Charles R. Farber
- B.S., Biochemistry – Western Kentucky University – 1993-1998
- M.S., Genetics – Michigan State University – 1998-2000
- Ph.D., Genetics – University of California, Davis – 2000 - 2005
- Postdoc, Genetics – University of California, Los Angeles – 2005-2008
Traditional genetic analysis identifies disease genes by correlating genotype with phenotype. While this approach has successfully identified genes contributing to disease, it fails to describe how genes function as members of complex cellular networks. Genomic technologies and analytical methods have made it possible to determine how genetic variation impacts disease on a systems-level. These advances have led to the creation of a new discipline, referred to as systems genetics, which seeks to elucidate how genetic information is integrated, organized, and transmitted through molecular, cellular, and physiological networks.
Osteoporosis is a condition of low bone strength and increased risk of fracture. In the U.S., there are approximately 12 million people diagnosed with osteoporosis. Osteoporotic fractures are debilitating, costly (costing the U.S. health care system ~$18 billion) and associated with increased morbidity and mortality. The Farber lab uses systems genetics to unravel the molecular basis of complex skeletal traits with the goal of developing a more comprehensive understanding of osteoporosis. Specifically, we use systems genetics to reverse engineer cellular networks that regulate skeletal phenotypes. Through the integration of genome-scale datasets using novel analytical strategies, we are able to develop hypotheses regarding the influence of genes and gene networks on bone function. The Farber lab tests these hypotheses using in vitro cell based assays and genetically modified mouse models.
Al-Barghouthi BM, Mesner LD, Calabrese GM, Brooks D, Tommasini SM, Bouxsein ML, Horowitz MC, Rosen CJ, Nguyen K, Haddox S, Farber EA, Onengut-Gumuscu S, Pomp D, Farber CR. Systems genetics in diversity outbred mice inform BMD GWAS and identify determinants of bone strength. Nature Communications. 2021 Jun 7;12(1):3408. doi: 10.1038/s41467-021-23649-0. PMID: 34099702; PMCID: PMC8184749.
Zhang Q, Mesner LD, Calabrese GM, Dirckx N, Li Z, Verardo A, Yang Q, Tower RJ, Faugere MC, Farber CR*, Clemens TL*. Genomic variants within chromosome 14q32.32 regulate bone mass through MARK3 signaling in osteoblasts. Journal of Clinical Investestigation. 2021 Apr 1;131(7):e142580. doi: 10.1172/JCI142580. PMID: 33792563; PMCID: PMC8011892. *Co-senior authors
Sabik OL, Calabrese GM, Taleghani E, Ackert-Bicknell CL, Farber CR. Identification of a Core Module for Bone Mineral Density through the Integration of a Co-expression Network and GWAS Data. Cell Reports. 2020 Sep 15;32(11):108145. doi: 10.1016/j.celrep.2020.108145. PMID: 32937138; PMCID: PMC8344123.
Calabrese GM, Mesner LD, Stains JP, Tommasini SM, Horowitz MC, Rosen CJ, Farber CR. Integrating GWAS and Co-expression Network Data Identifies Bone Mineral Density Genes SPTBN1 and MARK3 and an Osteoblast Functional Module. Cell Systems. 2017 Jan 25;4(1):46-59.e4. doi: 10.1016/j.cels.2016.10.014. Epub 2016 Nov 17. PMID: 27866947; PMCID: PMC5269473.