The shoot apical meristem (SAM) of plants contains a reservoir of stem cells that fuel above-ground growth, allowing the plant to grow and form organs throughout its lifetime. In Arabidopsis thaliana, stem cell maintenance in the SAM involves a negative-feedback loop between a secreted peptide known as CLAVATA3 (CLV3) and the transcription factor WUSCHEL (WUS). Now, Jennifer Fletcher and colleagues reveal that two CLV3-related peptides, CLE16 and CLE17, function to buffer stem cell homeostasis in the absence of CLV3. The authors first show that CLE16 and CLE17 transcripts are expressed at low levels in wild-type SAMs, whereas expression increases in clv3 mutants. They further show that, in the absence of CLV3 activity, CLE16 and CLE17 function independently to restrict stem cell accumulation in the SAM. In line with this, the treatment of clv3 mutants with synthetic CLE16 or CLE17 peptides significantly reduces SAM size. Following on from this, the researchers show that BARELY ANY MERISTEM (BAM) receptor kinases are required to transmit the CLE16 and CLE17 signals. Finally, they show that the function of CLE16 and CLE17 in SAM maintenance is dependent upon WUS activity. Overall, these findings uncover additional levels of complexity in CLE peptide signalling and identify novel roles for CLE16 and CLE17 in controlling stem cell homeostasis in the SAM.
