Temporal and spatial patterns of GAPDHc mRNA accumulation during an incompatible potato-Phytophthora infestans interaction. Comparison with a compatible interaction

BELIGNI, MV; LAXALT, AM; LAMATTINA, L

PHYSIOLOGIA PLANTARUM

Año: 1999 vol. 105 p. 280 - 287

0031-9317

Abstract: Most inducible defense responses of plants to pathogens are the result of transcriptional activation of specific genes. The cytosolic isoform of the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDHc, EC 1.2.1.12) increases under environmental constraints, including biological stress. This work was directed to investigate the temporal and spatial distribution of GAPDHc mRNA during an incompatible potato (Solanum tuberosum L. cv. Pampeana)-Phytophthora infestans interaction. GAPDHc mRNA accumulated earlier during an incompatible interaction (24 h upon infection) than during a compatible one (48 h) and remained over basal levels until late stages of infection (96 h). This different pattern for temporal accumulation in whole potato plants could be part of the rapid defense responses observed when plants are resistant to infection. During the incompatible interaction, the most important GAPDHc mRNA induction (20-fold increase) relative to basal levels, at 12 h post-inoculation, occurred at the site of infection, whereas a 13-fold increase occurred in the uninfected surrounding tissue of inoculated points. At later stages (24 h), the highest induction was observed in uninoculated leaflets (15-fold), whereas the levels in the inoculated leaflets (both the inoculated points and the surrounding areas) remained above the levels present at time zero of infection (8- and 11-fold, respectively). These results suggest that the signal responsible for GAPDHc mRNA accumulation in plants during infection is first activated in infected tissues, but is then transmitted to uninfected parts. Furthermore, biochemical responses in plants upon pathogen attack include components of primary metabolism, and this could be involved in physiological host adaptations against pathogen spreading.