The shoot apical meristem (SAM) is a structure at the growing tip of the plant that gives rise to all aboveground tissues throughout its life. Thus in certain species, the SAM has to be properly regulated for hundreds, or even thousands, of years. The genetic network that drives stem cell homeostasis in the model species Arabidopsis thaliana has been intensively studied over the last three decades. It involves a core regulatory feedback loop between the signalling peptide CLAVATA3, produced in stem cells, and the transcription factor WUSCHEL, expressed in the organising centre. Compromised CLAVATA activity leads to massive meristem overgrowth, which has been assumed to be caused by stem cell overproliferation. However, it is unknown how uncontrolled stem cell divisions lead to the specific changes observed in clavata mutants. Here we first quantitatively characterise these mutants to reveal hitherto unknown tissue buckling defects. Analytical models show how this altered morphology might be due perturbed mechanical properties and/or growth rates. Indeed, we find that clavata meristems are softer than the wild type, and that stereotypical wild-type meristem organisation is lost, with cells instead simultaneously expressing genetic markers from multiple, mutually exclusive domains. Lastly, we show that mutant meristematic cells are auxin-responsive, suggesting that they are also functionally different from wild-type stem cells. We propose that the clavata phenotype 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. We suggest that the current definition of stem cells is too restrictive, and should include genetic, mechanical and functional parameters.