ArticleGenome research2011
Deep congenic analysis identifies many strong, context-dependent QTLs, one of which, Slc35b4, regulates obesity and glucose homeostasis.
Article in Genome research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
- Genome Wide Analysis Approach Suggests Chromosome 2 Locus to be Associated with Thiazide and Thiazide Like-Diuretics Blood Pressure Response.Scientific reports · 2019Trial
- The SLC-ome of membrane transport: from molecular discovery to physiology and clinical applications.Physiological reviews · 2026Review
- Allograft inflammatory factor-1-like is a situational regulator of leptin levels, hyperphagia, and obesity.iScience · 2022Article
- Fine Mapping of the MouseGenes · 2021Article
- A model and test for coordinated polygenic epistasis in complex traits.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The complex role of genetic background in shaping the effects of spontaneous and induced mutations.Yeast (Chichester, England) · 2021Review
- Network-Based Functional Prediction Augments Genetic Association To Predict Candidate Genes for Histamine Hypersensitivity in Mice.G3 (Bethesda, Md.) · 2019Article
- A novel YAP1/SLC35B4 regulatory axis contributes to proliferation and progression of gastric carcinoma.Cell death & disease · 2019Article
- Structural basis for the delivery of activated sialic acid into Golgi for sialyation.Nature structural & molecular biology · 2019Article
- The virtuous cycle of human genetics and mouse models in drug discovery.Nature reviews. Drug discovery · 2019Review
- Article
- Lysine at position 329 within a C-terminal dilysine motif is crucial for the ER localization of human SLC35B4.PloS one · 2018Article
- Review
- Widespread epistasis regulates glucose homeostasis and gene expression.PLoS genetics · 2017Article
- From Peas to Disease: Modifier Genes, Network Resilience, and the Genetics of Health.American journal of human genetics · 2017Review
- N-acetylglucosamine: more than a silent partner in insulin resistance.Glycobiology · 2017Article
- Metabolic Reprogramming by Hexosamine Biosynthetic and Golgi N-Glycan Branching Pathways.Scientific reports · 2016Article
- Genetic control of obesity, glucose homeostasis, dyslipidemia and fatty liver in a mouse model of diet-induced metabolic syndrome.International journal of obesity (2005) · 2016Article
- Interactions between Gut Microbiota, Host Genetics and Diet Modulate the Predisposition to Obesity and Metabolic Syndrome.Cell metabolism · 2015Article
- Contrasting genetic architectures in different mouse reference populations used for studying complex traits.Genome research · 2015Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
Although central to many studies of phenotypic variation and disease susceptibility, characterizing the genetic architecture of complex traits has been unexpectedly difficult. For example, most of the susceptibility genes that contribute to highly heritable conditions such as obesity and type 2 diabetes (T2D) remain to be identified despite intensive study. We took advantage of mouse models of diet-induced metabolic disease in chromosome substitution strains (CSSs) both to characterize the genetic architecture of diet-induced obesity and glucose homeostasis and to test the feasibility of gene discovery. Beginning with a survey of CSSs, followed with genetic and phenotypic analysis of congenic, subcongenic, and subsubcongenic strains, we identified a remarkable number of closely linked, phenotypically heterogeneous quantitative trait loci (QTLs) on mouse chromosome 6 that have unexpectedly large phenotypic effects. Although fine-mapping reduced the genomic intervals and gene content of these QTLs over 3000-fold, the average phenotypic effect on body weight was reduced less than threefold, highlighting the "fractal" nature of genetic architecture in mice. Despite this genetic complexity, we found evidence for 14 QTLs in only 32 recombination events in less than 3000 mice, and with an average of four genes located within the three body weight QTLs in the subsubcongenic strains. For Obrq2a1, genetic and functional studies collectively identified the solute receptor Slc35b4 as a regulator of obesity, insulin resistance, and gluconeogenesis. This work demonstrated the unique power of CSSs as a platform for studying complex genetic traits and identifying QTLs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.