Unlabelled: The Supreme Court's decision in highlights the need for tools enabling nuanced and precise analysis of gene patents at the global level.
Supplementary Information: The online version of this article (doi:10.1038/nbt.
Variations in diabetic phenotypes are caused by complex interactions of genetic effects, environmental factors, and the interplay between the two. We tease apart these complex interactions by examining genome-wide genetic and epigenetic effects on diabetes-related traits among different sex, diet, and sex-by-diet cohorts in a Mus musculus model. We conducted a genome-wide scan for quantitative trait loci that affect serum glucose and insulin levels and response to glucose stress in an F(16) Advanced Intercross Line of the LG/J and SM/J intercross (Wustl:LG,SM-G16).
View Article and Find Full Text PDFVariation in serum cholesterol, free-fatty acids, and triglycerides is associated with cardiovascular disease (CVD) risk factors. There is great interest in characterizing the underlying genetic architecture of these risk factors, because they vary greatly within and among human populations and between the sexes. We present results of a genome-wide scan for quantitative trait loci (QTL) affecting serum cholesterol, free-fatty acids, and triglycerides in an F(16) advanced intercross line of LG/J and SM/J (Wustl:LG,SM-G16).
View Article and Find Full Text PDFObesity (Silver Spring)
January 2011
Although the current obesity epidemic is of environmental origin, there is substantial genetic variation in individual response to an obesogenic environment. In this study, we perform a genome-wide scan for quantitative trait loci (QTLs) affecting obesity per se, or an obese response to a high-fat diet in mice from the LG/J by SM/J Advanced Intercross (AI) Line (Wustl:LG,SM-G16). A total of 1,002 animals from 78 F₁₆ full sibships were weaned at 3 weeks of age and half of each litter placed on high- and low-fat diets.
View Article and Find Full Text PDFLevels of human obesity have increased over the past 20 years worldwide, primarily due to changes in diet and activity levels. Although environmental changes are clearly responsible for the increasing prevalence of obesity, individuals may show genetic variation in their response to an obesogenic environment. Here, we measure genetic variation in response to a high-fat diet in a mouse model, an F16 Advanced Intercross Line derived from the cross of SM/J and LG/J inbred mouse strains.
View Article and Find Full Text PDFObesity is one of the most serious threats to human health today. Although there is general agreement that environmental factors such as diet have largely caused the current obesity pandemic, the environmental changes have not affected all individuals equally. To model gene-by-environment interactions in a mouse model system, our group has generated an F(16) advanced intercross line (AIL) from the SM/J and LG/J inbred strains.
View Article and Find Full Text PDFMaternal effects on offspring phenotypes occur because mothers in many species provide an environment for their developing young. Although these factors are correctly "environmental" with respect to the offspring genome, their variance may have both a genetic and an environmental basis in the maternal generation. Here, reciprocal crosses between C57BL/6J and 10 LGXSM recombinant inbred (RI) strains were performed, and litters were divided at weaning into high-fat and low-fat dietary treatments.
View Article and Find Full Text PDFGenetic variation in response to high-fat diets is important in understanding the recent secular trends that have led to increases in obesity and type 2 diabetes. The examination of quantitative trait loci (QTLs) for both obesity- and diabetes-related traits and their responses to a high-fat diet can be effectively addressed in mouse model systems, including LGXSM recombinant inbred (RI) mouse strains. A wide range of obesity- and diabetes-related traits were measured in animals from 16 RI strains with 8 animals of each sex fed a high- or low-fat diet from each strain.
View Article and Find Full Text PDFObesity and its comorbidities, particularly type 2 diabetes, have become serious public health problems over the past few decades. Although the current pandemic is largely caused by societal environmental changes in diet, variation in response to these changes have, in part, a genetic basis. Here we address the genetic basis for both obesity- and diabetes-related traits themselves and dietary fat responses for these traits in a set of recombinant inbred mouse strains formed from the cross of LG/J with SM/J (LGXSM lines) fed a standard low-fat (15% calories from fat) or high-fat (42% calories from fat) diet.
View Article and Find Full Text PDFThe evolution of morphological modularity through the sequestration of pleiotropy to sets of functionally and developmentally related traits requires genetic variation in the relationships between traits. Genetic variation in relationships between traits can result from differential epistasis, where epistatic relationships for pairs of loci are different for different traits. This study maps relationship quantitative trait loci (QTLs), specifically QTLs that affect the relationship between individual mandibular traits and mandible length, across the genome in an F2 intercross of the LG/J and SM/J inbred mouse strains (N = 1045).
View Article and Find Full Text PDFObjective: To examine the differential response of obesity- and diabetes-related traits to a high- or low-fat diet in LG/J and SM/J mice. We also examined food consumption in these strains.
Research Methods And Procedures: Mice were placed on a high- or low-fat diet after weaning.
Pleiotropy refers to a single genetic locus that affects more than one phenotypic trait. Pleiotropic effects of genetic loci are thought to play an important role in evolution, reflecting functional and developmental relationships among phenotypes. In a previous study, we examined pleiotropic effects displayed by quantitative trait loci (QTLs) on murine mandibular morphology in relation to mandibular structure and function.
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