Melissa Borgen

Assistant Professor | Biomedical and Chemical Engineering and Sciences

Contact Information

mborgen@fit.edu
(321) 674-7133
Olin Life Sciences 222

Selected Publications

Autophagy is inhibited by ubiquitin ligase activity in the nervous system. Crawley O, Opperman KJ, Desbois M, Adrados I, Borgen MA, Giles AC, Duckett DR, Grill B. Nat Commun. 2019 Nov 1;10(1):5017.
Synapse maintenance is impacted by ATAT-2 tubulin acetyltransferase activity and the RPM-1 signaling hub. Borgen MA, Giles AC, Wang D, Grill B. Elife. 2019 Jan 18;8:e44040. doi: 10.7554/eLife.44040
The PHR proteins: intracellular signaling hubs in neuronal development and axon degeneration. Grill B, Murphey RK, Borgen MA. Neural Dev. 2016 Mar 23;11:8. doi: 10.1186/s13064-016-0063-0
RPM-1 regulates axon termination by affecting growth cone collapse and microtubule stability. Borgen MA, Wang D, Grill B. Development. 2017 Dec 15;144(24):4658-4672. doi: 10.1242/dev.154187
Netrin and Frazzled regulate presynaptic gap junctions at a Drosophila giant synapse. Orr BO, Borgen MA, Caruccio PM, Murphey RK. J Neurosci. 2014 Apr 16;34(16):5416-30. doi: 10.1523/JNEUROSCI.3183-13.2014

Research

What are the molecular mechanisms responsible for building and maintaining a functioning nervous system? Great strides have been made in the neuroscience field to identify molecules that regulate synapse formation. Synapse formation consists of several steps including axon outgrowth, target recognition, axon termination, synaptic assembly, and the final step, synapse maintenance. In addition to concluding the formation process, synapse maintenance is critical throughout an animal’s lifetime in order to retain circuitry and allow for synaptic plasticity. Understanding the molecular mechanisms and regulation of synapse formation and, especially, synapse maintenance, is critical, as synapse destabilization is an early hallmark of several neurodegenerative diseases, including Alzheimer’s disease. The molecular and cellular mechanisms of synapse formation and maintenance are complex. Indeed, we lack a clear understanding of how the molecular mechanisms of formation and maintenance differ, even when the same molecules are at play in both scenarios.

The goal of the Borgen Lab is to use genetics, cell biology, and live-imaging to study the intracellular molecular mechanisms that influence synapse maintenance and neurodegeneration using the C. elegans model system. Identifying new molecules that are part of the complex signaling processes that regulate synapse maintenance will be critical for developing future diagnostic and therapeutic targets for neurodegenerative diseases. C. elegans is a powerful genetic model system that is well established for studying synapse formation and maintenance. Importantly, C. elegans is a student-friendly model system. It has fast generation times and a simple and completely mapped nervous system consisting of 302-neurons. Additionally, previous work, including my own, shows that pharmacological treatment can impact synapse maintenance in C. elegans. This opens up future possibilities of using C. elegans to screen potential therapeutic compounds that affect synapse maintenance.