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生长素、 KANADI 和 III 类 HD-ZIP 转录因子在维管束组织形成中的相互作用。

Interplay of auxin, KANADI and Class III HD-ZIP transcription factors in vascular tissue formation.

机构信息

Institute of Biology, University of Neuchâtel, Rue Emile Argand 11, 2009 Neuchâtel, Switzerland.

出版信息

Development. 2010 Mar;137(6):975-84. doi: 10.1242/dev.047662.

Abstract

Class III HD-ZIP and KANADI gene family members have complementary expression patterns in the vasculature and their gain-of-function and loss-of-function mutants have complementary vascular phenotypes. This suggests that members of the two gene families are involved in the establishment of the spatial arrangement of phloem, cambium and xylem. In this study, we have investigated the role of these two gene families in vascular tissue differentiation, in particular their interactions with the plant hormone auxin. We have analyzed the vasculature of plants that have altered expression levels of Class III HD-ZIP and KANADI transcription factors in provascular cells. Removal of either KANADI or Class III HD-ZIP expression in procambium cells led to a wider distribution of auxin in internal tissues, to an excess of procambium cell recruitment and to increased cambium activity. Ectopic expression of KANADI1 in provascular cells inhibited procambium cell recruitment due to negative effects of KANADI1 on expression and polar localization of the auxin efflux-associated protein PIN-FORMED1. Ectopic expression of Class III HD-ZIP genes promoted xylem differentiation. We propose that Class III HD-ZIP and KANADI transcription factors control cambium activity: KANADI proteins by acting on auxin transport, and Class III HD-ZIP proteins by promoting axial cell elongation and xylem differentiation.

摘要

III 类 HD-ZIP 和 KANADI 基因家族成员在脉管系统中具有互补的表达模式,它们的功能获得和功能丧失突变体具有互补的脉管表型。这表明这两个基因家族的成员参与了韧皮部、形成层和木质部空间排列的建立。在这项研究中,我们研究了这两个基因家族在血管组织分化中的作用,特别是它们与植物激素生长素的相互作用。我们分析了在原形成层细胞中改变 III 类 HD-ZIP 和 KANADI 转录因子表达水平的植物的脉管系统。在原形成层细胞中去除 KANADI 或 III 类 HD-ZIP 的表达导致生长素在内部组织中的分布更广泛,原形成层细胞的募集增加,形成层活性增加。KANADI1 在原形成层细胞中的异位表达由于 KANADI1 对生长素外排相关蛋白 PIN-FORMED1 的表达和极性定位的负效应,抑制了原形成层细胞的募集。III 类 HD-ZIP 基因的异位表达促进了木质部分化。我们提出,III 类 HD-ZIP 和 KANADI 转录因子控制形成层活性:KANADI 蛋白通过作用于生长素运输,III 类 HD-ZIP 蛋白通过促进轴向细胞伸长和木质部分化。

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