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原形成层特异性基因Oshox1促进生长素极性运输能力并降低其对抑制作用的敏感性。

The procambium specification gene Oshox1 promotes polar auxin transport capacity and reduces its sensitivity toward inhibition.

作者信息

Scarpella Enrico, Boot Kees J M, Rueb Saskia, Meijer Annemarie H

机构信息

Institute of Molecular Plant Sciences, Leiden University, Clusius Laboratory, P.O. Box 9505, 2300 RA Leiden, The Netherlands.

出版信息

Plant Physiol. 2002 Nov;130(3):1349-60. doi: 10.1104/pp.009167.

DOI:10.1104/pp.009167
PMID:12428000
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC166654/
Abstract

The auxin-inducible homeobox gene Oshox1 of rice (Oryza sativa) is a positive regulator of procambial cell fate commitment, and its overexpression reduces the sensitivity of polar auxin transport (PAT) to the PAT inhibitor 1-N-naphthylphthalamic acid (NPA). Here, we show that wild-type rice leaves formed under conditions of PAT inhibition display vein hypertrophy, reduced distance between longitudinal veins, and increased distance between transverse veins, providing experimental evidence for a role of PAT in vascular patterning in a monocot species. Furthermore, we show that Oshox1 overexpression confers insensitivity to these PAT inhibitor-induced vascular-patterning defects. Finally, we show that in the absence of any overt phenotypical change, Oshox1 overexpression specifically reduces the affinity of the NPA-binding protein toward NPA and enhances PAT and its sensitivity toward auxin. These results are consistent with the hypothesis that Oshox1 promotes fate commitment of procambial cells by increasing their auxin conductivity properties and stabilizing this state against modulations of PAT by an endogenous NPA-like molecule.

摘要

水稻(Oryza sativa)的生长素诱导型同源异型盒基因Oshox1是原形成层细胞命运决定的正向调节因子,其过表达降低了极性生长素运输(PAT)对PAT抑制剂1-N-萘基邻苯二甲酸(NPA)的敏感性。在此,我们表明,在PAT抑制条件下形成的野生型水稻叶片表现出叶脉肥大、纵向叶脉之间的距离减小以及横向叶脉之间的距离增加,为PAT在单子叶植物物种的维管束模式形成中的作用提供了实验证据。此外,我们表明Oshox1过表达赋予了对这些PAT抑制剂诱导的维管束模式缺陷的不敏感性。最后,我们表明,在没有任何明显表型变化的情况下,Oshox1过表达特异性降低了NPA结合蛋白对NPA的亲和力,并增强了PAT及其对生长素的敏感性。这些结果与以下假设一致:Oshox1通过增加原形成层细胞的生长素传导特性并使其状态稳定,以抵抗内源性NPA样分子对PAT的调节,从而促进原形成层细胞的命运决定。

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