Figure 13.

Regulatory interactions in SAM development.

(A–F) In situ hybridizations of STM (A, B), CUC2 (C, D) and AS1 (E, F), in globular (A, C, E) and heart (B, D, F) stage embryos. Arrowheads in C and D point to the protoderm, where CUC2 is absent. The arrowhead in F indicates the SAM initials. Images A, B reproduced with permission from Macmillan Publishers Ltd: Nature, Long et al. (1996); C, D reproduced/adapted from Aida et al. (1999) with permission from The Company of Biologists; E, F reproduced with permission from Macmillan Publishers Ltd: Nature, Byrne et al. (2000).

(G) Schematic representation of the expression domain shown in A–F.

(H) Model of STM/CUC/AS interactions. The expression domains of STM and CUC2 (and the other CUC genes) are largely overlapping at the globular stage. Activity of CUCs promotes STM expression (A, C). Conversely, STM downregulates the CUCs. (B, D). STM activity promotes the establishment and maintenance of the SAM. This is in part accomplished by another function of STM: to inhibit expression of the genes AS1 and AS2 (here represented by AS1) in the SAM. The counter-acting activities of CUCs and STM lead to the formation of a torus of CUC expression around a STM domain centered on the SAM in the bent cotyledon stage, depicted in I.

(I) Schematic transverse section through the apex of a bent cotyledon embryo showing the inner STM expression domain surrounded by the CUC2 domain.