| Fusarium head blight (FHB), caused mainly by Fusarium graminearum Schwabe, and was a devastating disease of wheat in world regions that were warm and humid during flowering. FHB resistance had long been considered to be characteristic of quantitative inheritance. The breeding and populization of FHB resistance varieties were the most economical and effective and safe method to control FHB and reduce the loss of wheat yield. Application of marker-assisted selection method in a backcross project with the resistant cultivar Sumai3and Wangshuibai as the donor parent of FHB resistance gene Fhbl and Fhb2had provided a new tool to improve FHB resistance of wheat cultivar Yangmai13and Yangmai15which were the soft gluten wheat planted largely in China. Two recombinant inbred lines derived from the crosses of Sumai3×Annong2and Wang-shuibai×Annong8455were evaluated for FHB resistance using natural infection and single-floret injection, respectively, in three years2008through2010. FHB resistance QTLs of type II and type I were identified and mapped on the different chromosome in the two RIL populations. Some correlations were identified between FHB resistance and agronomic traits. The results obtained were listed as follows:1. It was practical and effective to develop wheat lines resistant to FHB using marker-assisted selection of Fhbl and Fhb2genes from the donor parents of Sumai3and Wangshuibai. The selection for Fhb1gene is more efficient in advanced generations, i.e. F4>F3, F3>F2, respectively. The Percentage of scabbed spikelet (PSS) of F3and F4gener-ations was higher within advancing backcross times and their FHB resistance decreasing lower in the same population, The resistance lines of Yangmai13and Yangmai15were bred carrying the Fhb1and Fhb2with better yield and higher resistance to FHB than that of recurrent parent to17.24%-26.72%,87.51%-91.82%and11.34%-23.08%,69.69%-73.67%, and named R Yangmai13-2, R Yangmai13-7, R Yangmai13-8and R Yangmai15-2, R Yangmai15-3, R Yangmai15-5, R Yangmai15-6, respectively. Therefore, the lines with FHB resistance genes could replace the susceptible FHB varieties Yangmai13or Yangmai15and be planted largely. Fhbl was verified to be a major effec-tive QTL for FHB resistance, and the additive effect was detected between Fhbl and Fhb2. The PSS of lines with Fhb1was44.60%lower than that of Yangmai13or Yang-mai15. Further study on FHB resistance of lines with Fhb1and Fhb2revealed that their PSS were significantly decreased by14.86%to55.06%when compared with that of the lines containing only one resistance gene Fhb1.2. The SSR molecular markers linkage maps of the two RIL populations were con-structed with the mapping software Joinmap4.0.833SSR markers were surveyed for polymorphism between the parents, and388and301polymorphic markers were detected and mapped in the two populations.The total length of the map was2980.9cM and cov-ered approximately75%of wheat genome and with an average genetic distance of each chromosome for141.9cM and10.7cM per interval density in the RIL of Sumai3×An nong2population. It was2554.1cM,127.7cM, and11.8cM in the RIL of Wangshuibai×Annog8455population, respectively.3. Two recombinant inbred lines derived from the crosses of Sumai3×Annong2and Wangshuibai×Annong8455were evaluated for type Ⅰ resistance to FHB in the natur-al infection condition from2009to2010. Fourteen QTLs were detected in two years. Three of them were located on chromosome1BS,3BS,5BL,5DL of Sumai3and explained6.76%to15.75%of the variation in FHB resistance in the two mapping populations. Three of them were located on chromosome1AS,3BS,5AS of Wangshuibai and explained7.84%to27.16%of the variation in FHB resistance. Two of them were located on chromosome3BS,6BS of the susceptible parental Annong2and explained12.15%to23.50%of the variation in FHB resistance. One QTL of them were located on chromosome4BS of the susceptible parental Annong8455could explain9.58%and19.97%of the variation in FHB resistance.4. Two recombinant inbred lines derived from the crosses of Sumai3×Annong2and Wangshuibai×Annong8455were evaluated for type Ⅱ resistance to FHB by SFI from2008to2010. Fifteen QTLs were detected in three years. Four QTLs of them were detected in every year and located on chromosome3BS.4BS.6BS and7AS in RIL of Sumai3×Annong2. SSR markers Xwmc615, Xgwm538, Xgwm705and Xbarc127linked tightly with QTLs above. One QTL nearby Xwmc118were detected in2008and2010year and located on chromosome5BL. QTLs on3BS,4BS,6AL and7AS of Sumai3could explain11.41%to27.70%of the variation in FHB resistance. QTLs on5BL,6BS and7AS of Annong2were FHB susceptibility loci and explained13.23%to25.99%of the variation in the mapping populations of Sumai3×Annong2. Seven QTLs were detected in2009and2010and were located on chromosome1AS,2DL,5AS and7BL in RIL of Wangshuibai×Annong8455. FHB resistance QTLs of Wangshuibai1AS,2DL and5AS diminished spreading of infection within the spike and explained11.04%to25.59%of the variation in FHB resistance. QTL on chromosome SAL and7BL of Annong8455could explain8.21%to11.24%of the variation in FHB susceptibility.5. Expressing amount and effective size and position on chromosome of FHB resistance QTL were nonidentity in different years and genetic populations. Inheritance of FHB spread resistance for Sumai3was controlled by2or3major QTLs and several minor QTLs. Hoverer1or2major QTLs and many minor QTLs were found out in FHB infection and spread resistance for Wangshuibai. Even though in the same mapping population, resistance QTLs didn’t show consistently effect on FHB.6. There were significant negative correlations between PSS of FHB spread and infection with plant height of RIL populations in different years, but positive correlation was identified between PSS of FHB infection with spikelet density. FHB resistance did not show consistent correlations with spikelet length and spikelet number and stem length under the spike in the different years. |
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