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MAP1S controls microtubule stability throughout the cell cycle in human cells

Understanding the molecular basis for proper cell division requires a detailed functional analysis of microtubule (MT)-associated proteins. MT-associated protein 1S (MAP1S), the most ubiquitously expressed MAP1 family member, is required for accurate cell division. Here, using quantitative analysis...

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Hauptverfasser: Tegha Dunghu, Justus (VerfasserIn) , Bausch, Elena (VerfasserIn) , Ellenberg, Jan (VerfasserIn) , Gruss, Oliver (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: November 30, 2014
In: Journal of cell science
Year: 2014, Jahrgang: 127, Heft: 23, Pages: 5007-5013
ISSN:1477-9137
DOI:10.1242/jcs.136457
Online-Zugang:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1242/jcs.136457
Verlag, lizenzpflichtig, Volltext: https://jcs.biologists.org/content/127/23/5007
Volltext
Verfasserangaben:Justus Tegha-Dunghu, Elena Bausch, Beate Neumann, Annelie Wuensche, Thomas Walter, Jan Ellenberg and Oliver J. Gruss
Beschreibung
Zusammenfassung:Understanding the molecular basis for proper cell division requires a detailed functional analysis of microtubule (MT)-associated proteins. MT-associated protein 1S (MAP1S), the most ubiquitously expressed MAP1 family member, is required for accurate cell division. Here, using quantitative analysis of MT plus-end tracking, we show that MAP1S knockdown alters MT dynamics throughout the cell cycle. Surprisingly, MAP1S downregulation results in faster growing, yet short-lived, MTs in all cell cycle stages and in a global loss of MT acetylation. These aberrations correlate with severe defects in the final stages of cell division. In monopolar cytokinesis assays, we demonstrate that MAP1S guides MT-dependent initiation of cytokinesis. Our data underline the key role of MAP1S as a global regulator of MT stability and demonstrate a new primary function of MAP1S to regulate MT dynamics at the onset of cytokinesis.
Beschreibung:Gesehen am 06.11.2020
Beschreibung:Online Resource
ISSN:1477-9137
DOI:10.1242/jcs.136457

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