Maize streak virus

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Maize streak virus
Common names MSV, streak of maize
Causal agents Maize streak virus
Hosts maize, Urochloa panicoides
Vectors leafhoppers (Cicadulina mbila, and other Cicadulina species, such as C. storeyi, C. arachidis and C. dabrowski)
EPPO code MSV000
Distribution sub-Saharan Africa
Maize streak virus
Virus classification
Group:
Group II (ssDNA)
Order:
Unassigned
Family:
Genus:
Species:
Maize streak virus

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Maize streak virus is a plant disease. It is an insect-transmitted maize pathogen in the genus Mastrevirus of the family Geminiviridae that is endemic in sub-Saharan Africa. The A-strain of MSV (MSV-A) causes sporadic maize streak disease epidemics throughout the maize growing regions of Africa.[1][2][3] MSV was first described by the South African entomologist Claude Fuller who referred to it in a 1901 report as “mealie variegation”.[4] The development of conventionally resistant maize varieties has been a priority since the 1950s in Kenya, Nigeria, South Africa and elsewhere, with a good deal of success: however, there are several genes associated with resistance, and breeding is complex. Transgenically resistant or genetically modified maize varieties are currently under development in South Africa.[5]

MSV is mainly transmitted by Cicadulina mbila, but other leafhopper species, such as C. storeyi, C. arachidis and C. dabrowski, are also able to transmit the virus.

Typical of all mastreviruses, MSV's circular, ~2.7-Kb monopartite single-stranded (ss) DNA genome encodes only four proteins. Bidirectional transcription from a long intergenic region (LIR) results in the virion-sense expression of a movement protein (MP) and a coat protein (CP), and the complementary-sense expression of the replication-associated proteins, Rep and RepA. Whereas the MP and CP are involved in virus movement and encapsidation,[6] Rep is an essential initiator of virus replication, and RepA is a regulator of host and viral gene transcription.[7][8][9][10] Due to genome size restrictions, MSV usurps host DNA replication and double-stranded DNA break repair proteins to replicate its genome via, respectively, rolling-circle [11] and recombination-dependent mechanisms.[12]

References

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External links

*http://www.sciencemag.org/cgi/content/summary/315/5809/182