|Brzostowski, Lilliam - University Of Illinois|
|Pruski, Timothy - University Of Illinois|
|Bond, Jason - Southern Illinois University|
|Wang, Dechun - Michigan State University|
|Cianzio, Silvia - Iowa State University|
|Diers, Brian - University Of Illinois|
Submitted to: Theoretical and Applied Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/18/2018
Publication Date: 4/24/2018
Citation: Brzostowski, L.F., Pruski, T.I., Hartman, G.L., Bond, J.P., Wang, D., Cianzio, S.R., Diers, B.W. 2018. Field evaluation of three sources of genetic resistance to sudden death syndrome of soybean. Theoretical and Applied Genetics. 131(7):1541-1552. doi.org/10.1007/s00122-018-3096-4.
DOI: https://doi.org/10.1007/s00122-018-3096-4 Interpretive Summary: Sudden death syndrome of soybean is a disease that causes yield loss in soybean growing regions across the USA and worldwide. Soybean resistance to this disease is not a single gene but is controlled by several genes each providing a minor (quantitative) contribution to resistance. The objective of this research was to incorporate sudden death syndrome quantitative resistance into elite breeding soybean lines. Regions within three soybean chromosomes were associated with sudden death syndrome resistance and several sources, including PI567374 and PI507531, were used to enhance SDS resistance. The information presented in this study can aid breeders in making decisions to improve resistance to SDS. This report is important to plant pathologist and breeders interested in plant disease management through host resistance.
Technical Abstract: Sudden death syndrome (SDS) of soybean [Glycine max (L.) Merrill] is a disease that causes yield loss in soybean growing regions across the USA and worldwide. While several quantitative trait loci (QTL) for SDS resistance have been mapped, studies to further evaluate these QTL are limited. The objective of our research was to map SDS resistance QTL and to test the effect of mapped resistance QTL on foliar symptoms when incorporated into elite soybean backgrounds. We mapped a QTL from Ripley to chromosome 10 (CHR10) and a QTL from PI507531 to chromosomes 1 and 18 (CHR1 and 18). Six populations were then developed to test the following QTL: cqSDS-001, with resistance originating from PI567374, CHR10, CHR1, and CHR18. The populations which segregated for resistant and susceptible QTL alleles were field tested in multiple environments and evaluated for SDS foliar symptoms. While foliar disease development was variable across environments and populations, a significant effect of each QTL on disease was detected within at least one environment. This includes the detection of cqSDS-001 in three genetic backgrounds. The QTL allele from the resistant parents was associated with greater resistance than the susceptible alleles for all QTL and backgrounds with the exception of the allele for CHR18, where the opposite occurred. This study highlights the importance and difficulties of evaluating QTL and the need for multi-year SDS field testing. The information presented in this study can aid breeders in making decisions to improve resistance to SDS.