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Glossy15,一种来自玉米的APETALA2类基因,可调控叶片表皮细胞特性。

Glossy15, an APETALA2-like gene from maize that regulates leaf epidermal cell identity.

作者信息

Moose S P, Sisco P H

机构信息

Department of Genetics, North Carolina State University, Raleigh 27695-7620, USA.

出版信息

Genes Dev. 1996 Dec 1;10(23):3018-27. doi: 10.1101/gad.10.23.3018.

DOI:10.1101/gad.10.23.3018
PMID:8957002
Abstract

Vegetative development in many plants progresses through distinct juvenile and adult phases. In maize, the transition from juvenile to adult shoot development affects a variety of leaf epidermal cell traits. These include epicuticular waxes, leaf hairs, and cell wall characteristics. Previous genetic and phenotypic analyses have shown that the maize Glossy15 (Gl15) gene is required for the expression of juvenile epidermal traits after leaf 2. We report here the molecular cloning of the Gl15 gene using a defective Suppressor-Mutator (dSpm) element insertion as a transposon-tag. Consistent with the gl15 mutant phenotype, the pattern of Gl15 mRNA expression was correlated with a juvenile leaf epidermal cell identity and was regulated by upstream factors such as Corngrass1. The Gl15 gene encodes a putative transcription factor with significant sequence similarity to the Arabidopsis regulatory genes APETALA2 and AINTEGUMENTA, which act primarily to regulate floral organ identity and ovule development. This finding expands the known functions of APETALA2-related genes to include the control of both vegetative and reproductive lateral organ identity and provides molecular support for the hypothesis that leaves and floral organs are related structures derived from a common growth plan.

摘要

许多植物的营养生长会经历不同的幼年和成年阶段。在玉米中,从幼年到成年茎发育的转变会影响多种叶片表皮细胞特征。这些特征包括表皮蜡质、叶毛和细胞壁特性。先前的遗传和表型分析表明,玉米光泽15(Gl15)基因是叶片2之后幼年表皮特征表达所必需的。我们在此报告使用缺陷型抑制子-突变体(dSpm)元件插入作为转座子标签对Gl15基因进行的分子克隆。与gl15突变体表型一致,Gl15 mRNA的表达模式与幼年叶片表皮细胞身份相关,并受上游因子如玉米草1的调控。Gl15基因编码一种推定的转录因子,与拟南芥调控基因APETALA2和AINTEGUMENTA具有显著的序列相似性,这两个基因主要作用是调控花器官身份和胚珠发育。这一发现将已知的APETALA2相关基因的功能扩展到包括对营养和生殖侧生器官身份的控制,并为叶片和花器官是源自共同生长计划的相关结构这一假说提供了分子支持。

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