Program in Molecular Medicine; RNA Therapeutics Institute
Cell Biology | Cellular and Molecular Physiology | Molecular Biology
The spindle midzone harbors both microtubules and proteins necessary for furrow formation and the completion of cytokinesis. However, the mechanisms that mediate the temporal and spatial recruitment of cell division factors to the spindle midzone and midbody remain unclear. Here we describe a mechanism governed by the conserved RNA-binding protein ATX-2/Ataxin-2, which targets and maintains ZEN-4 at the spindle midzone. ATX-2 does this by regulating the amount of PAR-5 at mitotic structures, particularly the spindle, centrosomes, and midbody. Preventing ATX-2 function leads to elevated levels of PAR-5, enhanced chromatin and centrosome localization of PAR-5-GFP, and ultimately a reduction of ZEN-4-GFP at the spindle midzone. Codepletion of ATX-2 and PAR-5 rescued the localization of ZEN-4 at the spindle midzone, indicating that ATX-2 mediates the localization of ZEN-4 upstream of PAR-5. We provide the first direct evidence that ATX-2 is necessary for cytokinesis and suggest a model in which ATX-2 facilitates the targeting of ZEN-4 to the spindle midzone by mediating the posttranscriptional regulation of PAR-5.
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© 2016 Gnazzo 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).
Mol Biol Cell. 2016 Oct 15;27(20):3052-3064. Epub 2016 Aug 24. Link to article on publisher's site
Molecular biology of the cell
Gnazzo, Megan M.; Uhlemann, Eva-Maria E.; Villarreal, Alex R.; Shirayama, Masaki; Dominguez, Eddie G.; and Skop, Ahna R., "The RNA-binding protein ATX-2 regulates cytokinesis through PAR-5 and ZEN-4" (2016). Open Access Articles. 2960.
Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-Share Alike 3.0 License.