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CLAVATA和无茎尖分生组织基因座竞争性调控拟南芥中的分生组织活性。

The CLAVATA and SHOOT MERISTEMLESS loci competitively regulate meristem activity in Arabidopsis.

作者信息

Clark S E, Jacobsen S E, Levin J Z, Meyerowitz E M

机构信息

Division of Biology, California Institute of Technology, Pasadena 91125, USA.

出版信息

Development. 1996 May;122(5):1567-75. doi: 10.1242/dev.122.5.1567.

DOI:10.1242/dev.122.5.1567
PMID:8625843
Abstract

The CLAVATA (CLV1 and CLV3) and SHOOT MERISTEMLESS (STM) genes specifically regulate shoot meristem development in Arabidopsis. CLV and STH appear to have opposite functions: c1v1 and Clv3 mutants accumulate excess undifferentiated cells in the shoot and floral meristem, while stm mutants fail to form the undifferentiated cells of the shoot meristem during embryonic development. We have identified a weak allele of stm (stm-2) that reveals STM is not only required for the establish- ment of the shoot meristem, but is also required for the continued maintenance of undifferentiated cells in the shoot meristem and for proper proliferation of cells in the floral meristem. We have found evidence of genetic interactions between the CLV and STM loci. clv1 and c1v3 mutations partially suppressed the stm-1 and stm-2 phenotypes, and were capable of suppression in a dominant fashion. clv stm double mutants and plants homozygous for stm but heterozygous for clv, while still lacking an embryonic shoot meristem, exhibited greatly enhanced postembryonic shoot and floral meristem development. Although stm phenotypes are recessive, stm mutations dominantly suppressed clv homozygous and heterozygous phenotypes. These results indicate that the stm phenotype is sensitive to the levels of CLV activity, while the clv phenotype is sensitive to the level of STM activity. We propose that these genes play related but opposing roles in the regulation of cell division and/or cell differentiation in shoot and floral meristems.

摘要

CLAVATA(CLV1和CLV3)基因以及无茎端分生组织(STM)基因专门调控拟南芥茎端分生组织的发育。CLV和STM似乎具有相反的功能:CLV1和CLV3突变体在茎端和花分生组织中积累过量未分化细胞,而STM突变体在胚胎发育过程中无法形成茎端分生组织的未分化细胞。我们鉴定出一个STM的弱等位基因(stm-2),该等位基因表明STM不仅对于茎端分生组织的建立是必需的,而且对于茎端分生组织中未分化细胞的持续维持以及花分生组织中细胞的正常增殖也是必需的。我们发现了CLV和STM基因座之间存在遗传相互作用的证据。CLV1和CLV3突变部分抑制了stm-1和stm-2的表型,并且能够以显性方式进行抑制。CLV-STM双突变体以及STM纯合但CLV杂合的植株,虽然仍然缺乏胚胎茎端分生组织,但在胚胎后茎端和花分生组织发育方面表现出极大增强。尽管STM表型是隐性的,但STM突变却能显性抑制CLV纯合和杂合表型。这些结果表明,STM表型对CLV活性水平敏感,而CLV表型对STM活性水平敏感。我们提出,这些基因在茎端和花分生组织的细胞分裂和/或细胞分化调控中发挥相关但相反的作用。

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