Genetic interactions between PXY and the ERECTA and PLETHORA gene families drive cell size and cell proliferation during vascular development in Arabidopsis thaliana.

Abstract

A significant proportion of terrestrial biomass is constituted of xylem cells that make up woody plant tissue (Etchells., 2015). This thesis further explores the genetic interactions that underpin the vascular developmental process in Arabidopsis thaliana stems, and the transition from primary to secondary growth in roots. To date, progress in the understanding of the underlying molecular mechanisms and genetic controls that underpin vascular development during secondary growth is incomplete. The PXY gene is one element in a ligand receptor pair that is a known central factor important for vascular development regulation and control. PXY signalling is known to be a part of a complex signalling system and it is clear that other interacting factors are also extremely important for the development of the vasculature. The research described as part of this thesis has shown that there exists a genetic interaction between the PXY gene and those of the PLETHORA3 and PLETHORA5 genes in Arabidopsis thaliana. This thesis has shown that PLETHORA3 and PLETHORA5 genes act redundantly and are in part responsible for the process of cellular proliferation within the vasculature during secondary growth. The loss of function mutations in PLT3 and PLT5 result in enhanced phenotypes in a pxy background for increased loss of cell proliferation. Further, they result in the suppression of hallmark characteristics and cellular proliferation in transgenic 35S::CLE41 over-expression backgrounds. Additionally, the interactions of PXY with the ERECTA family of genes has shown that ERECTA-LIKE genes interact with PXY to regulate the cell size in vascular cell types. Together PXY, ERECTA and PLETHORA interact to drive cell size and cell proliferation within the vascular cambium in regard to secondary growth.