Changes in the intraisolate genetic structure of Beet necrotic yellow vein virus populations associated with plant resistance breakdown
被引:40
作者:
Acosta-Leal, Rodolfo
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Texas A&M Univ, Texas Agr Res Stn, Amarillo, TX 79106 USATexas A&M Univ, Texas Agr Res Stn, Amarillo, TX 79106 USA
Acosta-Leal, Rodolfo
[1
]
Fawley, Marvin W.
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N Dakota State Univ, Dept Biol Sci, Fargo, ND 58105 USA
Univ Arkansas, Sch Math & Nat Sci, Monticello, AR 71656 USATexas A&M Univ, Texas Agr Res Stn, Amarillo, TX 79106 USA
Fawley, Marvin W.
[2
,3
]
Rush, Charles M.
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Texas A&M Univ, Texas Agr Res Stn, Bushland, TX 79012 USATexas A&M Univ, Texas Agr Res Stn, Amarillo, TX 79106 USA
Rush, Charles M.
[4
]
机构:
[1] Texas A&M Univ, Texas Agr Res Stn, Amarillo, TX 79106 USA
[2] N Dakota State Univ, Dept Biol Sci, Fargo, ND 58105 USA
[3] Univ Arkansas, Sch Math & Nat Sci, Monticello, AR 71656 USA
[4] Texas A&M Univ, Texas Agr Res Stn, Bushland, TX 79012 USA
The causal agent of rhizomania disease, Beet necrotic yellow vein virus (BNYVV), typically produces asymptomatic root-limited infections in sugar beets (Beta vulgaris) carrying the Rz1-allele. Unfortunately, this dominant resistance has been recently overcome. Multiple cDNA clones of the viral pathogenic determinant p25, derived from populations infecting susceptible or resistant plants, were sequenced to identify host effects on the viral population structure. Populations isolated from compatible plant-virus interactions (susceptible plant-wild type virus and resistant plant-resistant breaking variants) were large and relatively homogeneous, whereas those from the incompatible interaction (resistant plant-avirulent type virus) were small and highly heterogeneous. All populations from susceptible plants had the same dominant haplotype, whereas those from resistant cultivars had a different haplotype surrounded by a spectrum of mutants. Selection and diversification analyses suggest an evolutionary trajectory of BNYVV with positive selection for changes required to overcome resistance, followed by elimination of hitchhiking mutations through purifying selection. (c) 2008 Elsevier Inc. All rights reserved.