Timothy J. Hines, Ph.D.
My research combines my interests in genetics, neuroscience, and cell biology with my extensive training in mouse- and cell-based models of human diseases to understand how disruption of fundamental biological processes contributes to neurodegenerative disorders.
I completed my Ph.D. with Dr. Deanna Smith in the Department of Biological Sciences at the University of South Carolina in 2018. My thesis focused on the regulation of the microtubule motor, cytoplasmic dynein, through posttranslational modifications and protein-protein interactions using mouse models, primary neuron cultures, and cancer cell lines.
I did my postdoc with Dr. Rob Burgess at The Jackson Laboratory (JAX) in Bar Harbor, ME, where I studied the cellular and molecular mechanisms underlying peripheral axon degeneration in Charcot-Marie-Tooth disease (CMT), a genetic disorder characterized by demyelination and/or degeneration of motor and sensory nerves, leading to muscle weakness and atrophy. During my postdoc, we determined that CMT-associated mutations in tRNA synthetase (aaRS) genes inhibit release of charged tRNAs from the synthetase, effectively sequestering tRNAs from the ribosome. This leads to ribosome stalling and activation of the the integrated stress response (ISR), which has two major cellular consequences: decreased cap-dependent translation and increased expression of the transcription factor, ATF4, and stress response genes. Now, my lab is using preclinical mouse models and human induced pluripotent stem cell (hiPSC)-based neuromuscular models to study the role of ATF4/SRGs in different CMTs (see Research Projects page).
Outside of the lab, I enjoy long walks on the beach mountains, camping, death metal, hanging with my wife, ice fishing, eating spicy food until I cry, and gardening.