In plants, the shoot apical meristem (SAM) is an important stem cell niche, and stem cell maintenance is partly coordinated by the expression of CLAVATA3 (CLV3). Lack of CLV3 expression causes meristems to overgrow, and it has been suggested that this phenotype is due to stem cell overproliferation. Here, Léa Rambaud-Lavigne, Namrata Gundiah, Arezki Boudaoud, Pradeep Das and colleagues measure SAM curvature in Arabidopsis plants lacking CLV3 expression. They find that, in contrast to the smooth meristems of wild-type plants, the mutant meristems appear to be buckled. A mathematical modelling approach suggests that local differences in growth and stiffness within the mutant meristems could be sufficient to explain the morphological differences between the wild-type and mutant SAMs. The authors confirm the model’s predictions in vivo by showing that regions of heterogeneous cell growth in the mutant meristems correlate with regions of tissue buckling. Atomic force microscopy suggests that the mutant cells are softer and have more variable stiffness than wild-type cells. The mutant cells also lack characteristic stem cell properties, such as auxin insensitivity. Overall, this study suggests that CLV3 plays an important role in determining the physical properties of meristematic stem cells, and that a combination of these properties, as opposed to stem cell overproliferation alone, contribute to meristem morphology.
