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. 2018 Oct 24;9:478. doi: 10.3389/fgene.2018.00478

FIGURE 1.

FIGURE 1

Simplified model of the Genetic Regulatory Networks (GRN) controlling leaf development. (A) Leaves initiate from the flank of the shoot apical meristem (SAM) upon the formation of an auxin maxima caused by the cellular repolarisation of the auxin efflux carrier PIN1. This together with the activation of ARP will repress genes involved in the maintenance of SAM (KNOXI genes) at the site of leaf primordia initiation. The primordia will outgrow by increasing cell divisions through the activity of DRN and DRNL. (B) Early after its initiation, the primordia will acquire its adaxial-abaxial polarity through the activation of a complex GRN involving multiple negative feedback mechanisms. miR166 represses the adaxial HD-ZIPIII genes in the abaxial domain and miR390 induces tasiRNAs restricting ARF3 and 4 to the abaxial side. miR166 is itself inhibited by AS1-AS2 in the adaxial end where AS1-AS2 promote the tasiRNA-ARFs. AS1-AS2 are, in turn, inhibited by KAN in the abaxial domain. The establishment of the adaxial-abaxial polarity contributes to activate WOXs genes (WOX1 and PRS) in the medial domain, which result in the formation of the mediolateral axis. (C) Schematic representation of the main developmental processes involved in leaf growth. PRS and WOX1 activate KLUH at the margin of the leaf primordia (or marginal meristem). KLUH, in turn, promotes, in a non-cell autonomous manner, cell proliferation in the center of the leaves (or plate meristem). Later, cell divisions will be restricted to the proximal part of the leaves for several days while cell elongation will be initiated at the distal end. Subsequently, cell divisions will only continue at intercalary meristems before they completely stop. At this stage, leaves will mainly grow through cell elongation. (D) The cell division arrest front is established through the activation of the Class II TCPs at the distal end of the leaf primordia, where they will together with NGA inhibit PRS expression. Class II TCPs also activate miR396, which represses GRF/GIF function in the distal end. In the proximal side, miR319/JAW prevents Class II TCPs function.