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dc.contributor.authorHenrichs, Verena
dc.contributor.authorGrycova, Lenka
dc.contributor.authorBarinka, Cyril
dc.contributor.authorNahacka, Zuzana
dc.contributor.authorNeuzil, Jiri
dc.contributor.authorDiez, Stefan
dc.contributor.authorRohlena, Jakub
dc.contributor.authorBraun, Marcus
dc.contributor.authorLansky, Zdenek
dc.date.accessioned2020-07-30T23:35:21Z
dc.date.available2020-07-30T23:35:21Z
dc.date.issued2020
dc.identifier.issn2041-1723
dc.identifier.doi10.1038/s41467-020-16972-5
dc.identifier.urihttp://hdl.handle.net/10072/395965
dc.description.abstractIntracellular trafficking of organelles, driven by kinesin-1 stepping along microtubules, underpins essential cellular processes. In absence of other proteins on the microtubule surface, kinesin-1 performs micron-long runs. Under crowding conditions, however, kinesin-1 motility is drastically impeded. It is thus unclear how kinesin-1 acts as an efficient transporter in intracellular environments. Here, we demonstrate that TRAK1 (Milton), an adaptor protein essential for mitochondrial trafficking, activates kinesin-1 and increases robustness of kinesin-1 stepping on crowded microtubule surfaces. Interaction with TRAK1 i) facilitates kinesin-1 navigation around obstacles, ii) increases the probability of kinesin-1 passing through cohesive islands of tau and iii) increases the run length of kinesin-1 in cell lysate. We explain the enhanced motility by the observed direct interaction of TRAK1 with microtubules, providing an additional anchor for the kinesin-1-TRAK1 complex. Furthermore, TRAK1 enables mitochondrial transport in vitro. We propose adaptor-mediated tethering as a mechanism regulating kinesin-1 motility in various cellular environments.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherSpringer Science and Business Media LLC
dc.relation.ispartofpagefrom3123
dc.relation.ispartofissue1
dc.relation.ispartofjournalNature Communications
dc.relation.ispartofvolume11
dc.subject.fieldofresearchBiochemistry and Cell Biology
dc.subject.fieldofresearchcode0601
dc.titleMitochondria-adaptor TRAK1 promotes kinesin-1 driven transport in crowded environments
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationHenrichs, V; Grycova, L; Barinka, C; Nahacka, Z; Neuzil, J; Diez, S; Rohlena, J; Braun, M; Lansky, Z, Mitochondria-adaptor TRAK1 promotes kinesin-1 driven transport in crowded environments, Nature Communications, 2020, 11 (1), pp. 3123
dcterms.dateAccepted2020-06-02
dcterms.licensehttp://creativecommons.org/licenses/by/4.0/
dc.date.updated2020-07-27T23:59:51Z
dc.description.versionAccepted Manuscript (AM)
gro.rights.copyright© The Author(s) 2020. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
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gro.griffith.authorNeuzil, Jiri


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