Regulation of the KNOX-GA gene module induces heterophyllic alteration in North American lake cress.

Plants show leaf form alteration in response to changes in the surrounding environment, and this phenomenon is called heterophylly. Although heterophylly is seen across plant species, the regulatory mechanisms involved are largely unknown. Here, we investigated the mechanism underlying heterophylly in Rorippa aquatica (Brassicaceae), also known as North American lake cress. R. aquatica develops pinnately dissected leaves in submerged conditions, whereas it forms simple leaves with serrated margins in terrestrial conditions. We found that the expression levels of KNOTTED1-LIKE HOMEOBOX (KNOX1) orthologs changed in response to changes in the surrounding environment (e.g., change of ambient temperature; below or above water) and that the accumulation of gibberellin (GA), which is thought to be regulated by KNOX1 genes, also changed in the leaf primordia. We further demonstrated that exogenous GA affects the complexity of leaf form in this species. Moreover, RNA-seq revealed a relationship between light intensity and leaf form. These results suggest that regulation of GA level via KNOX1 genes is involved in regulating heterophylly in R. aquatica. The mechanism responsible for morphological diversification of leaf form among species may also govern the variation of leaf form within a species in response to environmental changes.

Xcl1 causes delayed oblique periclinal cell divisions in developing maize leaves, leading to cellular differentiation by lineage instead of position.

Differentiation of plant cells is regulated by position-dependent mechanisms rather than lineage. The maize Extra cell layers1 (Xcl1) mutation causes oblique, periclinal divisions to occur in the protoderm layer. These protodermal periclinal divisions occur at the expense of normal anticlinal divisions and cause the production of extra cell layers with epidermal characteristics, indicating that cells are differentiating according to lineage instead of position. Mutant kernels have several aleurone layers instead of one, indicating that Xcl1 alters cell division orientation in cells that divide predominantly in the anticlinal plane. Dosage analysis of Xcl1 reveals that the mutant phenotype is caused by overproduction of a normal gene product. This allows cells that have already received differentiation signals to continue to divide in aberrant planes and suggests that the timing of cell division determines differentiation. Cells that divide early and in the absence of differentiation signals use positional information, while cells that divide late after perceiving differentiation signals use lineage information instead of position.