Epistasis among genes is a universal phenomenon in obesity: Evidence from rodent models

Nutrition

Volumn 20, Issue 1, 2004, Pages 74-77

  Warden, Craig H ^a   Yi, Nengjun ^b   Fisler, Janis ^b  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b NONE

Author keywords

[No Author keywords available]

Indexed keywords

FURIN; GENOMIC DNA; LEPTIN; LEPTIN RECEPTOR; MELANOCORTIN 4 RECEPTOR; PEROXISOME PROLIFERATOR; PROOPIOMELANOCORTIN;

ALLELE; CHROMOSOME NOR; EPISTASIS; GENE; GENE IDENTIFICATION; GENE LOCATION; GENE LOCUS; GENE MUTATION; GENETIC ANALYSIS; KNOCKOUT MOUSE; NON INSULIN DEPENDENT DIABETES MELLITUS; NONHUMAN; OBESITY; PEROXISOME; PRIORITY JOURNAL; PROGENY; QUANTITATIVE TRAIT LOCUS MAPPING; REVIEW; STATISTICAL ANALYSIS;

RODENTIA;

EID: 0347123574     PISSN: 08999007     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.nut.2003.09.013     Document Type: Article

References (47)

1. Chagnon Y.C., Rankinen T., Snyder E.E., Weisnagel S.J., Perusse L., Bouchard C. The human obesity gene map the 2002 update . Obes Res. 11:2003;313.
2. Brockmann G.A., Bevova M.R. Using mouse models to dissect the genetics of obesity. Trends Genet. 18:2002;367.
3. Segal N.L., Allison D.B. Twins and virtual twins bases of relative body weight revisited . Int J Obes Relat Metab Disord. 26:2002;437.
4. Moore JH. The uniquitous nature of epistasis in determining susceptibility to common human diseases. Hum Hered 2003;56:73.
5. Warden C.H., Fisler J.S. Integrated methods to solve the biological basis of common diseases. Methods. 13:1997;347.
6. Coleman D.L., Hummel K.P. The influence of genetic background on the expression of the obese (Ob) gene in the mouse. Diabetologia. 9:1973;287.
7. Hummel K.P., Coleman D.L., Lane P.W. The influence of genetic background on expression of mutations at the diabetes locus in the mouse. I. C57BL-KsJ and C57BL-6J strains. Biochem Genet. 7:1972;1.
8. Bray G.A., York D.A., Fisler J.S. Experimental obesity a homeostatic failure due to defective nutrient stimulation of the sympathetic nervous system . Vitam Horm. 45:1989;1.
9. Leiter E.H., Chapman H.D., Coleman D.L. The influence of genetic background on the expression of mutations at the diabetes locus in the mouse. V. Interaction between the db gene and hepatic sex steroid sulfotransferases correlates with gender-dependent susceptibility to hyperglycemia. Endocrinology. 124:1989;912.
10. Harris R.B., Mitchell T.D., Yan X., Simpson J.S., Redmann S.M. Jr. Metabolic responses to leptin in obese db/db mice are strain dependent. Am J Physiol Regul Integr Comp Physiol. 281:2001;R115.
11. Hofmann W.E., Liu X., Bearden C.M., Harper M.E., Kozak L.P. Effects of genetic background on thermoregulation and fatty acid-induced uncoupling of mitochondria in UCP1-deficient mice. J Biol Chem. 276:2001;12460.
12. Bolivar V.J., Cook M.N., Flaherty L. Mapping of quantitative trait loci with knockout/congenic strains. Genome Res. 11:2001;1549.
13. Peirce J. Looking at old tools in new ways using knockouts as congenics to study QTLs . Genome Res. 11:2001;1469.
14. Cianflone K., Xia Z., Chen L.Y. Critical review of acylation-stimulating protein physiology in humans and rodents. Biochim Biophys Acta. 1609:2003;127.
15. Fisler J.S., Warden C.H. Mapping of mouse obesity genes a generic approach to a complex trait . J Nutr. 127:1997;1909S.
16. Stryke D., Kawamoto M., Huang C.C., et al. BayGenomics. a resource of insertional mutations in mouse embryonic stem cells. Nucleic Acids Res. 31:2003;278.
17. Cheverud J.M., Routman E.J. Epistasis and its contribution to genetic variance components. Genetics. 139:1995;1455.
18. Wade M.J. Epistasis, complex traits, and mapping genes. Genetica. 112:2001;59.
19. Kao C.H., Zeng Z.B., Teasdale R.D. Multiple interval mapping for quantitative trait loci. Genetics. 152:1999;1203.
20. Zeng Z.B., Kao C.H., Basten C.J. Estimating the genetic architecture of quantitative traits. Genet Res. 74:1999;279.
21. Sen S., Churchill G.A. A statistical framework for quantitative trait mapping. Genetics. 159:2001;371.
22. Yi N., Xu S. Mapping quantitative trait loci with epistatic effects. Genet Res. 79:2002;185.
