Dr. Ideraabdullah is interested in how genes and environment interact to result in traits (“phenotypes”), with a particular focus on nutrition.
Folami Ideraabdullah, Ph.D.
Assistant Professor of Genetics and Nutrition (University of North Carolina, Chapel Hill)
Dr. Ideraabdullah earned her B.S. from Pennsylvania State University and her Ph.D. from UNC Chapel Hill. She completed her post-doctoral training at the University of Pennsylvania in Marisa Bartolomei’s lab, where she studied a phenomenon called “imprinting”.
We inherit two copies of each gene — a “dad copy” and a “mom copy”. For most genes, each copy gets expressed (transcribed into RNA and then translated into a protein) in equal amounts, meaning that we have a 50/50 mix of “mom protein” and “dad protein” for any given protein. However, a subset of genes are “imprinted” — only one parent’s protein gets made. Which parent’s protein is made is consistent across all people; imprinted genes are either always “maternally imprinted” or “paternally imprinted”. However, when those genes get passed to the next generation, the imprinting gets re-set: if I pass on the copy I inherited from my mom, it will be my kid’s “dad” copy.
That’s how we know that imprinting is not a genetic process that changes the DNA, but rather an “epigenetic” process that changes how the DNA functions. (“epi” means “on top of”, so you can think of “epigenetic” modifications as “sitting on the DNA”.)
A major mechanism by which this happens is called DNA methylation. Genes have a regulatory region at the front called the promoter, which helps transcription factors attach to the DNA and start transcribing that gene into RNA (turning the gene “ON”). However, if methyl groups are attached to the promoter of a gene, it blocks transcription factors from binding (turning the gene “OFF”). A methyl group is just a carbon atom attached to 3 hydrogen atoms, and it physically blocks anything from getting to the promoter, especially if there are a bunch of them clustered at the same promoter. For most genes, these methyl groups are added or taken away depending on what’s happening and which genes are needed, but for imprinted genes, one parent’s copy is permanently methylated.
(There’s a second mechanism of epigenetic modification called histone modification, which is more complicated. We know a lot about it, but it’s still a pretty hot topic of research.)
Dr. Iderabdullah is interested in how imprinting (and gene expression more generally) is related to nutrition: does what we eat affect DNA methylation? Nutrients like folate and vitamin B12 contain methyl groups that are “donated” to the DNA, so it would make sense that if we didn’t eat enough of those nutrients, we might have trouble methylating our DNA.
Sure enough, in a recent paper, Dr. Iderabdullah and her colleagues showed that when female mice were deprived on vitamin D, they had decreased DNA methylation of imprinted genes, and that this effect was seen in the next two generations of offspring, even after they gave them normal amounts of vitamin D.