Key words: gene-environment interactions, epigenetic reprogramming, epigenetic plasticity, developmental programming, DOHAD, genetic susceptibility
Dr. Ideraabdullah is an Assistant Professor of Genetics in the School of Medicine and holds a joint appointment in the Department of Nutrition in the Gillings School of Global Public Health. She earned her PhD in comparative mouse genetics at UNC Chapel Hill and completed postdoctoral training in epigenetic regulation of genomic imprinting at the University of Pennsylvania.
The Ideraabdullah lab studies mechanisms of environmental modulation of the epigenome during development. We examine the impact on progeny development and health across the lifespan as well as potential for transmission to subsequent generations. A key focus is to identify naturally occurring genetic differences that contribute to variability in these outcomes for the purpose of identifying and helping susceptible populations. Ongoing projects investigate the impact of vitamin D deficiency, pesticide exposure, and hyperglycemia during pregnancy.
Role of environment in programming the DNA methylation landscape during development. DNA methylation patterns in mammals undergo two required stages of reprogramming. In (i) germ cells and (ii) preimplantation embryos, genome-wide methylation is erased and reset as development progresses. We have shown that vitamin D depletion during development has persistent effects on adiposity and DNA methylation landscapes into adulthood. Mouse somatic and germ cell lineages exhibited primarily loss of DNA methylation and the extent of methylation change was dependent on genomic/epigenomic context. Our ongoing studies combine findings from diet, toxicant, and metabolic models to elucidate mechanisms by which developmental environment perturbs the progeny epigenome and impacts long-term metabolic health.
Role of parental genome in developmental programming. Genetic screening for susceptibility to disease typically focuses on the genotype and disease outcome within an individual. We have used a combination of environmental exposure models and induced/targeted mutant mouse lines and naturally occurring (Collaborative Cross) genetic mouse models to demonstrate that maternal genotype plays a key role in developmental programming of progeny DNA methylomes and phenotypes across multiple generations. Our ongoing studies are aimed at identifying the causal regulatory genetic sequences and using these to screen for susceptible populations.
Please feel free to contact me by email or phone to discuss potential areas of my research where you would like to be involved or learn more.