TABLE 3.

Candidate genes for each QTL based on our data and published evidence—the genes to test first

					Evidence
Trait	QTL	Gene	Chr	Mb	mRNAa	Proteinb	Sequencec	Literatured
HDL	Hdlq20	Apoa2	1	173.1		4.1	X	Lilja et al. (2002)
		Fh1		177.5		−2.8	X
		Hsd11b1		194.9		−3.8		Morton et al. (2001)
	Hdlq1	Acads	5	115.3		−2.6	X
		Scarb1		125.6	−2.1			Acton et al. (1996)
	Hdlq24	Pparg	6	115.4			X	Chinetti et al. (2001)
		Rassf4		116.6	−8.2
		Adipor2		119.3	1.9		X	Yamauchi et al. (2003)
		Ndufa9		126.8		−2.6	X
Gallstone presence	Lith17	Scarb2	5	93.6			X	Acton et al. (1996)
		Acads		115.3		−2.6	X
	Lith19	Slc10a2	8	5.1	5.2			Shih et al. (2001)
	Lith21	Ctgf	10	24.3	−2.6		X	Koninger et al. (2005)
Obesity and body weight	Obwq3	Pparg	6	115.4			X	Cock et al. (2004)
		Rassf4		116.6	−8.2
		Adipor2		119.3	1.9		X	Yamauchi et al. (2003)
	Obwq4	Pgc	17	47.2			X	Puigserver et al. (1998)
	Obwq5	Atrnl1	19	57.7	3.4			Gunn et al. (1999)

Genes listed are in QTL regions that are not identical by descent between SM and NZB (Hsd11b1 maps close to Hldq20). Protein and mRNA fold changes are given where a positive value indicates upregulation and a negative one indicates downregulation in NZB relative to SM.

^aFold changes for mRNA are significant (F_s < 1 × 10⁻⁴).

^bProteins are significantly different as determined by Western analysis (Figure 3), except for APOA2, which is suggestive (P < 0.1) on the basis of MS/MS data.

^cGenes that contain known or extrapolated codon-changing SNPs leading to potential functional differences are indicated by “X.”

^dGene names from supplemental Table S2 were systematically interrogated against the PubMed database using relevant keywords (Stylianou et al. 2006).