Ke. Keller et al., POTYVIRUS GENOME-LINKED PROTEIN (VPG) DETERMINES PEA SEED-BORNE MOSAIC-VIRUS PATHOTYPE-SPECIFIC VIRULENCE IN PISUM-SATIVUM, Molecular plant-microbe interactions, 11(2), 1998, pp. 124-130
The mechanism of Pisum sativum pathotype-specific resistance to pea se
ed-borne mosaic potyvirus (PSbMV) was investigated and the coding regi
on determinant of PSbMV virulence was defined. Homozygous recessive sb
m-1 peas are unable to support replication of PSbMV pathotype 1 (P-l),
whereas biochemically and serologically related pathotype 4 (P-4) is
fully infectious in the sbm-1/sbm-1 genotype. We were unable to detect
viral coat protein or RNA with double antibody sandwich-enzyme-linked
immunosorbent assay and reverse transcription-polymerase chain reacti
on in sbm-1/sbm-1 P-1-inoculated protoplasts and plants. Lack of viral
coat protein or RNA in P-l transfected sbm-1/sbm-1 protoplasts sugges
ts that sbm-1 resistance is occurring at the cellular level and that i
nhibition of cell-to-cell virus movement is not the operating form of
resistance. In addition, because virus products were not detected at a
ny time post-inoculation, resistance must either be constitutive or ex
pressed very early in the virus infection process. P-l-resistant peas
challenged with full-length, infectious P-1/P-4 recombinant clones dem
onstrated that a specific P-4 coding region, the 21-kDa, genome-linked
protein (VPg), was capable of overcoming sbm-1 resistance, whereas cl
ones containing the P-l VPg coding region were noninfectious to sbm-1/
sbm-1 peas. VPg is believed to be involved in potyvirus replication an
d its identification as the PSbMV determinant of infectivity in sbm-1/
sbm-1 peas is consistent with disruption of an early P-l replication e
vent.