The Drosophila MAST kinase Drop out is required to initiate membrane compartmentalisation during cellularisation and regulates dynein-based transport

Daniel Hain, Alistair Langlands, Hannah C. Sonnenberg, Charlotte Bailey, Simon L. Bullock, H.-Arno J. Muller (Lead / Corresponding author)

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    6 Citations (Scopus)
    124 Downloads (Pure)

    Abstract

    Cellularisation of the Drosophila syncytial blastoderm embryo into the polarised blastoderm epithelium provides an excellent model with which to determine how cortical plasma membrane asymmetry is generated during development. Many components of the molecular machinery driving cellularisation have been identified, but cell signalling events acting at the onset of membrane asymmetry are poorly understood. Here we show that mutations in drop out (dop) disturb the segregation of membrane cortical compartments and the clustering of E-cadherin into basal adherens junctions in early cellularisation. dop is required for normal furrow formation and controls the tight localisation of furrow canal proteins and the formation of F-actin foci at the incipient furrows. We show that dop encodes the single Drosophila homologue of microtubule-associated Ser/Thr (MAST) kinases. dop interacts genetically with components of the dynein/dynactin complex and promotes dynein-dependent transport in the embryo. Loss of dop function reduces phosphorylation of Dynein intermediate chain, suggesting that dop is involved in regulating cytoplasmic dynein activity through direct or indirect mechanisms. These data suggest that Dop impinges upon the initiation of furrow formation through developmental regulation of cytoplasmic dynein.

    Original languageEnglish
    Pages (from-to)2119-2130
    Number of pages12
    JournalDevelopment
    Volume141
    Issue number10
    DOIs
    Publication statusPublished - May 2014

    Keywords

    • Drosophila
    • Protein kinase
    • Cell polarity
    • Microtubules
    • Dynein

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