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MBC in Press, published online ahead of print March 22, 2006
Mol. Biol. Cell 10.1091/mbc.E05-11-1010

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Submitted on November 3, 2005
Revised on February 24, 2006
Accepted on March 9, 2006

The Kinesin KIF1C and Microtubule Plus Ends Regulate Podosome Dynamics in Macrophages

Petra Kopp,* Reiner Lammers,{dagger} Martin Aepfelbacher,{ddagger} Günther Woehlke,{sect} Thomas Rudel,|| Nikolaus Machuy,|| Walter Steffen,¶ and Stefan Linder*

*Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten, Ludwig-Maximilians-Universität, 80336 München, Germany; {dagger}Medizinische Klinik IV, Universität Tübingen, 72076 Tübingen, Germany; {ddagger}Institut für Infektionsmedizin, Universitätsklinikum Hamburg Epppendorf, 20246 Hamburg, Germany; {sect}Institut für Zellbiologie, Ludwig-Maximilians-Universität, 80336 München, Germany; ||Max-Planck-Institut für Infektionsbiologie, 10117 Berlin, Germany; Institut für Molekular- und Zellphysiologie, Medizinische Hochschule Hannover, 30625 Hannover, Germany

Monitoring Editor: Paul Matsudaira

Microtubules are important for the turnover of podosomes, dynamic, actin-rich adhesions implicated in migration and invasion of monocytic cells. The molecular basis for this functional dependency, however, remained unclear. Here, we show that contact by microtubule plus-ends critically influences the cellular fate of podosomes in primary human macrophages. In particular, we identify the kinesin KIF1C, a member of the Kinesin-3 family, as a plus-end-enriched motor which targets regions of podosome turnover. Expression of mutation constructs or siRNA-/shRNA-based depletion of KIF1C resulted in decreased podosome dynamics and ultimately in podosome deficiency. Importantly, protein interaction studies showed that KIF1C binds to nonmuscle myosin IIA via its PTPD-binding domain, thus providing an interface between the actin and tubulin cytoskeletons, which may facilitate the subcellular targeting of podosomes by microtubules. This is the first report to implicate a kinesin in podosome regulation and also the first to describe a function for KIF1C in human cells.

Address correspondence to: Stefan Linder (stefan.linder{at}med.uni-muenchen.de)




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