Yu L P, Simon E J, Trotochaud A E, Clark S E
Department of Biology, University of Michigan, Ann Arbor, MI 48109-1048, USA.
Development. 2000 Apr;127(8):1661-70. doi: 10.1242/dev.127.8.1661.
Mutations at the CLAVATA loci (CLV1, CLV2 and CLV3) result in the accumulation of undifferentiated cells at the shoot and floral meristems. We have isolated three mutant alleles of a novel locus, POLTERGEIST (POL), as suppressors of clv1, clv2 and clv3 phenotypes. All pol mutants were nearly indistinguishable from wild-type plants; however, pol mutations provided recessive, partial suppression of meristem defects in strong clv1 and clv3 mutants, and nearly complete suppression of weak clv1 mutants. pol mutations partially suppressed clv2 floral and pedicel defects in a dominant fashion, and almost completely suppressed clv2 phenotypes in a recessive manner. These observations, along with dominant interactions observed between the pol and wuschel (wus) mutations, indicate that POL functions as a critical regulator of meristem development downstream of the CLV loci and redundantly with WUS. Consistent with this, pol mutations do not suppress clv3 phenotypes by altering CLV1 receptor activation.
CLAVATA基因座(CLV1、CLV2和CLV3)发生突变会导致茎尖和花分生组织中未分化细胞的积累。我们分离出了一个新基因座POLTERGEIST(POL)的三个突变等位基因,作为clv1、clv2和clv3表型的抑制子。所有pol突变体与野生型植株几乎没有区别;然而,pol突变对强clv1和clv3突变体中的分生组织缺陷提供了隐性的部分抑制,对弱clv1突变体则几乎完全抑制。pol突变以显性方式部分抑制了clv2的花和花梗缺陷,并以隐性方式几乎完全抑制了clv2的表型。这些观察结果,以及在pol和wuschel(wus)突变之间观察到的显性相互作用,表明POL作为CLV基因座下游分生组织发育的关键调节因子,与WUS存在功能冗余。与此一致的是,pol突变不会通过改变CLV1受体激活来抑制clv3表型。