DisplayTitle

<div>Fanleaf degeneration is one the most devastating viral diseases of grapevine. It is caused by a number of viruses of the genus <i>Nepovirus </i>(family<i> Secoviridae)</i>, including <i>Grapevine fanleaf virus </i>(GFLV). These viruses have a bipartite (+) sense RNA genome encapsidated in isometric particles and are transmitted by dagger nematodes. Grapevines infected with GFLV exhibit a range of symptoms such as fan-like leaf morphology, mosaics, vein yellowing, shortened internodes and premature death. Though GFLV is one of the most well characterized grapevine viruses, the mechanisms underlying symptom development remain poorly understood. Previous research revealed that symptom determinant(s) of GFLV strain GHu on <i>Nicotiana benthamiana</i>, a systemic herbaceous host, map to the 3’-end of the RNA-dependent RNA polymerase (1E^Pol) coding region. Mutagenesis of amino acids within this region of protein 1E^Pol followed by infectivity studies <i>in planta </i>ruled out several residues unique to strain GHu as being individually responsible for symptom development. Unexpectedly, some of the corresponding chimeric viruses failed to establish systemic infections in <i>N. benthamiana</i>,<i> </i>suggesting that this region may also be involved in systemic movement, a function not previously ascribed to the 1E^Pol protein. These results highlight the multi-functional nature of this GFLV protein and advance our understanding of molecular interactions that enable infection and symptom development by GFLV.</div>