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.
Author contributions
Z.L.N. and E.M.M. conceived the project. Z.L.N. created the vectors and plant lines and performed the confocal imaging and genetics. Y.Z. analyzed the T1 complementation assays in the clv1 background. P.T.T. performed all QRT-PCR analysis. B.A.P. analyzed some of the multiple mutants. Z.L.N. and E.M.M. analyzed the data. Z.L.N. wrote and revised the paper with P.T.T. and E.M.M.
Funding
This work was funded by a National Institutes of Health (NIH) grant [1R01GM086639] to E.M.M.; by funds from the Howard Hughes Medical Institute and the Gordon and Betty Moore Foundation [through grant GBMF3406]; and supported in part by start-up funds provided by Virginia Tech to Z.L.N. Deposited in PMC for release after 6 months.
