Wheat stripe rust, caused by Puccinia striiformis, is a common disease that was found primarily in the Pacific Northwest prior to 1990, with occasional minor outbreaks in the eastern wheat regions. A physiological adaptation to higher temperatures that occurred around 1990 led to stripe rust becoming a major disease problem in the Gulf Coast. Race (pathotype) changes have occurred several times since 2000, resulting in cultivars with previously effective resistance genes becoming susceptible. The cultivar LA 841, developed by the LSU AgCenter, has remained resistant to all races of stripe rust in the area for over 15 years. It contains the gene cluster Lr37/Yr17/Sr38 with Yr17, conferring broad-spectrum stripe rust resistance until recent years, when new races of stripe rust became virulent on Yr17. LA841 has remained resistant after Yr17 has lost its effectiveness, which indicates that LA 841 contains alternate/additional stripe rust resistance genes. Our objective was to determine the genetics of the resistance in LA 841. A mapping population consisting of 192 F2 progeny derived from a cross between the resistant line LA 841 and susceptible line NC06BGTAG12, was genotyped with 216 polymorphic SSR and AFLP markers. The F2:3 progeny was phenotyped for their reaction to stripe rust in replicated trials at three locations: Winnsboro, Louisiana; Plains, Georgia; and Fayetteville, Arkansas. Three QTL were identified - two on the short arm of chromosome 2A and one on chromosome 3B which together explained 43.2% of the total variation for stripe rust resistance. The QTL on chromosome 3B was flanked by SSR markers Barc164 and Barc1044. One QTL on the 2A chromosome was flanked by SSR markers gwm 636 and gwm 359 while the other QTL on the same chromosome was flanked by gwm 359 and AFLP marker gcg 800-2. Yr17, located on the short arm of chromosome 2A, is most likely the QTL closest to marker gwm 636, which is linked to the gene. This QTL explained 8.6% of the variation but has a LOD value of 11.2, which is the highest of the three. The QTL with the largest effect was found in the short arm of chromosome 2A, which accounted for 22% of the variation and had an LOD value of 9.8. The QTL on chromosome 3B explained 13% of the variation and has a LOD value of 2.7, just over the threshold of 2.5. Identification of new QTL linked to resistance genes is important in breeding programs for disease resistance due to the constant adaptation of pathogens which overcome previously effective resistance genes.
| Identifer | oai:union.ndltd.org:LSU/oai:etd.lsu.edu:etd-11112015-105214 |
| Date | 07 December 2015 |
| Creators | Castro Aviles, Alejandro |
| Contributors | Harrison, Stephen A., Baisakh, Niranjan, Padgett, Guy B., Myers, Gerald O. |
| Publisher | LSU |
| Source Sets | Louisiana State University |
| Language | English |
| Detected Language | English |
| Type | text |
| Format | application/pdf |
| Source | http://etd.lsu.edu/docs/available/etd-11112015-105214/ |
| Rights | unrestricted, I hereby certify that, if appropriate, I have obtained and attached herein a written permission statement from the owner(s) of each third party copyrighted matter to be included in my thesis, dissertation, or project report, allowing distribution as specified below. I certify that the version I submitted is the same as that approved by my advisory committee. I hereby grant to LSU or its agents the non-exclusive license to archive and make accessible, under the conditions specified below and in appropriate University policies, my thesis, dissertation, or project report in whole or in part in all forms of media, now or hereafter known. I retain all other ownership rights to the copyright of the thesis, dissertation or project report. I also retain the right to use in future works (such as articles or books) all or part of this thesis, dissertation, or project report. |
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