Leaves occur in a vast array of shapes and sizes, with complex diversity contributing to optimization of the principal function of photosynthesis. The program of development from a self-renewing stem cell population to a mature leaf has been of interest to biologists for years. Many genes involved in this process have been identified, particularly in the model eudicot Arabidopsis, so that now we have a greater understanding of mechanisms of stem cell maintenance, cell differentiation and organogenesis. One aspect of leaf development that is of particular interest is the establishment of dorsoventral polarity: the distinct adaxial (upper) and abaxial (lower) sides of the leaf. Early studies postulated conceptual models of how establishment of polarity leads to the development of planar leaves. Studies over the past decade have defined genetic details of this model, and uncovered diverse mechanisms of gene regulation that facilitate development of leaf dorsoventral polarity, including transcriptional regulation, chromatin modification, DNA modification, regulation by short RNAs and translational and post-translational regulation. This review will discuss these regulatory mechanisms in the context of leaf dorsoventrality, and will conclude with unresolved questions and areas of future research.

Leaves develop as planar organs, with a morphology that is specialized for photosynthesis. Development of a planar leaf requires genetic networks that set up opposing adaxial and abaxial sides of the leaf, which leads to establishment of dorsoventral polarity. While many genes have been identified that regulate adaxial and abaxial fate there is little information on how this is integrated with cellular function. EMBRYO DEFECTIVE DEVELOPMENT1 (EDD1) is a nuclear gene that encodes a plastid and mitochondrial localized glycyl-tRNA synthetase. Plants with partial loss of EDD1 function have changes in patterning of margin and distal regions of the leaf. In combination with mutations in the MYB domain transcription factor gene ASYMMETRIC LEAVES1 (AS1), partial loss of EDD1 function results in leaves with reduced adaxial fate. EDD1 may influence leaf dorsoventral polarity through regulating the abaxial fate genes KANADI1 (KAN1) and ETTIN (ETT)/AUXIN RESPONSE FACTOR3 (ARF3) since these genes are upregulated in the edd1 as1 double mutant. SCABRA3 (SCA3), a nuclear gene that encodes the plastid RNA polymerase is also required for leaf adaxial fate in the absence of AS1. These results add a novel component to networks of genetic regulation of leaf development and suggest that organelles, particularly plastids, are required in leaf patterning. Potentially, signalling from organelles is essential for coordination of different cell fates within the developing leaf.