Journal
MOLECULAR BIOLOGY OF THE CELL
Volume 20, Issue 1, Pages 438-451Publisher
AMER SOC CELL BIOLOGY
DOI: 10.1091/mbc.E08-08-0891
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Funding
- Natioanl Institutes of Health [GM-34107, EY-08538]
- Research to Prevent Blindness Foundation
- Dyson Foundation
- Deutsche Forschungsgemeinschaft (DFG)
- DFG
- Kultusministerium of the Land Sachsen-Anhalt
- NATIONAL EYE INSTITUTE [R01EY008538] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM034107] Funding Source: NIH RePORTER
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The functions of the actin cytoskeleton in post-Golgi trafficking are still poorly understood. Here, we report the role of LIM Kinase 1 (LIMK1) and its substrate cofilin in the trafficking of apical and basolateral proteins in Madin-Darby canine kidney cells. Our data indicate that LIMK1 and cofilin organize a specialized population of actin filaments at the Golgi complex that is selectively required for the emergence of an apical cargo route to the plasma membrane (PM). Quantitative pulse-chase live imaging experiments showed that overexpression of kinase-dead LIMK1 (LIMK1-KD), or of LIMK1 small interfering RNA, or of an activated cofilin mutant (cofilin S3A), selectively slowed down the exit from the trans-Golgi network (TGN) of the apical PM marker p75-green fluorescent protein (GFP) but did not interfere with the apical PM marker glycosyl phosphatidylinositol-YFP or the basolateral PM marker neural cell adhesion molecule-GFP. High-resolution live imaging experiments of carrier formation and release by the TGN and analysis of peri-Golgi actin dynamics using photoactivatable GFP suggest a scenario in which TGN-localized LIMK1-cofilin regulate a population of actin filaments required for dynamin-syndapin-cortactin-dependent generation and/or fission of precursors to p75 transporters.
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