Regulation of Cortex Glial Proliferation & Infiltration
Conference Year
January 2021
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
Faculty/Staff Collaborators
Hannah Boyd (Graduate Student), Grace Ross (Undergraduate Student), Emily Holt (Graduate Rotation Student), Jaeda Coutinho-Budd, PhD (Research Mentor)
Status
Undergraduate
Student College
College of Arts and Sciences
Program/Major
Neuroscience
Primary Research Category
Biological Sciences
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.