Double mutation in tomato ribosomal protein L3 cDNA confers tolerance to deoxynivalenol (DON) in transgenic tobacco.

The contamination of mycotoxins associated with head blight of wheat and other grains caused by Fusarium graminearum is chronic threat to crop, human and animal health throughout the world. Deoxinevalenol (DON), produced by the fungus, belonging to class trichothecene is believed to act as a virulence factor in fungal pathogenesis by inhibiting eukaryotic protein synthesis, thereby blocking or delaying the expression of defense related proteins induced by host plant. The putative site of action of DON is 60s ribosomal protein L3 (RPL3). In order to reduce the effects of DON in the host plants, we modified tomato RPL3 (LeRPL3) to introduce W25R/H259Y mutations so that amino acid residue 258 is changed from tryptophan to arginine and 259 from histidine to tyrosine. Transgenic tobacco plants expressing these modified LeRPL3 cDNAs were tested for growth pattern of T1 seedlings in presence of DON. When seedling of these transgenic tobacco plants were compared for growth in the presence of DON, a significant difference in growth rate and the ability to undergo differentiation was observed among those plants expressing the modified version of the Rp13 gene, compared to those expressing the wild-type Rp13 gene. Expression of the tagged gene product indicates that is was not due to somaclonal variation. These results indicate a possible mechanism of host plant resistance to the fungal pathogen F. graminearum among the susceptible cereal species based on the expression ofmodified Rp13 genes.