Current status, potential threat and challenges of Turnip Mosaic Virus (TUMV) management on Brassica crops

Keshav Saharan, Naresh Mehta GS Saharan and PD Meena


Turnip Mosaic Virus (TuMV) is the widest spread viral disease causing 30-90% yield losses in oilseeds Brassica crops at about 35 countries in the world especially when it is associated with Cauliflower Mosaic Virus (CaMV), and Beet Western Yellows Virus (BWYV). Its origin is from a virus of wild orchids, which acquired the pathogenicity on Allium spp. and then through wild Brassica plants became pathogenic to cultivated Brassica and Raphanus. The TuMV is a member of genus Potyvirus in the family potyviride has flexcious filamentous particles 135 Å wide with a model length of 729 nm, containing a single copy of a single stranded positive sense RNA (+ssRNA) genome. Virions are 720 x 15- 20nm, flexcious rods and are composed of 95 % coat protein (CP) and 5 % RNA. Under field conditions, it is transmitted by more than 89 species of aphids in non-persistent transmission mode, however, mainly by Myzus persicae and Brevicoryne brassicae. In general symptoms of TuMV infection are vein clearing, chlorotic mottling, leaf distortion, mosaic, necrosis, and plant stunting and in severe cases host death. Symptom variation in different Brassica species may be observed influenced by environmental conditions, virus strains, aphid vector activity, host genotypes, crop growth stage, and association of other viruses. Its host range is very wide infecting more than 318 species of 156 genera in dicots and monocots including several field crops, ornamentals and weeds. Pathogenic variability in TuMV has been recorded from more than 20 counties in the form of strains/pathotypes and phylogenetic groups infecting different hosts. The molecular mechanisms of host infection and pathogenesis have been observed through identification of effectors and determinant genes during host-virus interactions. The effectors alter the host metabolism to suit viral replication to increase its capability to become more virulent for increased cell infection and pathogenesis. Host resistance to TuMV in Brassica crops governed by both qualitative and quantitative genes. In B. rapa (A) genome, 15 dominants and 6 recessive genes have been mapped to provide resistance to different isolates/pathotypes of TuMV. Five dominant genes and QTLs have been mapped in Aand C genome of B. napus. One dominant and 3 recessive genes have been mapped in A genome of B. juncea lines. In B. oleracea (C) genome, one dominant gene TuRBO2 has been mapped to provide broad-spectrum resistance to TuMV isolates. The Raphanus sativus cv. Daikan has resistance to pathotypes 1 and 8, while cv. Sparkler has extreme resistance to pathotype 1, 7, 8 of TuMV. In Arabidopsis thaliana (A) genome, 5 dominant genes and 2 recessive genes have been mapped in different ecotypes to provide resistance to TuMV isolates/pathotypes. During Arabidopsis-TuMV interaction, upregulation of GSTs as well as cellular and apoplastic GGT with GR activities limits TuMV replication to exhibit resistance. It is difficult to control TuMV because of its wide host range as reservoirs of inoculum, high variability, numerous insect vectors, and development of resistance to insecticides in aphid vectors to make them ineffective. Use of host resistant cultivars is the most effective management method. The use of integrated approaches with precautionary measures to prevent introduction and spread of virus through early warning system for virus incidence can help in effective management TuMV.


Brassica crops, management, Turnip Mosaic Virus, transmission vectors

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