The Analysis of Two Receptor-like Kinases Redundantly Required for Pattern Formation during Arabidopsis Embryogenesis
KeywordsMolecular & Cellular Biology
AdvisorTax, Frans E.
Committee ChairTax, Frans E.
MetadataShow full item record
PublisherThe University of Arizona.
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AbstractThe coordination of various cellular differentiation and morphogenetic programs during plant embryogenesis is required to establish the basic adult body plan. The molecular basis of these patterning events remains to be fully understood. In particular, little is known about the roles of cell-cell signaling during embryonic pattern formation.I identified two receptor-like kinases, RECEPTOR-LIKE PROTEIN KINASE1 (RPK1) and TOADSTOOL2 (TOAD2), redundantly required for Arabidopsis thaliana embryonic pattern formation. Genetic analysis indicates that RPK1 and TOAD2 have overlapping embryonic functions. The zygotic gene dosage of TOAD2 in an rpk1 background is of critical importance, suggesting that signaling mediated by RPK1 and TOAD2 must be above a threshold level for proper embryo development. The localization of RPK1 and TOAD2 translational fusions to GFP coupled with the analysis of cell-type specific markers indicate that RPK1 and TOAD2 are redundantly required for both pattern formation along the radial axis and differentiation of the basal pole during early embryogenesis.I found that RPK1 and TOAD2 also have overlapping functions required for cotyledon primordia initiation during Arabidopsis embryogenesis. Genetic analyses indicate that cotyledon initiation is sensitive to TOAD2 gene dosage in an rpk1 background. Analysis of cell-specific markers suggest that RPK1 and TOAD2 are primarily required for the differentiation of cell types (i.e. the central domain protoderm) subjacent to the cotyledon primordia, and that the cotyledon initiation defects are caused by defects in the central domain protoderm. In addition, RPK1-GFP and TOAD2-GFP translational fusions had overlapping localization patterns in the central domain protodermal cells when cotyledon primordia were first recognizable. I propose that RPK1 and TOAD2 are primarily required to maintain central domain protoderm cell fate and that the loss of this key embryonic cell type in mutant embryos results in patterning defects throughout the embryo including the failure to initiate cotyledon primordia.This work has identified two putative receptors for cell-cell signals that mediate key patterning events during plant embryogenesis. The future identification of components in the RPK1 and/or TOAD2 signaling pathways will yield further insight into the molecular basis of the generation and assembly of diverse embryonic cell types.
Degree ProgramMolecular & Cellular Biology