Nimchuk Zachary L, Zhou Yun, Tarr Paul T, Peterson Brenda A, Meyerowitz Elliot M
Division of Biology 156-29, California Institute of Technology, Pasadena, CA 91125, USA Howard Hughes Medical Institute, California Institute of Technology, Pasadena, CA 91125, USA Department of Biological Sciences, Virginia Tech, Blacksburg, VA 24061, USA
Division of Biology 156-29, California Institute of Technology, Pasadena, CA 91125, USA.
Development. 2015 Mar 15;142(6):1043-9. doi: 10.1242/dev.119677.
The CLAVATA3 (CLV3)-CLAVATA1 (CLV1) ligand-receptor kinase pair negatively regulates shoot stem cell proliferation in plants. clv1 null mutants are weaker in phenotype than clv3 mutants, but the clv1 null phenotype is enhanced by mutations in the related receptor kinases BARELY ANY MERISTEM 1, 2 and 3 (BAM1, 2 and 3). The basis of this genetic redundancy is unknown. Here, we demonstrate that the apparent redundancy in the CLV1 clade is in fact due to the transcriptional repression of BAM genes by CLV1 signaling. CLV1 signaling in the rib meristem (RM) of the shoot apical meristem is necessary and sufficient for stem cell regulation. CLV3-CLV1 signaling in the RM represses BAM expression in wild-type Arabidopsis plants. In clv1 mutants, ectopic BAM expression in the RM partially complements the loss of CLV1. BAM regulation by CLV1 is distinct from CLV1 regulation of WUSCHEL, a proposed CLV1 target gene. In addition, quadruple receptor mutants are stronger in phenotype than clv3, pointing to the existence of additional CLV1/BAM ligands. These data provide an explanation for the genetic redundancy seen in the CLV1 clade and reveal a novel feedback operating in the control of plant stem cells.
CLAVATA3（CLV3）-CLAVATA1（CLV1）配体-受体激酶对负向调控植物茎尖干细胞的增殖。CLV1缺失突变体的表型比CLV3突变体弱，但CLV1缺失突变体的表型会因相关受体激酶BARELY ANY MERISTEM 1、2和3（BAM1、2和3）的突变而增强。这种遗传冗余的基础尚不清楚。在此，我们证明CLV1进化枝中明显的冗余实际上是由于CLV1信号对BAM基因的转录抑制。茎尖分生组织的肋状分生组织（RM）中的CLV1信号对于干细胞调控是必要且充分的。RM中的CLV3-CLV1信号在野生型拟南芥植物中抑制BAM表达。在CLV1突变体中，RM中异位的BAM表达部分弥补了CLV1的缺失。CLV1对BAM的调控不同于CLV1对拟议的CLV1靶基因WUSCHEL的调控。此外，四重受体突变体的表型比CLV3更强，这表明存在其他CLV1/BAM配体。这些数据为CLV1进化枝中观察到的遗传冗余提供了解释，并揭示了植物干细胞控制中存在的一种新型反馈机制。
