{"id":2931,"date":"2016-10-24T19:17:00","date_gmt":"2016-10-24T23:17:00","guid":{"rendered":"https:\/\/www.med.unc.edu\/genetics\/directory\/folami-ideraabdullah-phd\/"},"modified":"2025-04-15T14:16:45","modified_gmt":"2025-04-15T18:16:45","slug":"folami-ideraabdullah-phd","status":"publish","type":"directory","link":"https:\/\/www.med.unc.edu\/genetics\/directory\/folami-ideraabdullah-phd\/","title":{"rendered":"Folami Ideraabdullah, PhD"},"content":{"rendered":"

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Research Interests<\/h2>\n

Key words: gene-environment interactions, epigenetic reprogramming, epigenetic plasticity, developmental programming, DOHAD, genetic susceptibility<\/strong><\/p>\n

Dr. Ideraabdullah is an Associate 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.<\/p>\n

In addition to leading her research program, she serves as the Research Director for Healthy Development and Aging in the NIEHS-funded P-30 UNC Center for Environmental Health and Susceptibility [P30ES010126 (Troester)]. She also serves as Lead PI for the NHGRI-funded R25 training program, UNC EDGE Genomics (Educational Pathways to increase Diversity in Genomics) [R25HG012219-01 (Ideraabdullah, MPI)]. Learn more about UNC EDGE genomics here<\/a>.<\/p>\n

The Ideraabdullah lab studies the role of gene x environment interactions in modulating the epigenome<\/a><\/strong> and examines how these effects contribute to early origins of metabolic and reproductive diseases. A key focus is to develop more effective mouse models to help us understand the mechanisms driving interindividual responses to environment so we can better define the impacts of environmental exposures and associated disease risks across diverse human populations. Our ongoing research develops and characterizes mouse models of micronutrient insufficiencies (vitamin D) & environmental endocrine disruptors.<\/p>\n

Current projects<\/h3>\n

Role of environment in <\/u>programming the DNA methylation landscape during development.<\/u> 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.<\/a><\/strong> 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.<\/p>\n

Role of parental genome in developmental<\/u> programming.<\/u> 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\u00a0 induced\/targeted mutant mouse lines and naturally occurring (Collaborative Cross<\/em>) genetic mouse models to demonstrate that maternal genotype plays a key role in developmental programming of progeny DNA methylomes and phenotypes across multiple generations<\/a>.<\/strong> Our ongoing studies are aimed at identifying the causal regulatory genetic sequences and using these to screen for susceptible populations.<\/p>\n

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.<\/p>\n

Mentor Training:<\/h2>\n