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

Daniel Hain,Hannah C Sonnenberg,Alistair Langlands,Charlotte Bailey,Simon L Bullock,H.-Arno J Müller

doi:10.1242/dev.104711

Daniel Hain, Hannah C Sonnenberg + Show 4 more

Open Access

https://doi.org/10.1242/dev.104711

Copy DOI

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.

Highlights

Primary epithelium formation during embryonic cleavage divisions provides an excellent model with which to unravel the mechanisms that initiate the segregation of the plasma membrane cortex into distinct subdomains (Müller, 2001)
The results reported here demonstrate a requirement of Dop in the establishment of the furrow canal and the Basal adherens junctions (bAJs) at the cycle 14 transition
We propose that Dop acts upstream in furrow canal formation by controlling the formation of F-actin-rich foci, which initiate the assembly of a specific furrow membrane cortex

Summary

INTRODUCTION

Primary epithelium formation during embryonic cleavage divisions provides an excellent model with which to unravel the mechanisms that initiate the segregation of the plasma membrane cortex into distinct subdomains (Müller, 2001). The defects in apical h mRNA transport in dop mutants are similar to those exhibited by embryos in which components of the dynein-based mRNA transport machinery are compromised, including the RNAbinding protein Egalitarian, the adaptor protein Bicaudal D and the dynein co-factor Lissencephaly-1 (Bullock et al, 2006; Dix et al, 2013) These data provide direct evidence that Dop is important for normal dynein-dependent transport in the early embryo. We find that in dop mutants apical Golgi staining was reduced compared with control embryos (Fig. 8B,C) Together, these data indicate that dop is required for the normal distribution and transport of endomembrane systems that are crucial for membrane growth in cellularisation

DISCUSSION

Findings

MATERIALS AND METHODS