The proteins associated with schizophrenia might hang around longer than previously thought. Scientists have found that a particular protein doesn't only give cells a job, but also sticks around to tell them how to carry out these new assignments.
In this latest study, the researchers found that a protein by the name of TCF4 remained present in cells after neurogenesis. This is when they turn "jobless" cells into neurons, which are cells in the nervous system that send specific signals to each other. Surprisingly, it seems as if TCF4 sticks around and restricts the number of synapses neurons make.
"It seems these proteins are performing double duty," said Daniel Marenda, one of the researchers who is the director of the biology graduate program in Drexel's College of Arts and Sciences. "Not only do the proteins take a cell that doesn't have a job and give it one, but once the cell has a job, it tells that cell how to do it."
In this case, the researchers found that the equivalent protein in fruit flies, called daughterless, was present in neuron cells that already had a job (determining sex/gender). In the end, they found that daughterless was regulating the number of synapses in neurons. After looking at mice, the scientists found that TCF4 was doing exactly the same thing; the protein had not disappeared and was instead very active.
So what does this mean? TCF4 gene variants are associated with schizophrenia and Pitt-Hopkins syndrome. This means that understanding its role could be crucial to potentially treating these diseases.
"Mutations in TCF4 are associated with both," Marenda said. "So we think that TCF4 is most likely involved in helping to form the proper number of synapses a cell makes, so that the information flow in the nervous system doesn't get confused and dysfunctional. When you lose these proteins, you suddenly get too many synapses and it disrupts the nervous system function."
The findings could be huge when it comes to better understanding these diseases. More specifically, the researchers hope to see some correlation between the severity of the mutation on TCF4 and how it impacts what kind of disease is present. This, in turn, could reveal a bit more about the correlation between it and nervous system function.
The findings are published in the March 2016 journal Cell Reports.
