Speaker: Brian Zebosi, graduate student

Major: Genetics and Genomics

Major professor: GDCB Professor Erik Vollbrecht

Title: "Can plants survive without steroids?"

Abstract: Shoot architecture is a key determinant of grain yield in maize. Among the major plant growth regulators, brassinosteroids (BRs) affect multiple developmental processes and plant architecture traits, including organ size, sex determination, and leaf angle. However, genetic mechanisms by which BRs regulate plant architecture traits in maize remain poorly understood. We have generated and characterized several brassinosteroid biosynthesis and signaling mutants that emphasize the role of BRs in plant growth and development. Two of BR synthetic mutants include brassinosteroid deficient semi-dwarf (bds1) and bds2. The bds1 mutant is a point-nonsense EMS-induced mutation we localized to a gene that encodes an enzyme likely involved in BR biosynthesis. Using phylogenetic and sequence similarity analysis, we identified a bds1 close homolog, bds2 and generated several mutant alleles by remobilizing a nearby Ds transposable element. Contrary to bds1 mutants, the bds2 single mutants were indistinguishable from wild-type plants. However, the bds1-R; bds2-Ds double mutants exhibited enhanced bds1 developmental defects such as plant dwarfness and tassel feminization. Based on these results, we propose that bds1 and bds2 cooperatively regulate shoot architecture and BR biosynthesis. Cabbage (cbg1 and cbg2) are another pair of BR biosynthetic mutants that we identified using Mutator transposons and characterized. Neither single (cbg1 and cbg2) mutant displayed obvious developmental defects. However, their double-mutants (cbg1; cbg2) had extreme defects such extreme dwarf stature, smaller leaves, fewer tassel branches and reduced root growth. Thus, we hypothesize that cbg1 and cbg2 redundantly function plant growth and development via BR biosynthesis.

In addition to BR biosynthesis, we also investigated roles of Brassinosteroid Insensitive1 (BRI1), a receptor-like kinase to plant development and BR signaling. In Maize, there are five BRI1 gene members: a specific duplication of BRI1 (ZmBRI1a and ZmBRI1b), and an additional three homologs (BRL1, BRL2 and BRL3). To understand the tissue-specific functions of the individual receptors and their contributions to BR signaling, we identified transposon mutants either from public sources or for those genes without existing mutant alleles, we generated them using Ac/Ds transposon mutagenesis. To dissect genetic interactions between the BRI receptors, we stacked various receptor mutants to generate all higher-order mutant combinations (single, double, triple, quadruple and, quintuples). We characterized tissue-specific developmental defects in seedling shoots, coleoptile, mesocotyl and roots across the different mutant combinations. Neither single mutants nor higher mutants that contained a functional bri1a or bri1b showed obvious growth defects. However, bri1a; bri1b double mutants exhibited dwarfed plant stature and reduced root size. These plant growth defects were enhanced in specific higher order mutant combinations such as bri1a;bri1b;brl1 triple-mutants and bri1a;bri1b;brl1;brl3 quadruple-mutants, which implies these BRI1 receptor-like kinase members function collectively to regulate plant development. Our data show that brassinosteroids are essential for plant growth and development.