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Cell Morphogenesis

During differentiation cells typically adopt a specific cell shape according to their functions. Trichomes are an excellent model system to study the mechanism of cell morphogenesis as they have a predictable form and are accessible to a genetic approach. Many mutants affecting trichome shape in Arabidopsis are caused by mutations in genes involved in the regulation of the actin or microtubule cytoskeleton. We currently focus on two genes that seem to regulate new not yet understood pathways.

Analysis of the SPIRRIG Gene

Mutations in the SPIRRIG gene result in a distorted trichome phenotype and various other cell morphogenesis phenotypes similar as found in arp2/3 mutants. The SPIRRIG gene encodes a BEACH domain protein. The BEACH domain is named after the human CHS and its mouse homolog beige gene (beige and Chediak-Higashi-Syndrom). BEACH domain proteins are thought to be involved in membrane transport processes. Little is known about the molecular function of BEACH domain proteins in plants. We use genetic, cell biological and molecular tools to unravel the role of SPIRRIG in plant cell morphogenesis.

Analysis of the ANGUSTIFOLIA Gene

Mutations in ANGUSTIFOLIA cause a pleiotropic phenotype including underbranched trichomes, narrow leaves and twisted siliques.

The ANGUSTIFOLIA (AN) gene encodes a protein with sequence similarity to C-terminal binding proteins (CtBP) and brefeldin A-ribosylated proteins (BARS). As CtBPs act as transcriptional co-repressors while BARS proteins become ADP-ribosylated after treatment with the fungal toxin brefeldin A its molecular function in plants is still unclear. We use cell biological, genetic and biochemical approaches to understand the molecular mechanism of ANGUSTIFOLIA function.