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LAX1基因和FRIZZY PANICLE 2基因通过控制穗轴分支和小穗发育来决定水稻的花序结构。

The LAX1 and FRIZZY PANICLE 2 genes determine the inflorescence architecture of rice by controlling rachis-branch and spikelet development.

作者信息

Komatsu M, Maekawa M, Shimamoto K, Kyozuka J

机构信息

Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology, 8916-5, Takayama, Ikoma, 630-0101, Japan

出版信息

Dev Biol. 2001 Mar 15;231(2):364-73. doi: 10.1006/dbio.2000.9988.

DOI:10.1006/dbio.2000.9988
PMID:11237465
Abstract

We have analyzed two mutants that exhibit altered panicle architecture in rice (Oryza sativa L.). In lax1-2, which is a new and stronger allele of the previously reported lax mutant, initiation and/or maintenance of rachis-branches, lateral spikelets, and terminal spikelets was severely prevented. In situ hybridization analysis using OSH1, a rice knotted1 (kn1) ortholog, confirmed the absence of lateral meristems in lax1-2 panicles. These defects indicate that the LAX1 gene is required for the initiation/maintenance of axillary meristems in the rice panicle. In addition to its role in forming lateral meristems, the wild-type LAX1 gene acts as a floral meristem identity gene which specifies the terminal spikelet meristem. A comparison of the defects in lax1-1 and lax1-2 plants suggested that the sensitivities to reduced LAX1 activity were not uniform among different types of meristems. In the fzp2 mutant panicle, the basic branching pattern of the panicle was indistinguishable from that of the wild type; however, specification of both terminal and lateral spikelet meristems was blocked, and sequential rounds of branching occurred at the point where the spikelet meristems are initiated in the wild-type panicle. This resulted in the generation of a panicle composed of excessive ramification of rachis-branches. The lax1-1 fzp2 double mutants exhibited a novel, basically additive, phenotype, which suggests that LAX1 and FZP2 function in genetically independent pathways.

摘要

我们分析了两个在水稻(Oryza sativa L.)中表现出穗型结构改变的突变体。在lax1-2中,它是先前报道的lax突变体的一个新的更强的等位基因,穗轴分支、侧生小穗和顶生小穗的起始和/或维持受到严重阻碍。使用水稻knotted1(kn1)直系同源基因OSH1进行的原位杂交分析证实,lax1-2穗中没有侧生分生组织。这些缺陷表明,LAX1基因是水稻穗中腋生分生组织起始/维持所必需的。除了在形成侧生分生组织中的作用外,野生型LAX1基因还作为一种花分生组织特征基因,指定顶生小穗分生组织。对lax1-1和lax1-2植株缺陷的比较表明,不同类型的分生组织对LAX1活性降低的敏感性并不一致。在fzp2突变体穗中,穗的基本分支模式与野生型无法区分;然而,顶生和侧生小穗分生组织的指定都被阻断,并且在野生型穗中启动小穗分生组织的位置发生了连续几轮的分支。这导致产生了一个由穗轴分支过度分支组成的穗。lax1-1 fzp2双突变体表现出一种新的、基本上是累加的表型,这表明LAX1和FZP2在遗传上独立的途径中发挥作用。

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