Characterisation of morphogenesis mutants in Arabidopsis

Abstract

In this thesis is described the identification and characterisation of two morphogenesis mutants of Arabidopsis thaliana. One, vertically challenged (vch1) exhibits much reduced cellular elongation. The second, altered suspensor fate (asf1) is embryonic- lethal. A thorough phenotypic analysis of both mutants is presented, as are the results of genetic analysis. Vch1 exhibits a severe reduction in cellular elongation throughout the plant, resulting in a dwarfed phenotype. Despite its stunted morphology, vch1 exhibits normal cellular patterning, demonstrating that cell morphogenesis can be uncoupled from correct cellular pattern formation, vch1 follows a normal life history by all parameters examined demonstrating that the timing of developmental events can be uncoupled from correct morphogenesis. The phenotype of vch1 cannot be rescued by the exogenous supply of a range of hormones, signalling inhibitors or growth conditions, although it can respond to each, in a proportionately similar manner to wild type seedlings. No defects in cell wall architecture nor in cytoskeletal organisation were detected during this study. Speculative models for the role of the VCH gene are proposed. In asf1, the embryo proper arrests at the transition stage of embryogenesis. The wild type suspensor is a single file of cells which serves to anchor the embryo proper to the maternal tissue and acts as a conduit for, and source of, nutrients to the developing embryo. In asf1, suspensor cells undergo inappropriate proliferation following the arrest of the embryo proper. Evidence is presented from cytological and ultrastructural examination, and expression of spatially restricted gus-fusion marker genes, that the ectopically divided suspensor cells take on aspects of embryo proper-like character. Models for the role of the ASF1 gene are proposed. It is likely that the mutant phenotype results from disruption of intercellular communication between the embryo proper and suspensor.