Archivio Journal of Plant Pathology

Abstract:

Abutilon mosaic virus (AbMV) and Bean dwarf mosaic virus (BDMV) are phylogenetically related, bipartitegenome begomoviruses. AbMV is limited to the plant host phloem but BDMV is not. We have previously provided evidence that the genomic DNA-A component of BDMV contains determinants involved in movement (Levy and Czosnek, 2003). We report here that the DNA-A-encoded genes AC2 and AC3 are involved in virus accumulation and spread. To follow AbMV and BDMV movement in inoculated bean plants, we replaced their coat protein genes (CP) with DNA encoding the green or the red fluorescent proteins (GFP, RFP) to create BDMV-CP:GFP, BDMV-CP:RFP, and AbMV-CP:GFP. Frame-shift mutations in BDMV AC2 and AC3 to produce BDMV-CP:GFP-mC23 resulted in inhibition of BDMV movement when co-inoculated with BDMV DNA-B. The mutation reverted to wildtype and movement was restored when BDMVCP: GFP-mC23 was co-inoculated with BDMV-CP:RFP and BDMV DNA-B, which strongly suggests that the AC2/AC3 region is important for BDMV movement. Consequently we replaced the AC2/AC3 region of Ab- MV-CP:GFP with that of BDMV to create AbMVCP: GFP-C23: BDMV. AbMV-CP: GFP-C23: BDMV inoculated together with AbMV DNA-B moved from cell to cell in the epidermis towards the phloem, and long-distance in the entire plant, even though inocula lacked part of all of BDMV DNA-B. AbMV-CP:GFP with its cognate DNA-B was unable to move. Inoculation of bean with AbMV-CP:GFP-C23:BDMV and BDMV DNA-B resulted in the accumulation of very large amounts of viral DNA, in remarkably fast systemic movement, and in the early appearance of severe symptoms, which in most cases, resulted in an inhibition of germination. These results suggest that interactions between AC2/AC3 of BDMV and other proteins encoded by AbMV DNA-A and DNA-B influence the ability of AbMV to overcome the phloem barrier and move in non-phloem cells. Furthermore, they suggest that proteins encoded by AbMV DNA-A also interact with those encoded by BDMV DNA-B, resulting in an enhancement of systemic spread and of symptom development.