作者: Lu Lu , Ashutosh K. Pandey , M. Trevor Houseal , Megan K. Mulligan
DOI: 10.1371/JOURNAL.PONE.0148230
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摘要: Glutathione S-transferase (GST) genes play a protective role against oxidative stress and may influence disease risk drug pharmacokinetics. In this study, massive multiscalar trait profiling across large population of mice derived from cross between C57BL/6J (B6) DBA2/J (D2)--the BXD family--was combined with linkage bioinformatic analyses to characterize mechanisms controlling GST expression identify downstream consequences variation. Similar humans, show wide range in family members. Variation the Gsta4, Gstt2, Gstz1, Gsto1, Mgst3 is modulated by local QTLs (eQTLs) several tissues. Higher Gsto1 brain liver strains strongly associated (P < 0.01) inheritance B6 parental allele whereas higher Gsta4 liver, Gstt2 Gstz1 D2 allele. Allele-specific assays confirmed that are sequence variants within or near each gene locus. We exploited endogenous variation coexpression networks targets mouse human. Through systems genetics approach, we provide new insight into biological naturally occurring genes.