Figure 1

A model integrating the multiple layers of regulation that account for the development and polarization of leaf primordia from the shoot apical meristem (SAM) in plants. (a) The role of auxin effluxes, based on the models of Meyerowitz and Kuhlemeier. Top view of a shoot, showing the SAM (inside the dotted line) and three developing leaf primordia at different stages. Dark green, high levels of auxin; light green, low auxin levels; arrows, movement of auxin; PIN1 and CUC2 are expressed in the high and low auxin regions, respectively. In both models, the PIN1 distribution in a given cell depends on the relative auxin concentration in neighboring cells. PIN1 preferentially polarizes towards adjacent cells with the highest auxin content, pumping more auxin into these cells. (b) Regulation of gene expression by transcription factor proteins. Expression of ASYMMETRIC LEAVES1 (AS1) is restricted to the leaf primordia; this maintains the repression of KNOX proteins in the leaf primordia and enables leaf initiation when auxin accumulates. KNOXs, which specify meristem identity, are thus confined to the SAM. HD-ZIPIII and KANADI (KAN) genes have complementary expression patterns in leaf primordia; they act antagonistically to each other to specify the polarity of the emerging leaf. (c) A close-up of the leaf primordium in (b), showing opposing gradient of protein and small RNA expression. Cell-to-cell movement might cause a reduction in levels of TAS3 from the SAM vasculature to the abaxial side of the developing primordium. This might confine HD-ZIPIII expression to the adaxial domain. The model is based on the proposal by Timmermans that miR166 expression is transcriptionally controlled by ETT, which is itself a known target of TAS3. (d) The pathway of ta-siRNA biogenesis. First, a non-coding transcript is cleaved by the miRNA-loaded Argonaute1 (AGO1), the 'slicer' component of the RISC complex. Cleavage fragments are then converted into dsRNA by SGS3 and RDR6, from which ta-siRNAs are generated by the action of DCL4. The ta-siRNAs then cleave and degrade target transcripts bearing sequences complementary to the ta-siRNA, possibly through the recruitment of an AGO7-programmed RISC.