Abstract

The generation of form in living embryos, a process termed “morphogenesis” from the Greek word μορφογένeση, is one of the most fascinating unsolved problems in biology. In embryonic epithelia, most attention has been paid to events occurring at the apical surface of epithelia, particularly the regulation of actomyosin contractility during morphogenetic change. In a new report, De Renzis and colleagues demonstrate a key role for regulated actomyosin contractility at the basal surface of the epithelium during formation of the first epithelial fold in Drosophila (the “ventral furrow”) (Krueger et al, 2018).

Highlights

  • The generation of form in living embryos, a process termed “morphogenesis” from the Greek word lοqφοcέmerg, is one of the most fascinating unsolved problems in biology

  • The Drosophila ventral furrow has since become an excellent model system for understanding how epithelial folding can occur, with numerous studies demonstrating the importance of apical actomyosindriven constriction in driving indentation of the epithelium (Leptin & Grunewald, 1990; Sweeton et al, 1991; Dawes-Hoang et al, 2005; Martin et al, 2009)

  • The models suggest that apical constriction must be accompanied by basal relaxation to achieve the pyramidal cell shape observed in folds

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Summary

Introduction

The generation of form in living embryos, a process termed “morphogenesis” from the Greek word lοqφοcέmerg, is one of the most fascinating unsolved problems in biology. Establishment of the first epithelium is followed by formation of a single epithelial fold, namely the “primitive streak” in vertebrates or the “ventral furrow” in Drosophila. Genetic screens in Drosophila identified the twist and snail genes as being required for epithelial folding and the subsequent process of epithelial-to-mesenchymal transition (EMT) that produces mesodermal tissues inside the protective outer epithelium (Simpson, 1983; Nusslein-Volhard et al, 1984).

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