In plants, the shoot apical meristem (SAM) provides all the cells that are needed for post-embryonic growth and development of the leaves, stems and flowers. In Arabidopsis, a peptide ligand derived from CLAVATA3 (CLV3) regulates the SAM stem cell pool by signalling through two receptor complexes – a homodimer of the receptor-like kinase CLV1 and a heterodimer consisting of the receptor-like protein CLV2 and the protein kinase CRN/SOL2. Now, Shinichiro Sawa and colleagues report that the receptor-like kinase RPK2 also has a vital role in SAM maintenance (see ). They show that loss-of-function mutations in RPK2 result in SAM stem cell expansion and increased numbers of floral organs, as seen in clv1 and clv2 mutants. Notably, the RPK2 mutant phenotypes are additive with those of clv1 and clv2 mutations. Moreover, biochemical analyses in Nicotiana benthamiana reveal that RPK2 forms homodimers but does not associate with CLV1 or CLV2. The researchers propose, therefore, that three, rather than two, CLV3 signalling pathways regulate meristem homeostasis.
