New developmental functions of WAVE and ARP2/3 genes in Arabidopsis, maize and rice
Abstract
Plant organogenesis is a direct result of coordinated and specific cell division and growth where cell shape and function are directly related. Plant cell shape is determined by vacuolar turgor pressure driven expansion and cellulose microfibril orientation regulated growth. At the cellular level, actin cytoskeleton provides dynamic tracks for the delivery of cell wall biogenesis enzymes and materials to their required locations on the cell surface. In plants the WAVE and ARP2/3 complexes regulate actin cytoskeleton filament formation. In Arabidopsis and maize, mutations in genes of these complexes are referred to as the distorted and brick mutants respectively, and have been shown to cause cell morphogenesis defects in epidermal pavement cells and trichomes. However, little is known about the overall physiological or developmental effects these mutations have at the plant tissue or organ level. Additionally, while it has been shown that mutations in homologous genes of maize have similar cellular phenotypes as those seen in Arabidopsis, there are distinct differences that are not fully explained in the current model. How can the cellular models for WAVE and ARP2/3 function in Arabidopsis be applied to the organism as a whole? How can the cellular models for WAVE and ARP2/3 function in Arabidopsis be used to explain the phenotypic observations in other physiologically distinct plants such as maize and rice? My MS thesis identifies the maize and rice homologous sequences to the known Arabidopsis SPIKE1, WAVE complex, and ARP2/3 complex genes through bioinformatic analysis. I further characterize the basic maize plant phenotype of the brick mutants and identify potentially useful rice T-DNA insertion alleles for the SPIKE1, SRA1, and ARPC1 genes. Finally, I establish new developmental functions for the WAVE and ARP2/3 complexes in lateral root emergence.
Degree
M.S.
Advisors
Szymanski, Purdue University.
Subject Area
Agronomy
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