Folami Ideraabdullah is an American geneticist and assistant professor in the Department of Genetics and the Department of Nutrition at the Gillings School of Global Public Health at the University of North Carolina at Chapel Hill. Ideraabdullah explores how maternal nutrition and environmental toxin exposure affect development through exploring epigenetic changes to DNA. She has found that maternal Vitamin D deficiencies can cause genome-wide changes in methylation patterns that persist for several generations and impact offspring health. Her international collaboration with the University of Witwatersrand represents the first time that metal levels in the placenta have been investigated in relation to birth outcomes in South Africa.
Early life and education
Ideraabdullah wanted to be a scientist from a young age. It was in her high school biology class that she learned that DNA is the blueprint for biology, and this idea fascinated her. She wanted to understand how this blueprint could generate and sustain a healthy organism, and became dedicated to science ever since.
In 1997, Ideraabdullah pursued her undergraduate studies at Pennsylvania State University in University Park, Pennsylvania. She majored in biology with a concentration in genetics and explored undergraduate research opportunities in the lab of Andrew Clark. She conducted genetics research in Drosophila, which spearheaded a continued career in genetics. Ideraabdullah graduated in 2001 with a Bachelors of Science.
Following her undergraduate degree, Ideraabdullah moved to Chapel Hill, North Carolina to conduct her graduate research at the University of North Carolina at Chapel Hill in 2002. She worked under the mentorship of Fernando Pardo-Manuel de Villena in the Department of Genetics. She explored genetic diversity through a clear evolutionary framework. Her first work in the lab helped to elucidate the sequence diversity of 20 inbred mouse strains based on substitutions, insertions, and deletions. She found that deletions are more frequent than insertions and that sequence diversity is about two orders of magnitude higher among these strains than within the human population. Her thesis worked explored the genetic architecture of DDK syndrome and the genetic basis for embryonic lethality in mice. She found that the maternal and paternal components of the DDK syndrome are non-allelic based on characterizing the candidate intervals for the gene encoding the maternal and paternal factors. She also characterized the genetic modifiers that lead to a rescue phenotype for DDK syndrome. Ideraabdullah completed her graduate training in 2007.
Following her graduate training, Ideraabdullah pursued postdoctoral work under the mentorship of Marisa Bartolomei at the Perelman School of Medicine at the University of Pennsylvania. Here, Ideraabdullah gained expertise in the study of epigenetics. She studied the molecular mechanisms of genomic imprinting, where gene expression is dependent on whether the gene was inherited from the mother or the father. Since regulation of imprinted genes was thought to be governed by the epigenetic modifications to the imprinting control region (ICR), Ideraabdullah explored whether there are regions outside the ICR that are important in the regulation of imprinted genes. She mutated different regions within the ICR for H19/IGF2 and this caused a loss of repression of the imprinted gene, yet the methylation patterns at the imprinted gene's ICR and promoter region did not change. Her findings were the first to suggest that mechanisms outside the ICR are necessary to mediate the fully repressed state of an imprinted gene. Following this finding, Ideraabdullah generated and characterized a mouse model of Beckwith-Wiedemann Syndrome (BWS), a disorder caused by aberrations in gene imprinting. Using this tool, she explored how microdeletions in the imprinting control region for H19/IGF2 cause dysregulation of epigenetic marks and imprinted gene expression. She found that the deletion did not perturb DNA methylation, though it did impact gene repression and further that the impacts of the deletion on insulator function are tissue specific, in that only mesodermal tissues have disrupted insulator function. Ideraabdullah completed her postdoctoral training in 2012.