Potential ROBO1-Ankyrin Interaction Within Mouse Brain Tissue
Date
April 2020
Description
The formation of neural circuitry without neurodevelopmental or neurodegenerative disorder rests upon precise axonal guidance (Stoekli, 2018). Signaling between the axonal growth-cone receptor Roundabout homolog 1 (ROBO1) and the long-range chemorepulsant, SLIT mediates axonal turning through actin polymerization or disintegration within the growth-cone, though the protein players of this mechanism remain unknown. Studies (Levinger & Wright, 2017; Schlatter et al., 2007) revealed binding of close-homolog of L1 (CHL1), a colocalized partner of ROBO1, with the scaffolding protein Ankyrin to establish spectrin-actin linkages for axonal collapse. Extending these findings, we explored the possibility of ROBO1 and Ankyrin colocalization, which could suggest a role in SLIT-mediated repulsion. Repeated trials of indirect immunofluorescence staining of sectioned mouse brains with monoclonal ROBO-1 and Ankyrin antibodies remain inconclusive; however we continue our efforts to establish evidence of ROBO1-Ankyrin interaction. Discerning axonal guidance mechanisms including potential ROBO1-Ankyrin interaction offers implications for understanding neurodevelopmental and neurodegenerative diseases.
Presentation Type
Poster
Potential ROBO1-Ankyrin Interaction Within Mouse Brain Tissue
The formation of neural circuitry without neurodevelopmental or neurodegenerative disorder rests upon precise axonal guidance (Stoekli, 2018). Signaling between the axonal growth-cone receptor Roundabout homolog 1 (ROBO1) and the long-range chemorepulsant, SLIT mediates axonal turning through actin polymerization or disintegration within the growth-cone, though the protein players of this mechanism remain unknown. Studies (Levinger & Wright, 2017; Schlatter et al., 2007) revealed binding of close-homolog of L1 (CHL1), a colocalized partner of ROBO1, with the scaffolding protein Ankyrin to establish spectrin-actin linkages for axonal collapse. Extending these findings, we explored the possibility of ROBO1 and Ankyrin colocalization, which could suggest a role in SLIT-mediated repulsion. Repeated trials of indirect immunofluorescence staining of sectioned mouse brains with monoclonal ROBO-1 and Ankyrin antibodies remain inconclusive; however we continue our efforts to establish evidence of ROBO1-Ankyrin interaction. Discerning axonal guidance mechanisms including potential ROBO1-Ankyrin interaction offers implications for understanding neurodevelopmental and neurodegenerative diseases.
Comments
This poster based on an individual research project.