01) were detected for TGW at both locations and for GY in Hangzhou, whereas a marginal effect (P = 0.0622) was observed for GY in Lingshui. The directions of allelic effect were consistent across the two locations, with alleles from MY46

increasing TGW and enhancing GY. In the same population, no significant effect was detected for HD or NP, but significant effects (P < 0.05) were detected for NGP in Lingshui. These results indicated that QTL for grain weight and yield were located Ponatinib cost in the target interval and the allelic difference between ZS97 and MY46 was detected in the background of ZS97. In addition, the QTL had little effect on HD. Linkage maps covering the three segregating regions were constructed, spanning 25.0, 49.4 and 43.7 cM in populations I, II and III, respectively. QTL for TGW and HD were determined with Windows QTL Cartographer 2.5. None of the regions showed significant effects on HD, but QTL were detected MK-1775 ic50 for TGW in all the three populations (Table 3). In population III, the MY46 allele increased TGW by 0.62 g, explaining 39.1% of the phenotypic variance. These effects were consistent with estimates in the previous generation, verifying

the segregation of a QTL for TGW in this population. In populations I and II, the MY46 alleles decreased and increased TGW by 0.26 g and 0.27 g, explaining 9.2% and 9.8% of the phenotypic variance, respectively. These effects were much lower than those detected in population III. Together with the small sample size in BC2F5, it is not surprising that the effects in populations I and II were not detected in the previous experiment. Comparison among the allelic effects and their directions

detected in the three populations, two QTL for TGW could be resolved (Fig. 2). While qTGW1.1 was located in the interval RM11437–RM11615 and had a smaller effect with the enhancing allele from ZS97, qTGW1.2 was located in RM11615–RM11800 and had a larger effect with the enhancing allele from MY46. Population I segregated for qTGW1.1 only, with a smaller effect and the enhancing allele coming from ZS97. Population III segregated for qTGW1.2 only, with a larger effect and the enhancing allele coming from MY46. Populations II segregated for both qTGW1.1 and qTGW1.2, thus a residual effect with the enhancing allele from MY46 was detected. The detection of over-dominance in population II and partial dominance in the two other populations not ( Table 3) provided evidence for segregation of two QTL in population II. The NIL sets in BC2F7 were identical to those in BC2F5 in the segregating regions, but they included more lines with a more homogenous background. Two-way ANOVA for phenotypic difference between two homozygous genotypic groups in each of the three NIL sets are shown in Table 4. As expected, major effects were detected for TGW in all the three populations, with the largest effect observed in population III and the enhancing alleles from ZS97 in population I but from MY46 in the two other populations.