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Plant and Cell Physiology, 2004, Vol. 45, No. 6 770-780
© 2004 Oxford University Press

Up-Regulation and Localization of Asparagine Synthetase in Tomato Leaves Infected by the Bacterial Pathogen Pseudomonas syringae

Francisco Olea1, Alejandro Pérez-García1, Francisco R. Cantón2, M. Eugenia Rivera1, Rafael Cañas2, Concepción Ávila2, Francisco M. Cazorla1, Francisco M. Cánovas2 and Antonio de Vicente1,3

1 Departamento de Microbiología, Facultad de Ciencias, Universidad de Málaga, E-29071 Málaga, Spain
2 Departamento de Biología Molecular y Bioquímica-Unidad Asociada UMA-CSIC, Facultad de Ciencias-Instituto Andaluz de Biotecnología, Universidad de Málaga, E-29071 Málaga, Spain

Nitrogen metabolism is one aspect of basic metabolism, which is still quite unknown in the field of plant–pathogen interactions. Evidence derived from previous studies conducted in our laboratory strongly suggests that during microbial pathogenesis an important nitrogen mobilization process takes place in diseased tissues. Here we describe the expression pattern of asparagine synthetase (AS; EC 6.3.5.4) in tomato leaves infected by the bacterial pathogen Pseudomonas syringae pv. tomato. Using an homologous AS cDNA probe isolated by RT-PCR from infected leaves, we have observed a high level induction of AS expression during the course of infection. Concomitantly, a single AS polypeptide also accumulated in response to bacterial infection. Furthermore, immunohistochemical analysis of AS in infected leaves revealed a strong immunostaining in phloem cells of the main vascular bundles and in secondary veins of the leaf blade. These data correlate with those previously reported for expression of a cytosolic isoform of glutamine synthetase (GS1) also induced during development of the infectious process. Taken together, our results suggest the existence of a GS1/AS pathway representing a metabolic route for transferring ammonium released from protein catabolism into asparagine, an amino acid that may have a major role in nitrogen mobilization from diseased tissues.

3 Corresponding author: Fax: +34-952132000. E-mail: adevicente{at}uma.es


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