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The CLAVATA1 (CLV1), CLV2 and CORYNE (CRN) receptors egulate cell proliferation in shoot meristems through inhibition of WUSCHEL (WUS). Mutations in these receptors produce more floral organs. The prevailing model proposes that the extra organs are generated from enlarged floral meristems. Using forward and reverse genetics, I identified new alleles in clv1, clv2 and crn and found that most alleles only affect fruit organ number and not sepal, petal or stamen number. Analysis of inflorescence and floral meristems of clv1, clv2 and crn mutants revealed that most mutants do not have altered meristem size. I show that mutations in the ERECTA gene enhance the extra valve phenotype in crn mutants by increasing proliferation in floral meristems. Further data indicate that all mutants tested generate extra organs during fruit development and that CLV1, CLV2 and CRN expression in developing fruit overlaps with regions of increased cell division and extra organs formation. In addition, I provide evidence that CLV1 regulates the transcription factor SHOOTMERISTEMSLESS (STM) in these same regions, as mutations in STM suppress the fruit development phenotype in clv1 mutants.Analysis of the relationship between CLV pathway receptors in meristems and fruit revealed that during fruit development, all three are required to regulate fruit organ number. In meristems, I find that CLV1 appears to play a predominant role, based on evidence that the CLV1 homolog BARELY ANY MERISTEM1 (BAM1) compensates for the absence of CLV1 in the meristem but not in fruit. The fact that BAM1 does not interact genetically with CLV2 or CRN in meristems, further supports the hypothesis that BAM1/CLV1 receptor complexes play key roles in meristems. My analyses suggest that CLV3 acts specifically in the meristem pathway, and not in fruit. Also, I provide genetic data for a CLV3-related CLE gene as a ligand for the fruit-specific pathway. The work presented here provides evidence that a CLV/CRN-STM pathway acts in fruit to restrict cell division and consequently organ number via a mechanism analogous to the CLV/CRN-WUS pathway in shoot meristems, supporting the hypothesis that plants use conserved CLE/Receptor-like kinase/Homeodomain signaling module to maintain meristematic regions throughout the plant.

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