The 2-dimensional to 3-dimensional growth transition in Physcomitrella patens

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An important event in evolutionary history was the colonisation of the land by plants. In the charophyte green algae, the sister group of land plants, growth occurs from apical initial cells with only one or two cutting faces, producing simple forms. The movement from water to land was accompanied by the acquisition of apical initial cells that could cleave in three planes. 3-dimensional (3D) growth is thus a defining feature of all land plants, which underpins structurally complex biomes that form the foundation of important terrestrial ecosystems. The onset of 3D growth in flowering plants occurs during embryogenesis. For this reason, flowering plants such a Arabidopsis thaliana cannot easily be exploited to investigate the genetic basis of 3D growth. However, it is possible to genetically dissect 3D growth in the model moss Physcomitrella patens, an extant representative of one of the earliest diverging land plant lineages. In P. patens, a 2-dimensional (2D) growth phase precedes 3D growth initiation and this 2D phase can be maintained indefinitely. Consequently, forward genetics can be used to create viable 3D-defective mutants in P. patens and a somatic hybidisation based approach can then be used to identify causative mutations, and help elucidate the underlying regulatory networks underpinning 3D growth in plants. It was previously shown that the NO GAMETOPHORES 1 (PpNOG1) gene is essential for 3D growth in P. patens. The aim of this project is to perform further functional characterisation of PpNOG1 in P. patens, and through a comparative approach, in A. thaliana. The first strand of the project will determine the PpNOG1 interaction partners. Next, the function of NOG1 in A. thaliana will be explored. Additionally, the project will examine the effect of PpNOG1 on cell division planes and investigate phytohormone signalling during the transition to 3D growth. Finally, transcriptomics will be used to glean a full picture of how the 3D-defective mutants Ppnog1 & 2 differ transcriptionally from wild type.