Erik C. Andersen Genetics and genomics of complex traits

Research Interests

We differ in our susceptibilities to cancer, diabetes, and other common diseases because of each individual’s unique genetic makeup and the effects of their particular environment. The greatest challenge in genetics today is to read an individual’s genome and make predictions about disease and drug susceptibilities. The Andersen laboratory uses quantitative and molecular genetics in nematode roundworms, like Caenorhabditis elegans, to identify the genes that vary within populations to cause differences in these traits. Nematodes are a powerful experimental platform for many reasons, including a high-level of conservation with humans, ease of manipulation, a powerful genetic and genomic toolkit, a large wild strain collection that contains variation comparable to that of humans, and the ability to connect gene function to tissues and cells in an intact organism. In addition to genetics, we use new sequencing technologies, high-throughput robotic phenotyping assays, and other genomic tools to determine the molecular mechanisms for how genetic variation causes phenotypic differences.

Selected Publications

Balancing selection maintains hyper-divergent haplotypes in Caenorhabditis elegans. Lee D, Zdraljevic S, Stevens L, Wang Y, Tanny RE, Crombie TA, Cook DE, Webster AK, Chirakar R, Baugh LR, Sterken MG, Braendle C, Félix M-A, Rockman MV, and Andersen EC. Nature Ecology & Evolution. 2021 June;5(6):794-807.

Deep sampling of Hawaiian Caenorhabditis elegans reveals high genetic diversity and admixture with global populations. Crombie TA, Zdraljevic S, Cook DE, Tanny RE, Brady SC, Wang Y, Evans KS, Hahnel S, Lee D, Rodriguez BC, Zhang G, van der Zwagg J, Kiontke K, and Andersen EC. eLife. 2019 December 3;8:e50465.

Selection and gene flow shape niche-associated variation in pheromone response. Lee D, Zdraljevic S, Cook DE, Frézal L, Hsu J-C, Sterken MG, Riksen JAG, Wang J, Kammenga JE, Braendle C, Félix M-A, Schroeder FC, and Andersen EC. Nature Ecology & Evolution. 2019 October;3(10):1455-1463.

Natural variation in C. elegans arsenic toxicity is explained by differences in branched chain amino acid metabolism. Zdraljevic S, Fox BW, Strand C, Panda O, Tenjo FJ, Brady SC, Crombie TA, Doench JG, Schroeder FC, and Andersen EC. eLife. 2019 April 8;8:e40260.

Extreme allelic heterogeneity at a Caenorhabditis elegans beta-tubulin locus explains natural resistance to benzimidazoles. Hahnel SR, Zdraljevic S, Rodriguez BC, Zhao Y, McGrath PT, and Andersen EC. PLoS Pathogens. 2018 October 29;14(10):e1007226.

View all publications by Erik C. Andersen listed in the National Library of Medicine (PubMed). Current and former IBiS students in blue.