Brandon Walters

Campus

UTM

CSB Appointment

Full

Research Areas

Neurobiology

Education

B.S. (Biology, Purdue University)
M.S. (Forensic Science, University of Alabama Birmingham)
Ph.D. (Neurobiology, University of Alabama at Birmingham)
Postdoctoral Fellow: (Developmental Neurobiology, St. Jude Children’s Research Hospital)
Postdoctoral Fellow: (Neuroscience and Mental Health, Hospital for Sick Children)

Primary Undergraduate Department

Biology, UTM

Graduate Programs

Cell & Systems Biology

Research Description

My research focuses on how memory is encoded in rodents at the molecular level, and how these molecular changes support the establishment and persistence of a memory. Even though we have known of the molecular basis of memory for over a decade, how the molecular events sum together to give rise to memory is still not understood. Currently I am focused on “transient” players in memory formation, focusing on mRNA itself. This view was spurred by the observation that the synapse is capable of local translation (IE within the synapse)  of mRNA into proteins, giving synapses a vital role in local regulation of translation and thus how synapses respond to experience.

Epitranscriptomic modifications (m6A is the most common) regulate nearly every aspect of mRNA, from transport, to translation, and ultimately its degradation. These modifications are added to mRNA (in this case a methylation on adenosine) during transcription. The outcome depends on the location of the m6A within the mRNA and which reader protein is engaged to ‘read’ it. The end result is a highly regulatable system that can promote or inhibit protein production in specific locations within the cell, thus allowing synaptic and nuclear locations to have different translational programs in response to synaptic activity, IE the same mRNA can be handled in opposing ways depending on WHERE in the neuron the mRNA is located. My lab was the first to discover that in the hippocampus m6A is actively promoted (by loss of the m6A eraser FTO) during memory formation. This lead to an overall increase in m6A after memory formation, and viral mediated removal of FTO promoted memory formation in rodents. These findings introduced epitranscriptomics as an active and vital process in memory formation, and FTO specifically as a memory inhibitor.

My interests focus on the synapse, its molecular makeup, and how that changes with memory formation. My current focus on m6A is a logical application of this interest as epitranscriptomics have quickly positioned themselves as key regulators in the protein makeup of the synapse, and importantly they control how that makeup changes with memory. Projects in the laboratory are centered around this idea but are not limited to it. We are also actively researching how stress, sex, and neurological diseases affect synaptic dynamics and ultimately memory formation.