Presentation Title

Regulation of Cortex Glial Proliferation & Infiltration

Project Collaborators

Hannah Boyd (Graduate Student), Grace Ross (Undergraduate Student), Emily Holt (Graduate Rotation Student), Jaeda Coutinho-Budd, PhD (Research Mentor)

Abstract

Glial cells regulate numerous functions of neuronal biology, yet these cells are relatively understudied in any system. Drosophila provides a sophisticated model for studying glia, with a number of different subtypes, and a plethora of genetic tools to target each one. Cortex glia, the least-studied glial subset, are known to infiltrate throughout the central nervous system to enwreathe and support neuronal cell bodies. Cortex glial cells differentiate in embryonic development, and proliferate between the second and third larval stages (Coutinho-Budd et al., 2017). Loss of soluble NSF Attachment Protein alpha (ɑSNAP) causes abnormal, “blob-like” cortex glia that no longer proliferate (Coutinho-Budd et al., 2017), raising the question of whether infiltration and proliferative potential are linked. Previous research in the lab has revealed that knockdown of CycA results in fewer, yet larger cortex glial nuclei compared to controls. This loss of proliferation does not affect infiltration, establishing that infiltration and proliferation are not necessarily linked; however whether driving proliferation affects infiltration or could even rescue the morphological defect seen with loss of ɑSNAP had not been explored. Here we investigate knockdown and overexpression of cell cycle machinery in cortex glia to further explore the relationship between proliferation, infiltration, and morphology.

Primary Faculty Mentor Name

Jaeda Coutinho-Budd, PhD

Status

Undergraduate

Student College

College of Arts and Sciences

Program/Major

Neuroscience

Primary Research Category

Biological Sciences

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Regulation of Cortex Glial Proliferation & Infiltration

Glial cells regulate numerous functions of neuronal biology, yet these cells are relatively understudied in any system. Drosophila provides a sophisticated model for studying glia, with a number of different subtypes, and a plethora of genetic tools to target each one. Cortex glia, the least-studied glial subset, are known to infiltrate throughout the central nervous system to enwreathe and support neuronal cell bodies. Cortex glial cells differentiate in embryonic development, and proliferate between the second and third larval stages (Coutinho-Budd et al., 2017). Loss of soluble NSF Attachment Protein alpha (ɑSNAP) causes abnormal, “blob-like” cortex glia that no longer proliferate (Coutinho-Budd et al., 2017), raising the question of whether infiltration and proliferative potential are linked. Previous research in the lab has revealed that knockdown of CycA results in fewer, yet larger cortex glial nuclei compared to controls. This loss of proliferation does not affect infiltration, establishing that infiltration and proliferation are not necessarily linked; however whether driving proliferation affects infiltration or could even rescue the morphological defect seen with loss of ɑSNAP had not been explored. Here we investigate knockdown and overexpression of cell cycle machinery in cortex glia to further explore the relationship between proliferation, infiltration, and morphology.