Rochester Institute of Technology
Jeff Rathmell lab
Mtm1 is gene for Myotubularin 1, which when mutated can cause X-linked myotubular myopathy and functions as a lipid phosphatase. Through large and small library T cell CRISPR screens of inborn errors of metabolism genes, Th0 and iTreg cells were found to have increased proliferation when Mtm1 was knocked out. I will be studying the affects of Mtm1 on basic T cell biology and metabolism. I will test the hypothesis that Mtm1 can regulate phosphatidylinositol-3-phosphate signaling and downstream Akt and mTORC1 signaling. I will also test the hypothesis that Mtm1 can act similarly to a tumor suppressor and inhibition or loss of Mtm1 will increase T cell function in vivo, which would have potential applications to a new immunotherapy target in cancer.