Search

Research reveals that plant disease resistance is mediated by MAP kinase 4 (MPK4) activity and its inactivation by transposons result in the development of systemic acquired resistance, elevated salicylic acid levels, and resistance to virulent pathogens.

The Cf genes in tomatoes are responsible for resistance against Cladosporidium fulvum. There are several copies of this gene and 11 of these copies were analyzed for amino acid composition. Results revealed seven hypervariable amino acid residues in the leucine-rich domain. The predicted structure of the protein exposes these residues to the solvent. Further analysis of this domain reveals selection for sequence diversification.

The host gene Prf was found to encode a protein with leucine-zipper, nucleotide-binding and leucine-rich repeat motifs in tomato. Four prf mutant alleles were found to carry alterations within the Prf coding sequence, and a genomic fragment containing Prf was found to complement a prf mutant tomato line for sensitivity to the insecticide Fenthion and for resistance to Pst strains expressing avrPto. In addition, Prf was found to reside in the center of the Pto gene cluster, 500 bp from the Fen gene and 24 kb from the Pto gene.

The replicase enzymes of tobacco inhibit the transcription or movement of the cucumber mosaic viruses (CMV) by directly acting on the viral RNA. The binding of replicase to an inactive 2a transgene protein, encoded by the CMV-RNA2 gene, inhibits the formation of a functional complex. In the absence of a functional complex, the CMV is unable to replicate. Replicase also confers resistance by inhibiting the movement of CMV. The accumulation and transcription of viral RNA is unaffected.

The phosphorylation cascade induced by phosphorylation of the tomato Pto-interacting 1 (Pti1) protein kinase by Pto induces the hypersensitive response (HR). Pti1 expressed in tobacco plants increases HR in response to an avirulence gene. Pti1 is a serine/threonine kinase and acts downstream of Pto. It is unable to phosphorylate Pto or Fen, a related kinase. The HR confers gene-for-gene disease resistance to the plants.

Cloning of four new plant resistant (R) genes gives an insight into the molecular components of plant-pathogen interactions. The four R genes are RPS2 from Arabidopsis, N from tobacco, Cf-9 from tomato and L6 from flax. The diversity in R genes can be attributed to structural differences in genome organization at the loci of R genes. Recombination is mediated by R gene sequences, which might give rise to novel, altered or aberrently regulated R genes due to intragenic recombination or unequal crossing over.

The generation of reactive oxygen intermediates during avirulent pathogen infection leads to H2O2 production that controls the cross-linking of membrane proteins. H2O2 signals apoptosis in the infected cells and serves as a diffusible signal that activates the genes that code for cellular protective enzymes such as glutathione S-transferase in neighboring cells. A combined model that describes the organization of the hypersensitive resistance response to plant disease is proposed.

A screening for suppressors of npr1-1 was conducted to identify additional regulators of systemic acquired resistance (SAR). Results revealed the sni1 mutant that displays near wild-type levels of PR1 expression and resistance to pathogens after induction. The recessive sni1 mutation was found to restore SAR in npr1-1, suggesting that wild-type SNI1 may function as a negative regulator of SAR. The cloning of the SNI1 gene showed that it encodes a leucine-rich nuclear protein.