  Existing mathematical models of the shoot apical meristem (SAM) explain
nucleation and confinement of a stem cell domain by Turing's mechanism,
assuming that the diffusion coefficients of the activator (WUSCHEL) and
inhibitor (CLAVATA) are significantly different. As there is no evidence for
this assumption of differential diffusivity, we recently proposed a new
mechanism based on a bistable switch model of the SAM. Here we study the
bistable-switch mechanism in detail, demonstrating that it can be understood as
localized switches of WUSHEL activity in individual cells driven by a
non-uniform field of a peptide hormone. By comparing domain formation by Turing
and bistable-switch mechanisms on a cell network, we show that the latter does
not require the assumptions needed by the former, which are not supported by
biological evidences.
