American Society of Plant Biologists 
CONTACT US     SITE MAP     SEARCH     PRIVACY POLICY     ADVERTISE  
Abstract Center . Session List .
Search:
Poster: Vegetative Development

Abs # 445: Apyrase expression is critical for normal vegetative growth in Arabidopsis

Presenter: Roux, Stanley J., sroux@uts.cc.utexas.edu
AuthorsRoux, Stanley J. (A)   Steinebrunner, Iris  (A)   Arnold, David  (A)  
Affiliations: (A): The University of Texas at Austin

Arabidopsis has two highly similar apyrases, AtAPY1 and AtAPY2. Single knockout (KO) mutants of either gene lacked a discernible phenotype, but the double KO (DKO) mutants showed a complete inhibition of pollen germination. Complementation with either apyrase gene under the control of a steroid-inducible promoter rescued pollen germination. Subsequent development in the absence of apyrase expression could proceed through flowering, but the DKO mutants were dwarf. Microscopic analysis revealed that DKO plants generally developed the same tissue patterns as wild-type plants, except in the area of cell expansion. DKO cells in stem and root tissues appeared “early post mitotic” with nuclei appearing more or less normal size, but other cell dimensions were greatly reduced compared to wild type. Mesophyll leaf cells of DKO plants cells failed to expand normally and had greatly reduced vacuoles. Primary root meristems of DKO plants often died soon after germination. This loss of the primary root meristem resulted in adventitious roots, most of them developing just above the hypocotyls. Current evidence suggests that AtAPY1 and AtAPY2 are ectoapyrases, anchored in the plasma membrane with their active site facing to the outside of the cell. Loss of ectoapyrase activity could allow the build-up of the main apyrase substrate, ATP, in the ECM. Tang et al. (Plant Physiol. 131: 147, 2003) have shown that mM levels of external ATP can inhibit auxin transport. We will discuss the speculative possibility that the dwarf phenotype of the apyrase double KO mutants may be partially explained by defective auxin transport in the mutants. Supported by NSF IBN-0080363.

Abstract Center . Session List .
Search: