ArticleArchives of virology2026
P3, P3N-PIPO and 6K1 from soybean mosaic virus strain N are involved in host specificity for systemic infection in cultivated and wild soybeans.
Article in Archives of virology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Soybean mosaic virus-N (SMV-N) and clover yellow vein virus (ClYVV-No.30) are two recognized potyviruses with distinct host ranges and host specificities. Both infect systemically wild soybean (Glycine soja) whereas SMV-N, but not ClYVV-No.30, infects systemically cultivated soybean (G. max) as well. In contrast, ClYVV-No.30, but not SMV-N, infects systemically broad bean (Vicia faba). To investigate whether P3, P3N-PIPO, and 6K1 from SMV-N play role in host specificity for systemic infection, each was replaced precisely with those from ClYVV-No.30 including the corresponding NIaPro protease recognition sequences at the junctions between P3-6K1 or 6K1-CI cistrons. A second set of SMVN/ClYVV-No.30 chimeras were also synthesized with the P3, P3N-PIPO, and 6K1 from ClYVV-No.30 but with NIaPro protease recognition site at P3-6K1 or 6K1-CI junctions from SMV-N. Regardless of the origin of NIaPro recognition sites, none of the SMV-N-derived chimeras gained the ability to infect systemically broad bean. On the contrary, unlike parental SMV-N, all SMV-N-derived chimeras lost the ability to infect systemically cultivated and wild soybeans. Site-directed mutagenesis of SMV-N NIaPro recognition site at P3-6K1 junction showed replacement of one of the amino acids with the corresponding residue from ClYVV-No.30 at proximal C-terminus of P3 abolished systemic infection of the SMV-N-derived mutant in both cultivated and wild soybeans. Our data suggest that in addition to processing of the NIaPro recognition site at the P3-6K1 junction, P3N-PIPO and 6K1 are also involved in systemic infection of cultivated and wild soybeans by SMV-N.
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