Page Banner

United States Department of Agriculture

Agricultural Research Service

Research Project: RESPONSE OF DIVERSE RICE GERMPLASM TO BIOTIC AND ABIOTIC STRESSES Title: Phenotypic gain from introgression of two QTLs, qSB9-2 and qSB12-1, for rice sheath blight resistance

Authors
item Wang, Yueguang -
item Pinson, Shannon
item Fjellstrom, Robert
item Tabien, Rodante -

Submitted to: Molecular Breeding
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 23, 2011
Publication Date: August 14, 2011
Citation: Wang, Y., Pinson, S.R., Fjellstrom, R.G., Tabien, R.E. 2011. Phenotypic gain from introgression of two QTLs, qSB9-2 and qSB12-1, for rice sheath blight resistance. Molecular Breeding. 30:293-303.

Interpretive Summary: Sheath blight is one of the most important diseases in rice production and causes yield losses worldwide. Research has been conducted to identify resistance genes to this disease that can be used by breeders to develop improved rice cultivars. Eighteen genes have been identified that affect sheath blight resistance with two of these, named qSB9-2 and qSB12-1, appearing to contribute more to the resistance response. A study was conducted to accurately determine the impact of these two chromosomal regions on sheath blight resistance. Rather than using a standard gene mapping population, we first backcrossed these chromosomal regions into the sheath blight susceptible U.S. rice variety, Lemont and then measured how much they reduced disease development in both a greenhouse and a field study. Both regions were seen to provide a significant reduction in disease when evaluated individually. When the two were combined, another small gain in resistance was observed compared to the rice lines containing just one or the other. However, the impact was not additive which indicates that the development of rice varieties highly resistant to sheath blight disease must involve incremental improvements from combining many genes together. This process is facilitated by having genetic markers that are linked to the various chromosomal regions that possess resistance genes. Both qSB9-2 and qSB12-1 have genetic markers closely associated that can be used by breeders to accomplish marker assisted breeding for improved sheath blight resistance.

Technical Abstract: F2:3 families from crosses between three indica introgression lines and their common japonica recurrent parent were used to evaluate two quantitative trait loci (QTLs) for sheath blight (SB) resistance. Three selected ‘TeQing’-into-‘Lemont’ backcross introgression lines (TILs) were more resistant than their susceptible parent (Lemont) in inoculated field plots, and molecularly verified to contain TeQing alleles at qSB9-2 and/or qSB12-1. F2 individuals homozygous for qSB9-2 and qSB12-1 provided F2:3 families that fit four genotypic classes: containing the resistant TeQing allele for qSB9-2TQ alone, qSB12-1TQ alone, both qSB9-2TQ and qSB12-1TQ, and neither SB QTL introgression. By comparing the SB resistance of these four genotypic classes in micro-chamber evaluations and inoculated field plots, the phenotypic values of the QTLs were measured. Under both study conditions, disease resistance ranked qSB9-2+qSB12-1 > qSB9-2 > qSB12-1> no QTLs, with both qSB9-2 and qSB12-1 acting as dominant resistance genes. In micro-chamber studies, qSB9-2TQ reduced disease an average of 1.0 disease index units and qSB12-1TQ by 0.7 using a scale of 0-9. Field effects of qSB9-2TQ and qB12-1TQ were less pronounced, with average phenotypic gains of 0.5 and 0.2 units, respectively. TIL642 proved to contain qSB9-2TQ in an introgression so small it was tagged by just RM205 on the tip of chromosome 9. These studies verify that the indica introgression of qSB9-2TQ or qSB12-1TQ can measurably improve resistance to sheath blight disease in a highly susceptible tropical japonica cultivar, and fine-mapped the qSB9-2 locus. Markers presently verified as linked to these QTLs can support marker assisted breeding to improve disease resistance.

Last Modified: 4/20/2014
Footer Content Back to Top of Page