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乙烯介导的拟南芥黄化幼苗顶端弯钩形成增强是依赖赤霉素的。

Ethylene-mediated enhancement of apical hook formation in etiolated Arabidopsis thaliana seedlings is gibberellin dependent.

作者信息

Vriezen Wim H, Achard Patrick, Harberd Nicholas P, Van Der Straeten Dominique

机构信息

Department of Molecular Genetics, Ghent University, K.L. Ledeganckstraat 35, B-9000 Ghent, Belgium.

出版信息

Plant J. 2004 Feb;37(4):505-16. doi: 10.1046/j.1365-313x.2003.01975.x.

Abstract

Dark-grown Arabidopsis seedlings develop an apical hook by differential elongation and division of hypocotyl cells. This allows the curved hypocotyl to gently drag the apex, which is protected by the cotyledons, upwards through the soil. Several plant hormones are known to be involved in hook development, including ethylene, which causes exaggeration of the hook. We show that gibberellins (GAs) are also involved in this process. Inhibition of GA biosynthesis with paclobutrazol (PAC) prevented hook formation in wild-type (WT) seedlings and in constitutive ethylene response (ctr)1-1, a mutant that exhibits a constitutive ethylene response. In addition, a GA-deficient mutant (ga1-3) did not form an apical hook in the presence of the ethylene precursor 1-aminocyclopropane-1-carboxylate (ACC). Analysis of transgenic Arabidopsis seedlings expressing a green fluorescent protein (GFP)-repressor of ga1-3 (RGA) fusion protein suggested that ACC inhibits cell elongation in the apical hook by inhibition of GA signaling. A decreased feedback of GA possibly causes an induction of GA biosynthesis based upon the expression of genes encoding copalyl diphosphate synthase (CPS; GA1) and GA 2-oxidase (AtGA2ox1). Furthermore, expression of GASA1, a GA-response gene, suggests that differential cell elongation in the apical hook might be a result of differential GA-sensitivity.

摘要

暗中生长的拟南芥幼苗通过下胚轴细胞的差异伸长和分裂形成顶端弯钩。这使得弯曲的下胚轴能够轻柔地拉动被子叶保护的顶端向上穿过土壤。已知几种植物激素参与弯钩发育,包括导致弯钩过度伸长的乙烯。我们发现赤霉素(GA)也参与这一过程。用多效唑(PAC)抑制GA生物合成可阻止野生型(WT)幼苗和组成型乙烯反应(ctr)1-1突变体(该突变体表现出组成型乙烯反应)形成弯钩。此外,GA缺陷型突变体(ga1-3)在乙烯前体1-氨基环丙烷-1-羧酸(ACC)存在的情况下不形成顶端弯钩。对表达绿色荧光蛋白(GFP)-ga1-3抑制子(RGA)融合蛋白的转基因拟南芥幼苗的分析表明,ACC通过抑制GA信号传导来抑制顶端弯钩中的细胞伸长。GA反馈的减少可能基于编码贝壳杉烯二磷酸合酶(CPS;GA1)和GA 2-氧化酶(AtGA2ox1)的基因表达导致GA生物合成的诱导。此外,GA反应基因GASA1的表达表明,顶端弯钩中细胞的差异伸长可能是GA敏感性差异的结果。

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