 |
 |
Carol Rivin
Associate Professor, Botany and Plant Pathology
|
 |
||||||||||||||
RESEARCH:
The genetic programming of plant development is the major focus of research in our laboratory, using maize as our research organism. The maize plant is an excellent model system for plant development, having a large array of described mutants, well-developed molecular biology tools and superb genetics. Maize is also an important crop plant around the world, so while our research concerns basic science issues, we also hope to contribute to crop improvement. Our research program is centered on the study of genes expressed during embryogenesis. In maize, as in most angiosperms, embryogenesis actually encompasses two distinct developmental programs: embryogeny, which involves the morphogenesis and differentiation of the embryo from the single-celled zygote, and maturation, a process whereby the embryo is diverted from continued growth and directed towards dormancy and desiccation. We have isolated mutants and studied gene expression during both these phases of embryo development.
One of our most exciting recent findings is a mutant that is unable to make a shoot apical meristem---the cell population that will give rise to all shoot structures in the course of embryonic and post-embryonic development. How genes control the establishment of the basic elements of the body plan is a central question in development. We are studying this mutant at the genetic, morphological and molecular levels to determine what cellular process has been disrupted, and how this participates in the formation or function of the meristem. We have just cloned the putative gene for the shootless phenotype and begun to analyze its function and expression. We are also studying the expression of a protein kinase family that appears to be associated with shoot meristem function, and evaluating a potential mutant for one of these genes.
To study the maturation phase of embryogenesis, we have pursued two experimental strategies: isolating and characterizing mutants that disrupt this process in a variety of ways, identifying endogenous and environmental cues that switch embryos from a growth to a maturation pathway. We have been particularly interested in abscisic acid regulation of maturation genes and the maturation developmental pathway, and the involvement of an antagonizing hormone, gibberellin in mediating this developmental switch.