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Drosophila PAT1 is required for kinesin-1 to transport cargo and to maximize its motility
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Loiseau, P., Davies, T., Williams, L. S., Mishima, Masanori and Palacios, I. M. (2010) Drosophila PAT1 is required for kinesin-1 to transport cargo and to maximize its motility. Development , 137 (16). pp. 2763-2772. doi:10.1242/dev.048108 ISSN 0950-1991.
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Official URL: http://dx.doi.org/10.1242/dev.048108
Abstract
Kinesin heavy chain (KHC), the force-generating component of Kinesin-1, is required for the localization of oskar mRNA and the anchoring of the nucleus in the Drosophila oocyte. These events are crucial for the establishment of the anterior-posterior and dorsal-ventral axes. KHC is also essential for the localization of Dynein and for all ooplasmic flows. Interestingly, oocytes without Kinesin light chain show no major defects in these KHC-dependent processes, suggesting that KHC binds its cargoes and is activated by a novel mechanism. Here, we shed new light on the molecular mechanism of Kinesin function in the germline. Using a combination of genetic, biochemical and motor-tracking studies, we show that PAT1, an APP-binding protein, interacts with Kinesin-1, functions in the transport of oskar mRNA and Dynein and is required for the efficient motility of KHC along microtubules. This work suggests that the role of PAT1 in cargo transport in the cell is linked to PAT1 function as a positive regulator of Kinesin motility.
| Item Type: | Journal Article | ||||
|---|---|---|---|---|---|
| Divisions: | Faculty of Science, Engineering and Medicine > Medicine > Warwick Medical School | ||||
| Journal or Publication Title: | Development | ||||
| Publisher: | The Company of Biologists Ltd. | ||||
| ISSN: | 0950-1991 | ||||
| Official Date: | 15 August 2010 | ||||
| Dates: |
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| Volume: | 137 | ||||
| Number: | 16 | ||||
| Page Range: | pp. 2763-2772 | ||||
| DOI: | 10.1242/dev.048108 | ||||
| Status: | Peer Reviewed | ||||
| Publication Status: | Published | ||||
| Access rights to Published version: | Restricted or Subscription Access |
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