The movement protein of Cucumber mosaic virus determines systemic infection in the melon accession PI161375

GUIU-ARAGONÉS, CÈLIA; DÍAZ-PENDÓN, JUAN; PEÑA, EDUARDO; HEINLEIN, MANFRED; MARTÍN-HERNÁNDEZ, ANA

Bischoffsheim

Workshop; EMBO-workshop Intercellular communication in plant development and disease; 2014

Exotic melon accession PI161375 shows a complex resistance to CMV infection, qualitative or quantitative depending on the strain. Previously, we had reported the presence of a recessive gene (cmv1) in the linkage group XII conferring total resistance to CMV strains of subgroup II, but not to strains of subgroup I (Essafi et al., 2009). Strains of subgroup II are not able to complete the infectious cycle in presence of cmv1, whereas those of subgroup I can infect systemically. Using infectious clones of strains CMV-LS (subgroup II) and CMV-FNY (subgroup I) we made combinations between RNAs of both strains showing that the determinant of the virulence is located in RNA3. Chimaeras between CMV-FNY and CMV-LS showed that the determinant of the virulence is in the N-terminal 209 amino acids of the movement protein (MP). By directed mutagenesis, we identified 4 specific positions that confer to LS the ability to overcome cmv1- mediated resistance when exchanged for the corresponding FNY residues. We have also analysed the mechanisms of the resistance provided by cmv1. The strain CMV-LS is able to replicate and to move cell to cell in the inoculated leaf of the resistant line. However, it is not able to invade the sieve elements since we haven?t been able to detect the virus in the phloem of the resistant line. Moreover, by ?in situ? hybridization, we have observed that the virus does not invade the phloem cells. Our current work is focused on identifying by electron microscopy the cell type of the phloem tissue where the virus invasion is interrupted. Altogether, our results demonstrate that resistance determined by cmv1 involves interruption of the virus entry into the vascular system and therefore, inability to develop a systemic infection