Dev119677 1043..1049
نویسندگان
چکیده
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 BARELYANYMERISTEM1, 2and3 (BAM1,2and 3). Thebasis of this genetic redundancy isunknown.Here,wedemonstrate that theapparent redundancy in the CLV1 clade is in fact due to the transcriptional repression ofBAM 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, ectopicBAM expression in theRMpartially complements the loss ofCLV1.BAM regulation byCLV1 is distinct fromCLV1 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.
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