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dc.contributor.authorAwata, Junya
dc.contributor.authorSong, Kangkang
dc.contributor.authorLin, Jianfeng
dc.contributor.authorKing, Stephen M.
dc.contributor.authorSanderson, Michael J.
dc.contributor.authorNicastro, Daniela
dc.contributor.authorWitman, George B.
dc.date2022-08-11T08:08:03.000
dc.date.accessioned2022-08-23T15:40:46Z
dc.date.available2022-08-23T15:40:46Z
dc.date.issued2015-08-01
dc.date.submitted2015-10-13
dc.identifier.citationMol Biol Cell. 2015 Aug 1;26(15):2788-800. doi: 10.1091/mbc.E15-01-0018. <a href="http://dx.doi.org/10.1091/mbc.E15-01-0018">Link to article on publisher's site</a>.
dc.identifier.issn1059-1524 (Linking)
dc.identifier.doi10.1091/mbc.E15-01-0018
dc.identifier.pmid26063732
dc.identifier.urihttp://hdl.handle.net/20.500.14038/26477
dc.description.abstractThe nexin-dynein regulatory complex (N-DRC), which is a major hub for the control of flagellar motility, contains at least 11 different subunits. A major challenge is to determine the location and function of each of these subunits within the N-DRC. We characterized a Chlamydomonas mutant defective in the N-DRC subunit DRC3. Of the known N-DRC subunits, the drc3 mutant is missing only DRC3. Like other N-DRC mutants, the drc3 mutant has a defect in flagellar motility. However, in contrast to other mutations affecting the N-DRC, drc3 does not suppress flagellar paralysis caused by loss of radial spokes. Cryo-electron tomography revealed that the drc3 mutant lacks a portion of the N-DRC linker domain, including the L1 protrusion, part of the distal lobe, and the connection between these two structures, thus localizing DRC3 to this part of the N-DRC. This and additional considerations enable us to assign DRC3 to the L1 protrusion. Because the L1 protrusion is the only non-dynein structure in contact with the dynein g motor domain in wild-type axonemes and this is the only N-DRC-dynein connection missing in the drc3 mutant, we conclude that DRC3 interacts with dynein g to regulate flagellar waveform.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=26063732&dopt=Abstract">Link to Article in PubMed</a>
dc.rights<p>© 2015 Awata, Song, et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).</p>
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/
dc.subjectcytoskeleton
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectGenetics
dc.titleDRC3 connects the N-DRC to dynein g to regulate flagellar waveform
dc.typeJournal Article
dc.source.journaltitleMolecular biology of the cell
dc.source.volume26
dc.source.issue15
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1161&amp;context=cellbiology_pp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/cellbiology_pp/162
dc.identifier.contextkey7709829
refterms.dateFOA2022-08-23T15:40:47Z
html.description.abstract<p>The nexin-dynein regulatory complex (N-DRC), which is a major hub for the control of flagellar motility, contains at least 11 different subunits. A major challenge is to determine the location and function of each of these subunits within the N-DRC. We characterized a Chlamydomonas mutant defective in the N-DRC subunit DRC3. Of the known N-DRC subunits, the drc3 mutant is missing only DRC3. Like other N-DRC mutants, the drc3 mutant has a defect in flagellar motility. However, in contrast to other mutations affecting the N-DRC, drc3 does not suppress flagellar paralysis caused by loss of radial spokes. Cryo-electron tomography revealed that the drc3 mutant lacks a portion of the N-DRC linker domain, including the L1 protrusion, part of the distal lobe, and the connection between these two structures, thus localizing DRC3 to this part of the N-DRC. This and additional considerations enable us to assign DRC3 to the L1 protrusion. Because the L1 protrusion is the only non-dynein structure in contact with the dynein g motor domain in wild-type axonemes and this is the only N-DRC-dynein connection missing in the drc3 mutant, we conclude that DRC3 interacts with dynein g to regulate flagellar waveform.</p>
dc.identifier.submissionpathcellbiology_pp/162
dc.contributor.departmentDepartment of Microbiology and Physiological Systems
dc.contributor.departmentDepartment of Cell and Developmental Biology
dc.source.pages2788-800


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<p>© 2015 Awata, Song, et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).</p>
Except where otherwise noted, this item's license is described as <p>© 2015 Awata, Song, et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).</p>