DLK1 and DLK2 are two genes that are unique to vertebrates and we believe they are essential for the development of key physiological and neurological processes.

Dlk1 is imprinted throughout development; it is expressed only from the paternally inherited gene. Interestingly, in adult neurogenic niches of the mouse brain, where neural stem cells reside, extra DLK1 is required and it is selectively expressed from both parental chromosomes. These cells lose their imprinting. One goal of my PhD is to investigate whether this phenomenon is unique to the brain or if stem cell niches in other adult tissues also loose their imprinting.

DLK2 is a related to DLK1, however virtually nothing is known about it. During my PhD, I have been working towards determining the role of DLK2 in mice and investigating how it interacts with DLK1. Using classical molecular biology approaches, I am demonstrating when and where both genes are expressed throughout mouse development and in adult mouse brains. I’ve been using the latest advances in genome editing technology to try to remove DLK2 from the mouse genome; this will enable me to determine the function of DLK2.

DLK1 is implicated in several diseases, including metabolic disorders and cancer. I have initiated a collaboration to investigate the role of DLK1 in diabetes. Collectively these approaches will provide insights into the function and regulation of these important players in health and disease.