Recessive resistance in Pisum sativum and potyvirus pathotype resolved in a gene-for-cistron correspondence between host and virus

Pea seed-borne mosaic potyvirus (PSbMV) isolates are divided into pathotype s P-1, P-2, and P-4 according to their infection profile on a panel of Pisu m sativum lines. P. sativum PI 269818 is resistant to P-1 and P-2 isolates and is susceptible to P-4 isolates. Resistance to P-1 is inherited as a sin gle recessive gene, denoted sbm-1, and the pathogenicity determinant has pr eviously been mapped to the virus-coded protein VPg. In the cultivar Bonnev ille, a second recessive gene, sbm-2, confers specific resistance to P-2. B y exchanging cistrons between a P-2 and a P-4 isolate, the P3-6k1 cistron w as identified as the PSbMV host-specific pathogenicity determinant on Bonne ville. Exchange of P3-6k1 did not affect infection on PI 269818, and infect ion of Bonneville was not altered by substitution of the VPg cistron, indic ating that P3-6k1 and VPg are independent determinants of pathotype-specifi c infectivity. On PI 269818 the pathogenicity determinant of both P-l and P -2 mapped to the N terminus of VPg. This suggests that VPg from the P-1 and P-2 isolates are functionally similar on this host and that resistance to P-1 and P-2 in PI 269818 may operate by the same mechanism. Identification of VPg-sbm-1 and P3-6k1-sbm-2 as independent pairs of genetic interactors b etween PSbMV and P. sativum provides a simple explanation of the three know n pathotypes of PSbMV. Furthermore, analysis of P-glucuronidase-tagged P-2 virus indicated that sbm-2 resistance affected an early step in infection, implying that the P3-6k1 region plays a critical role in potyvirus replicat ion or cell-to-cell movement.