SAT-749 Using the NLG-1 GRASP marker to investigate the role of sensory activity in Synaptic Partner Recognition in Caenorhabditis elegans

Saturday, October 13, 2012: 8:40 AM
Hall 4E/F (WSCC)
Luis Perez , NSF REU Research for Undergraduates using Molecular Biological Applications, San José State University, San José, CA
Benjamin Barsi-Rhyne , HHMI SCRIBE Program, San José State University, San José, CA
Kristine Miller , Department of Biological Sciences, San José State University, San José, CA
Christopher Vargas , NSF REU Research for Undergraduates using Molecular Biological Applications, San José State University, San José, CA
Emma Holdrich , Department of Biological Sciences, San José State University, San José, CA
Kristine Andersen , NSF REU Research for Undergraduates using Molecular Biological Applications, San José State University, San José, CA
Miri VanHoven, PhD , Department of Biological Sciences, San José State University, San José, CA
An important step in neural development is the formation of neuronal connections called synapses. During the development of these connections, long cellular extensions called neurites contact many potential partners, but faithfully form synapses with the correct synaptic partners through a process called synaptic partner recognition (SPR). To understand the molecular mechanisms that mediate SPR, we utilize NLG-1 GRASP (GFP Reconstitution Across Synaptic Partners), which is a transgenic fluorescent marker that labels synapses in the genetic model organism Caenorhabditis elegans. Specifically, we have labeled synapses between the left and right PHB sensory neurons and the left and right AVA interneurons.  Our aim is to determine if genes required for sensory activity are also required for PHB-to-AVA SPR.  We have found that odr-3, a G-protein α-subunit previously identified for its role in chemosensation, is required for PHB-to-AVA SPR. Our preliminary data indicates that odr-3 mutants have a 54% reduction in NLG-1 GRASP intensity, but maintain normal neurite contact. This suggests that sensory activity mediates PHB-to-AVA SPR. To determine if odr-3 is required for establishment or maintenance of SPR, we are conducting a time-course.  We are also testing additional sensory mutants to determine if they have similar SPR defects. By understanding the role of sensory activity in SPR, we can better understand this fundamental process.