No abstract

Stem cell homeostasis in the shoot apical meristem involves a core regulatory feedback loop between the signalling peptide CLAVATA3, produced in stem cells, and the transcription factor WUSCHEL, expressed in the underlying organising centre. Compromised CLAVATA activity leads to massive meristem overgrowth, which is thought to be caused by stem cell overproliferation. However, it is unknown how uncontrolled stem cell divisions lead to the specific changes observed inclavatamutants. Here we first quantitatively characterise these mutants, to reveal underlying tissue curvature defects. We use analytical models to show how perturbed mechanical properties and/or growth rates may contribute to altered meristem morphology. Indeed, we find thatclavatameristems are softer than the wild type, and that stereotypical meristem organisation is lost, with cells instead simultaneously expressing multiple domain markers. Furthermore, we show that mutant meristematic cells are auxin-responsive, suggesting that they are functionally different from wild-type stem cells. We propose that theclavataphenotype is not caused by stem cell overproliferation, but rather by the disruption of a more complex regulatory framework that is key to maintaining distinct genetic and functional domains at the shoot apex.