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The UNC-6/Netrin receptors UNC-40/DCC and UNC-5 inhibit growth cone filopodial protrusion via UNC-73/Trio, Rac-like GTPases and UNC-33/CRMP
dc.contributor.author | Norris, Adam D. | |
dc.contributor.author | Sundararajan, Lakshmi | |
dc.contributor.author | Morgan, Dyan E. | |
dc.contributor.author | Roberts, Zachary J. | |
dc.contributor.author | Lundquist, Erik A. | |
dc.date.accessioned | 2015-03-05T21:00:20Z | |
dc.date.available | 2015-03-05T21:00:20Z | |
dc.date.issued | 2014-11-15 | |
dc.identifier.citation | Norris, Adam D. et. al. "The UNC-6/Netrin receptors UNC-40/DCC and UNC-5 inhibit growth cone filopodial protrusion via UNC-73/Trio, Rac-like GTPases and UNC-33/CRMP." Development. 2014 November 15; 141(22): 4395–4405. http://dx.doi.org/10.1242/dev.110437 | en_US |
dc.identifier.uri | http://hdl.handle.net/1808/16976 | |
dc.description.abstract | UNC-6/Netrin is a conserved axon guidance cue that can mediate both attraction and repulsion. We previously discovered that attractive UNC-40/DCC receptor signaling stimulates growth cone filopodial protrusion and that repulsive UNC-40–UNC-5 heterodimers inhibit filopodial protrusion in C. elegans. Here, we identify cytoplasmic signaling molecules required for UNC-6-mediated inhibition of filopodial protrusion involved in axon repulsion. We show that the Rac-like GTPases CED-10 and MIG-2, the Rac GTP exchange factor UNC-73/Trio, UNC-44/Ankyrin and UNC-33/CRMP act in inhibitory UNC-6 signaling. These molecules were required for the normal limitation of filopodial protrusion in developing growth cones and for inhibition of growth cone filopodial protrusion caused by activated MYR::UNC-40 and MYR::UNC-5 receptor signaling. Epistasis studies using activated CED-10 and MIG-2 indicated that UNC-44 and UNC-33 act downstream of the Rac-like GTPases in filopodial inhibition. UNC-73, UNC-33 and UNC-44 did not affect the accumulation of full-length UNC-5::GFP and UNC-40::GFP in growth cones, consistent with a model in which UNC-73, UNC-33 and UNC-44 influence cytoskeletal function during growth cone filopodial inhibition. | en_US |
dc.description.sponsorship | We thank E. Struckhoff for technical assistance and J. Culotti for kindly providing the pU5GFP plasmid. Some strains were provided by the CGC, which is funded by the NIH Office of Research Infrastructure Programs [P40OD010440]. | en_US |
dc.publisher | Company of Biologists | en_US |
dc.rights | © 2014. Published by The Company of Biologists Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed. | |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
dc.subject | UNC-40/DCC | en_US |
dc.subject | UNC-5 | en_US |
dc.subject | UNC-6 | en_US |
dc.subject | Axon repulsion | en_US |
dc.subject | Filopodia | en_US |
dc.subject | Growth cone | en_US |
dc.subject | Caenorhabditis elegans | en_US |
dc.title | The UNC-6/Netrin receptors UNC-40/DCC and UNC-5 inhibit growth cone filopodial protrusion via UNC-73/Trio, Rac-like GTPases and UNC-33/CRMP | en_US |
dc.type | Article | |
kusw.kuauthor | Norris, Adam D. | |
kusw.kuauthor | Sundararajan, Lakshmi | |
kusw.kuauthor | Morgan, Dyan E. | |
kusw.kuauthor | Roberts, Zachary J. | |
kusw.kuauthor | Lundquist, Erik A. | |
kusw.kudepartment | Department of Molecular Biosciences | en_US |
dc.identifier.doi | 10.1242/dev.110437 | |
kusw.oaversion | Scholarly/refereed, publisher version | |
kusw.oapolicy | This item meets KU Open Access policy criteria. | |
dc.rights.accessrights | openAccess |
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Except where otherwise noted, this item's license is described as: © 2014. Published by The Company of Biologists Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.