|Miklas, Phillip - Phil|
Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/1/2002
Publication Date: 3/1/2003
Citation: STRAUSBAUGH, C.A., MIKLAS, P.N., SINGH, S.P., MYERS, J.R., FORSTER, R.L. GENETIC CHARACTERIZATION OF DIFFERENTIAL REACTIONS AMONG HOS GROUP 3 COMMON BEAN CULTIVARS TO NL-3K STRAIN OF BEAN COMMON MOSAIC NECROSIS VIRUS. PHYTOPATHOLOGY, 93:683-690. 2003. Interpretive Summary: Worldwide, bean common mosaic is a serious seed-borne viral disease of dry edible bean and garden snap bean. Yield loss caused by this disease can exceed 80%. Genetic resistance in the host is the primary means of disease control. Although genetic resistance within the host is well understood, there is still genetic variability that has yet to be characterized or fully exploited in breeding programs. We describe the identification of a new recessive resistance gene that is amenable to exploitation by breeders. This gene conditions resistance to the major endemic strains that plague certified seed production in the west and commercial production in the midwest U.S. This newly identified gene will likely contribute to the development of common bean cultivars with more effective and durable resistance to this pesky virus in both regions.
Technical Abstract: A previously unrecognized recessive resistance gene was identified in three putative Host Group 3 common bean (Phaseolus vulgaris) cultivars: Olathe, Victor, and UI 37; based on genetic analysis of plants from five populations screened with the NL-3 K strain of bean common mosaic necrosis virus (BCMNV). The gene was primarily associated with resistance to leaf stunting and deformity and reduction in plant height. The gene provides similar, but slightly better resistance than the bc-12 gene that is characteristic of Host Group 3 cultivars. Traditional Host Group 3 cultivars like RGB possess the bc-12 gene but are susceptible to NL-3 K, whereas cultivars possessing the new gene condition resistance to NL-3 K. Other slight variations in disease reaction pattern to a wide array of BCM inducing strains was noted among Host Group 3 differentials indicating that additional resistance to BCM exists, but has yet to be fully exploited by breeders. To gage the full breeding value of this newly identified gene, allelism tests with existing genes namely bc-12, and further characterization of response to all BCMV and BCMNV strains, need to be conducted. Meanwhile breeders should seriously consider introgressing this highly effective recessive resistance gene into their programs, while pathologists continue to decipher the genetic variability present among Host Group 3 differential cultivars.