Abstract
The coordination between membrane trafficking and actomyosin networks is essential to the regulation of cell and tissue shape. Here, we examine Rab protein distributions during Drosophila epithelial tissue remodeling and show that Rab35 is dynamically planar polarized. Rab35 compartments are enriched at contractile interfaces of intercalating cells and provide the first evidence of interfacial monopolarity. When Rab35 function is disrupted, apical area oscillations still occur and contractile steps are observed. However, contractions are followed by reversals and interfaces fail to shorten, demonstrating that Rab35 functions as a ratchet ensuring unidirectional movement. Although actomyosin forces have been thought to drive interface contraction, initiation of Rab35 compartments does not require Myosin II function. However, Rab35 compartments do not terminate and continue to grow into large elongated structures following actomyosin disruption. Finally, Rab35 represents a common contractile cell-shaping mechanism, as mesoderm invagination fails in Rab35 compromised embryos and Rab35 localizes to constricting surfaces.
Highlights
The coordination between membrane trafficking and actomyosin networks is essential to the regulation of cell and tissue shape
There is a system of planar polarized protein distributions during cell intercalation, with F-actin and Myosin II enrichments at AP interfaces and apical domains, and adherens junction-associated proteins such as Bazooka/Par-3, E-cadherin, and Armadillo/ßcatenin enriched at dorsal and ventral (DV) neighboring interfaces[8,9,10]
To identify the relevant trafficking pathways in epithelial cells undergoing cell intercalation, we focused on the behaviors of Rab proteins in vivo by screening the expression and localization of the 31 Drosophila Rab proteins as driven by Rab-Gal[4] knock-ins[40, 41]
Summary
The coordination between membrane trafficking and actomyosin networks is essential to the regulation of cell and tissue shape. The oriented contraction of T1 (or vertical, AP) interfaces followed by the growth of T3 interfaces leads to tissue narrowing and extension This cellular reshaping requires the function of apical and junctional cytoskeletal and adhesion proteins[8,9,10,11,12,13]. There is a system of planar polarized protein distributions during cell intercalation, with F-actin and Myosin II enrichments at AP interfaces and apical domains, and adherens junction-associated proteins such as Bazooka/Par-3, E-cadherin, and Armadillo/ßcatenin enriched at dorsal and ventral (DV) neighboring interfaces[8,9,10] This combination of tension-producing actomyosin networks and cadherin-dependent adhesion complexes are believed to be central determinants directing early morphogenesis in the Drosophila embryo; the role of membrane trafficking in guiding these events has been less clear[20, 21]. These compartments further function as endocytic hubs that have transient interactions late in their formation with Rab[5] and Rab[11] endosomes
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