Drosophila TNF Modulates Tissue Tension in the Embryo to Facilitate Macrophage Invasive Migration

Publication date: 7 May 2018
Source:Developmental Cell, Volume 45, Issue 3
Author(s): Aparna Ratheesh, Julia Biebl, Jana Vesela, Michael Smutny, Ekaterina Papusheva, S.F. Gabriel Krens, Walter Kaufmann, Attila Gyoergy, Alessandra Maria Casano, Daria E. Siekhaus
Migrating cells penetrate tissue barriers during development, inflammatory responses, and tumor metastasis. We study if migration in vivo in such three-dimensionally confined environments requires changes in the mechanical properties of the surrounding cells using embryonic Drosophila melanogaster hemocytes, also called macrophages, as a model. We find that macrophage invasion into the germband through transient separation of the apposing ectoderm and mesoderm requires cell deformations and reductions in apical tension in the ectoderm. Interestingly, the genetic pathway governing these mechanical shifts acts downstream of the only known tumor necrosis factor superfamily member in Drosophila, Eiger, and its receptor, Grindelwald. Eiger-Grindelwald signaling reduces levels of active Myosin in the germband ectodermal cortex through the localization of a Crumbs complex component, Patj (Pals-1-associated tight junction protein). We therefore elucidate a distinct molecular pathway that controls tissue tension and demonstrate the importance of such regulation for invasive migration in vivo.

Teaser

It is important to understand how the mechanical properties of surrounding tissues influence immune cells' progress during their in vivo migration. Here, Ratheesh et al. show that Drosophila TNF facilitates macrophage invasion by lowering active Myosin levels and thus apical tension in the ectoderm through enhanced localization of Patj.


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