David J. Cutler, Ph.D.

Department of Human Genetics

Phone: 404-727-5388

Email: djcutle@emory.edu


I am a theoretical population geneticist by training and inclination, and the work my lab does is most easily thought of as population genetics applications to human disease studies. In particular my lab devotes most of its time and energy to building tools to analyze whole genome data sets in an attempt to discover alleles associated with disease. Most of our work lies in the intersection of human genomics / population genetics / biostatistics and computer science. Loosely put, we take human genomics data, think about that data like a population geneticist, develop relatively straightforward biostatistical tests for that data, and then implement those tests using somewhat sophisticated computer science approaches. The motto of our lab might be "Everything is easier with a 1000 CPU computer cluster!"

In particular, my lab has existence experience with whole genome SNP studies, beginning with techniques to infer genotypes from arrays, to assessing the effects of genotyping error on genetic inference. The Cutler lab designed and performed all the initial quality control procedures for the International HapMap project, and developed techniques for Haplotype reconstruction at genomic scales. We have also developed techniques for association testing of all haplotypes in all sliding windows at a genomic scale with multiple test correction by permutation. My lab has been an integral part of the analysis team for numerous past and ongoing whole genome association studies, including published studies of stem cell populations, and Autism, and ongoing WGAs including the GAIN bipolar project and an international consortium studying modifiers of Cystic Fibrous. Recently my lab has developed techniques to estimate error and missing data rates in genomic data, and distinguish random error from copy number variation. My lab also has numerous side projects involving more basic population genetics questions, including assessing the effects of population bottlenecks on human genomic variation.