Marenda is an assistant professor of biology, co-director of the Cell Imaging Center and director of the biology graduate program in the College of Arts and Sciences.
The discovery that a particular protein doesn’t just give cells jobs but also sticks around to teach them to perform their new assignments could provide insight into schizophrenia.
D’Rozario was formerly a Drexel graduate student and is now a post-doctoral researcher at Washington University School of Medicine.
A team of Drexel researchers discovered that the protein, called TCF4, remains present in cells after neurogenesis — the process by which jobless cells are turned into signal-carrying neurons that transmit information through the body.
Scientists believed that TCF4 degraded and disappeared at that stage, but researchers found that TCF4 actually sticks around and restricts the number of synapses these neurons make, effectively instructing the cells’ job performance.
The protein is called “Daughterless” in Drosophila, or fruit flies, where its persistence was discovered.
“We think that TCF4 is most likely involved in helping to form the proper number of synapses a neuron makes, so that the information flow in the nervous system doesn’t get confused and dysfunctional,” says Daniel Marenda, associate professor in the College of Arts and Sciences and a program director at the National Science Foundation. “When you lose these proteins, you suddenly get too many synapses and it disrupts nervous system function.”
The findings are particularly important because of the association TCF4 gene variants have with schizophrenia and Pitt-Hopkins Syndrome, a neurodevelopmental disorder.
There is also evidence that neurons making too many synapses are associated with autism.