Natalie K. Barker

Abstract The E3 ubiquitin ligase TRIM67 is enriched in the central nervous system and is required for proper neuronal development. Previously we demonstrated TRIM67 coordinates with the closely related E3 ubiquitin ligase TRIM9 to regulate cytoskeletal dynamics downstream of the netrin-1 during axon guidance and axon branching in early neuronal morphogenesis. Interestingly, loss of Trim67 impacts cognitive flexibility in a spatial learning and memory task.

Abstract During neuronal development, dynamic filopodia emerge from dendrites and mature into functional dendritic spines during synaptogenesis. Dendritic filopodia and spines respond to extracellular cues, influencing dendritic spine shape and size as well as synaptic function. Previously, the E3 ubiquitin ligase TRIM9 was shown to regulate filopodia in early stages of neuronal development, including netrin-1 dependent axon guidance and branching.

Research ArticlePain David I. Duron1, Wei Lei1, Natalie K. Barker2, Carrie Stine1, Sanket Mishra3, Brian S. J. Blagg3, Paul R. Langlais2, and John M. Streicher1,* 1Department of Pharmacology, College of Medicine, University of Arizona, Tucson, AZ 85724, USA. 2Division of Endocrinology, Department of Medicine, College of Medicine, University of Arizona, Tucson, AZ 85724, USA. 3Department of Chemistry and Biochemistry, College of Science, University of Notre Dame, Notre Dame, IN 46556, USA.