Leslie L. Domier,
Houston A. Hobbs,
Nancy K. McCoppin,
Charles R. Bowen,
Todd A. Steinlage,
Yi Wang, and
Glen L. Hartman
First, third, fourth, and eighth authors: United States Department of Agriculture–Agricultural Research Service and Department of Crop Sciences, University of Illinois, Urbana 61801; and second, fifth, sixth, and seventh authors: Department of Crop Sciences, University of Illinois, Urbana.
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Accepted for publication 19 January 2011.
Infection of soybean plants with Soybean mosaic virus (SMV), which is transmitted by aphids and through seed, can cause significant reductions in seed production and quality. Because seedborne infections are the primary sources of inoculum for SMV infections in North America, host-plant resistance to seed transmission can limit the pool of plants that can serve as sources of inoculum. To examine the inheritance of SMV seed transmission in soybean, crosses were made between plant introductions (PIs) with high (PI88799), moderate (PI60279), and low (PI548391) rates of transmission of SMV through seed. In four F2 populations, SMV seed transmission segregated as if conditioned by two or more genes. Consequently, a recombinant inbred line population was derived from a cross between PIs 88799 and 548391 and evaluated for segregation of SMV seed transmission, seed coat mottling, and simple sequence repeat markers. Chromosomal regions on linkage groups C1 and C2 were significantly associated with both transmission of isolate SMV 413 through seed and SMV-induced seed coat mottling, and explained ≈42.8 and 46.4% of the variability in these two traits, respectively. Chromosomal regions associated with seed transmission and seed coat mottling contained homologues of Arabidopsis genes DCL3 and RDR6, which encode enzymes involved in RNA-mediated transcriptional and posttranscriptional gene silencing.
quantitative trait loci, RNA silencing, virus movement.
This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 2011.