Author
Listed:
- Li Tao
(University of Hawaii at Hilo, 200 West Kawili Street, Hilo, Hawaii 96720, USA
Cellular and Developmental Biology, University of California)
- Barbara Fasulo
(Cellular and Developmental Biology, University of California)
- Brandt Warecki
(Cellular and Developmental Biology, University of California)
- William Sullivan
(Cellular and Developmental Biology, University of California)
Abstract
Centralspindlin is essential for central spindle and cleavage furrow formation. Drosophila centralspindlin consists of a kinesin-6 motor (Pav/kinesin-6) and a GTPase-activating protein (Tum/RacGAP). Centralspindlin localization to the central spindle is mediated by Pav/kinesin-6. While Tum/RacGAP has well-documented scaffolding functions, whether it influences Pav/kinesin-6 function is less well-explored. Here we demonstrate that both Pav/kinesin-6 and the centralspindlin complex (co-expressed Pav/Tum) have strong microtubule bundling activity. Centralspindlin also has robust plus-end-directed motility. In contrast, Pav/kinesin-6 alone cannot move microtubules. However, the addition of Tum/RacGAP or a 65 amino acid Tum/RacGAP fragment to Pav/kinesin-6 restores microtubule motility. Further, ATPase assays reveal that microtubule-stimulated ATPase activity of centralspindlin is seven times higher than that of Pav/kinesin-6. These findings are supported by in vivo studies demonstrating that in Tum/RacGAP-depleted S2 Drosophila cells, Pav/kinesin-6 exhibits severely reduced localization to the central spindle and an abnormal concentration at the centrosomes.
Suggested Citation
Li Tao & Barbara Fasulo & Brandt Warecki & William Sullivan, 2016.
"Tum/RacGAP functions as a switch activating the Pav/kinesin-6 motor,"
Nature Communications, Nature, vol. 7(1), pages 1-11, September.
Handle:
RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11182
DOI: 10.1038/ncomms11182
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