these, the Chr 9 QTL has been best characterized; putative QTGs are Hyou1 (Orp150; hypoxia upregulated protein 1) and Scn4b (sodium channel subunit beta-4; Mulligan et al. 2006). The overlap of the two data-sets is on Chr 4; however, the Chr 4 congenic strain, which captured the withdrawal QTL (see Fehr et al. 2002), did not differ in ethanol consumption (Buck, unpublished observation). Of the seven reciprocal QTLs detected in the current study, only three (Chr 6, 11, and 17) have a haplotype where the B6 differs from the D2 strain. Thus, the only potential overlap with the QTLs noted above is for the withdrawal QTL on Chr 11; however, the reciprocal Chr 11 QTL is distal to the QTL detected in the B6×D2 crosses. The question arises as to whether or not we detected any of the B6×D2 withdrawal or consumption QTLs. Although we have not looked at this issue extensively, we have been unable to detect the Chr 4 withdrawal QTL in either the withdrawal selected lines or in the parental HS4 population; in contrast, we have reliably detected the Chr 9 QTL for consumption. Although, overall, the QTL data collected in this and previous studies appear generally
