Dynein-mediated transport and membrane trafficking control PAR3 polarised distribution
Abstract
The scaffold protein PAR3 and the kinase PAR1 are essential proteins that control cell polarity. Their precise opposite localisations define plasma membrane domains with specific functions. PAR3 and PAR1 are mutually inhibited by direct or indirect phosphorylations, but their fates once phosphorylated are poorly known. Through precise spatiotemporal quantification of PAR3 localisation in the Drosophila oocyte, we identify several mechanisms responsible for its anterior cortex accumulation and its posterior exclusion. We show that PAR3 posterior plasma membrane exclusion depends on PAR1 and an endocytic mechanisms relying on RAB5 and PI(4,5)P2. In a second phase, microtubules and the dynein motor, in connection with vesicular trafficking involving RAB11 and IKK-related kinase, IKKε, are required for PAR3 transport towards the anterior cortex. Altogether our results point to a connection between membrane trafficking and dynein-mediated transport to sustain PAR3 asymmetry.
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All data generated or analysed during this study are included in the manuscript and supporting files.
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Funding
Fondation ARC pour la Recherche sur le Cancer (SLR20130607102)
- Antoine Guichet
Ligue Contre le Cancer (RS14/75-58)
- Antoine Guichet
Fondation ARC pour la Recherche sur le Cancer (PJA 20141201756)
- Antoine Guichet
Fondation ARC pour la Recherche sur le Cancer (PJA 20161204931)
- Antoine Guichet
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Copyright
© 2019, Jouette et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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