The postsynaptic t-SNARE Syntaxin 4 controls traffic of Neuroligin 1 and Synaptotagmin 4 to regulate retrograde signaling
Postsynaptic cells can induce synaptic plasticity through the release of activity-dependent retrograde signals. We previously described a Ca[superscript 2+]-dependent retrograde signaling pathway mediated by postsynaptic Synaptotagmin 4 (Syt4). To identify proteins involved in postsynaptic exocytosi...
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eLife Sciences Publications, Ltd.
2016
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Online Access: | http://hdl.handle.net/1721.1/103859 https://orcid.org/0000-0001-7463-977X https://orcid.org/0000-0001-5576-2887 |
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author | Zhang, Yao Piccioli, Zachary David Perrimon, Norbert Troy, J. Troy Littleton, J. Troy Harris, Kathryn P. |
author2 | Massachusetts Institute of Technology. Department of Biology |
author_facet | Massachusetts Institute of Technology. Department of Biology Zhang, Yao Piccioli, Zachary David Perrimon, Norbert Troy, J. Troy Littleton, J. Troy Harris, Kathryn P. |
author_sort | Zhang, Yao |
collection | MIT |
description | Postsynaptic cells can induce synaptic plasticity through the release of activity-dependent retrograde signals. We previously described a Ca[superscript 2+]-dependent retrograde signaling pathway mediated by postsynaptic Synaptotagmin 4 (Syt4). To identify proteins involved in postsynaptic exocytosis, we conducted a screen for candidates that disrupted trafficking of a pHluorin-tagged Syt4 at Drosophila neuromuscular junctions (NMJs). Here we characterize one candidate, the postsynaptic t-SNARE Syntaxin 4 (Syx4). Analysis of Syx4 mutants reveals that Syx4 mediates retrograde signaling, modulating the membrane levels of Syt4 and the transsynaptic adhesion protein Neuroligin 1 (Nlg1). Syx4-dependent trafficking regulates synaptic development, including controlling synaptic bouton number and the ability to bud new varicosities in response to acute neuronal stimulation. Genetic interaction experiments demonstrate Syx4, Syt4, and Nlg1 regulate synaptic growth and plasticity through both shared and parallel signaling pathways. Our findings suggest a conserved postsynaptic SNARE machinery controls multiple aspects of retrograde signaling and cargo trafficking within the postsynaptic compartment. |
first_indexed | 2024-09-23T16:16:53Z |
format | Article |
id | mit-1721.1/103859 |
institution | Massachusetts Institute of Technology |
language | en_US |
last_indexed | 2024-09-23T16:16:53Z |
publishDate | 2016 |
publisher | eLife Sciences Publications, Ltd. |
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spelling | mit-1721.1/1038592022-10-02T07:32:32Z The postsynaptic t-SNARE Syntaxin 4 controls traffic of Neuroligin 1 and Synaptotagmin 4 to regulate retrograde signaling Zhang, Yao Piccioli, Zachary David Perrimon, Norbert Troy, J. Troy Littleton, J. Troy Harris, Kathryn P. Massachusetts Institute of Technology. Department of Biology Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences Picower Institute for Learning and Memory Harris, Kathryn Zhang, Yao Piccioli, Zachary David Littleton, J. Troy Postsynaptic cells can induce synaptic plasticity through the release of activity-dependent retrograde signals. We previously described a Ca[superscript 2+]-dependent retrograde signaling pathway mediated by postsynaptic Synaptotagmin 4 (Syt4). To identify proteins involved in postsynaptic exocytosis, we conducted a screen for candidates that disrupted trafficking of a pHluorin-tagged Syt4 at Drosophila neuromuscular junctions (NMJs). Here we characterize one candidate, the postsynaptic t-SNARE Syntaxin 4 (Syx4). Analysis of Syx4 mutants reveals that Syx4 mediates retrograde signaling, modulating the membrane levels of Syt4 and the transsynaptic adhesion protein Neuroligin 1 (Nlg1). Syx4-dependent trafficking regulates synaptic development, including controlling synaptic bouton number and the ability to bud new varicosities in response to acute neuronal stimulation. Genetic interaction experiments demonstrate Syx4, Syt4, and Nlg1 regulate synaptic growth and plasticity through both shared and parallel signaling pathways. Our findings suggest a conserved postsynaptic SNARE machinery controls multiple aspects of retrograde signaling and cargo trafficking within the postsynaptic compartment. National Institutes of Health (U.S.) (NIH grant NS40296) 2016-08-05T16:25:23Z 2016-08-05T16:25:23Z 2016-05 Article http://purl.org/eprint/type/JournalArticle 2050-084X http://hdl.handle.net/1721.1/103859 Harris, Kathryn P., Yao V. Zhang, Zachary D. Piccioli, Norbert Perrimon, and J. Troy Littleton. "The postsynaptic t-SNARE Syntaxin 4 controls traffic of Neuroligin 1 and Synaptotagmin 4 to regulate retrograde signaling." eLife 2016;5:e13881. https://orcid.org/0000-0001-7463-977X https://orcid.org/0000-0001-5576-2887 en_US http://dx.doi.org/10.7554/eLife.13881 eLife Creative Commons Attribution 4.0 International License http://creativecommons.org/licenses/by/4.0/ application/pdf eLife Sciences Publications, Ltd. eLife |
spellingShingle | Zhang, Yao Piccioli, Zachary David Perrimon, Norbert Troy, J. Troy Littleton, J. Troy Harris, Kathryn P. The postsynaptic t-SNARE Syntaxin 4 controls traffic of Neuroligin 1 and Synaptotagmin 4 to regulate retrograde signaling |
title | The postsynaptic t-SNARE Syntaxin 4 controls traffic of Neuroligin 1 and Synaptotagmin 4 to regulate retrograde signaling |
title_full | The postsynaptic t-SNARE Syntaxin 4 controls traffic of Neuroligin 1 and Synaptotagmin 4 to regulate retrograde signaling |
title_fullStr | The postsynaptic t-SNARE Syntaxin 4 controls traffic of Neuroligin 1 and Synaptotagmin 4 to regulate retrograde signaling |
title_full_unstemmed | The postsynaptic t-SNARE Syntaxin 4 controls traffic of Neuroligin 1 and Synaptotagmin 4 to regulate retrograde signaling |
title_short | The postsynaptic t-SNARE Syntaxin 4 controls traffic of Neuroligin 1 and Synaptotagmin 4 to regulate retrograde signaling |
title_sort | postsynaptic t snare syntaxin 4 controls traffic of neuroligin 1 and synaptotagmin 4 to regulate retrograde signaling |
url | http://hdl.handle.net/1721.1/103859 https://orcid.org/0000-0001-7463-977X https://orcid.org/0000-0001-5576-2887 |
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