Kinesin I and cytoplasmic dynein orchestrate glucose-stimulated insulin-containing vesicle movements in clonal MIN6 beta-cells |
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Authors: | Varadi Aniko Tsuboi Takashi Johnson-Cadwell Linda I Allan Victoria J Rutter Guy A |
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Institution: | Henry Wellcome Laboratories for Integrated Cell Signaling, Department of Biochemistry, School of Medical Sciences, University Walk, University of Bristol, Bristol BS8 1TD, UK. |
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Abstract: | Glucose-stimulated mobilization of large dense-core vesicles (LDCVs) to the plasma membrane is essential for sustained insulin secretion. At present, the cytoskeletal structures and molecular motors involved in vesicle trafficking in beta-cells are poorly defined. Here, we describe simultaneous imaging of enhanced green fluorescent protein (EGFP)-tagged LDCVs and microtubules in beta-cells. Microtubules exist as a tangled array, along which vesicles describe complex directional movements. Whilst LDCVs frequently changed direction, implying the involvement of both plus- and minus-end directed motors, inactivation of the minus-end motor, cytoplasmic dynein, inhibited only a small fraction of all vesicle movements which were involved in vesicle recovery after glucose-stimulated exocytosis. By contrast, selective silencing of the plus-end motor, kinesin I, with small interfering RNAs substantially inhibited all vesicle movements. We conclude that the majority of LDCV transport in beta-cells is mediated by kinesin I, whilst dynein probably contributes to the recovery of vesicles after rapid kiss-and-run exocytosis. |
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Keywords: | Secretion Vesicle Insulin Islet Kinesin Dynein Trafficking |
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