23. Kao C.H., Zeng Z.B. Modeling epistasis of quantitative trait loci using Cockerham's model. Genetics. 160:2002;1243.
24. Gauderman W.J., Thomas D.C. The role of interacting determinants in the localization of genes. Adv Genet. 42:2001;393.
25. Jansen R.C., Stam P. High resolution of quantitative traits into multiple loci via interval mapping. Genetics. 136:1994;1447.
26. Lander E.S., Botstein D. Mapping mendelian factors underlying quantitative traits using RFLP linkage maps. Genetics. 121:1989;185.
27. Zeng Z.B. Theoretical basis for separation of multiple linked gene effects in mapping quantitative trait loci. Proc Natl Acad Sci USA. 90:1993;10972.
28. Zeng Z.B. Precision mapping of quantitative trait loci. Genetics. 136:1994;1457.
29. Haley C.S., Knott S.A. A simple regression method for mapping quantitative trait loci in line crosses using flanking markers. Heredity. 69:1992;315.
30. Chase K., Adler F.R., Lark K.G. EPISTAT a computer program for identifying and testing interactions between pairs of quantitative trait loci . Theor Appl Genet. 94:1997;724.
31. Routman E.J., Cheverud J.M. Gene effects on a quantitative trait. Two-locus epistatic effects measured at microsatellite markers and at estimated QTL. Evolution. 51:1997;1654.
32. Wang D.L., Zhu J., Li Z.K., Paterson A.H. Mapping QTLs with epistasis effects and QTL × environment interactions by mixed linear model approaches. Theor Appl Genet. 99:1999;1255.
33. Carlborg O., Andersson L., Kinghorn B. The use of a genetic algorithm for simultaneous mapping of multiple interacting quantitative trait loci. Genetics. 155:2000;2003.
34. Jannink J.L., Jansen R. Mapping epistatic quantitative trait loci with one-dimensional genome searches. Genetics. 157:2001;445.
35. Boer M.P., Ter Braak C.J., Jansen R.C. A penalized likelihood method for mapping epistatic quantitative trait loci with one-dimensional genome searches. Genetics. 162:2002;951.
36. Yi N, Xu S, Allison DB. Bayesian model choice and search strategies for mapping interacting quantitative trait loci. Genetics 2003;165:867.
37. Fisler J.S., Pace M.J., Lusis A.J. BSB a new mouse model of multigenic obesity . Obes Res. 1:1993;271.
38. Warden C.H., Fisler J.S., Shoemaker S.M., et al. Identification of four chromosomal loci determining obesity in a multifactorial mouse model. J Clin Invest. 95:1995;1545.
39. Brockmann G.A., Kratzsch J., Haley C.S., Renne U., Schwerin M., Karle S. SingleQTL effects, epistasis, and pleiotropy account for two-thirds of the phenotypic F(2) variance of growth and obesity in DU6i × DBA/2 mice. Genome Res. 10:2000;1941.
40. Cheverud J.M., Vaughn T.T., Pletscher L.S., et al. Genetic architecture of adiposity in the cross of LG/J and SM/J inbred mice. Mamm Genome. 12:2001;3.
41. Corva P.M., Horvat S., Medrano J.F. Quantitative trait loci affecting growth in high growth (hg) mice. Mamm Genome. 12:2001;284.
42. Masinde G.L., Li X., Gu W., et al. Quantitative trait loci (QTL) for lean body mass and body length in MRL/MPJ and SJL/J F(2) mice. Funct Integr Genomics. 2:2002;98.
43. Monti J., Plehm R., Schulz H., Ganten D., Kreutz R., Hubner N. Interaction between blood pressure quantitative trait loci in rats in which trait variation at chromosome 1 is conditional upon a specific allele at chromosome 10. Hum Mol Genet. 12:2003;435.
44. Rapp J.P., Garrett M.R., Deng A.Y. Construction of a double congenic strain to prove an epistatic interaction on blood pressure between rat chromosomes 2 and 10. J Clin Invest. 101:1998;1591.
45. Galli J., Fakhrai-Rad H., Kamel A., Marcus C., Norgren S., Luthman H. Pathophysiological and genetic characterization of the major diabetes locus in GK rats. Diabetes. 48:1999;2463.
46. Risch N., Ghosh S., Todd J.A. Statistical evaluation of multiple-locus linkage data in experimental species and its relevance to human studies application to nonobese diabetic (NOD) mouse and human insulin-dependent diabetes mellitus (IDDM) . Am J Hum Genet. 53:1993;702.
47. Cordell H.J., Todd J.A., Hill N.J., et al. Statistical modeling of interlocus interactions in a complex disease rejection of the multiplicative model of epistasis in type 1 diabetes . Genetics. 158:2001;357.