘乙酸(NAA),促进了辅助细胞母细胞(SMC)极性的建立以及随后的辅助细胞的建立。在用生长素运输抑制剂2,3,5-三碘苯甲酸(TIBA)和1-萘氧基乙酸(NOA)处理的过程中,其形成可以特异性地阻止SMC极化和不对称分裂。此外,在年轻的保卫细胞母细胞(GMC)中,PIN1生长素外排载体主要位于GMC的横向面上,而在高级GMC中,它们既出现在与SMC相邻的横向也包括横向。考虑到磷脂酰肌醇-3-激酶(PI3K)是植物生长素信号转导的活性成分,并且磷脂信号传导有助于极性的建立,因此用PI3K的特异性抑制剂进行了治疗。 SMCs极化的抑制和防止它们的不对称分裂的存在,而外源添加NAA的联合治疗并限制了生长素对辅助细胞形成的促进作用。这些发现支持以下观点:生长素参与了玉米双歧杆菌的辅助细胞形成,可能是不对称SMC分裂的诱导剂。总的来说,从生长素运输抑制剂处理得到的结果以及在GMC侧面的PIN1蛋白的出现表明生长素从GMC到SMC的局部转移。此外,生长素信号转导似乎由PI3K的催化功能介导。

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