The cellular and molecular mechanisms that establish the mechanics of Drosophila gastrulation.

Abstract

In this review, we cover advances in the field that have contributed to our mechanistic understanding of how tissues internalize during Drosophila melanogaster gastrulation. The changes in tissue shape and architecture that are associated with mesoderm and endoderm invagination in the early Drosophila embryo are accompanied by cell shape changes which are driven by actomyosin contractility. The activation of signal transduction pathways is patterned by embryonic transcription factors, which define distinct geometries of gene expression and the tissue contractile domains. At the subcellular level, outputs from signaling pathways that activate actomyosin contractility are highly polarized and their behavior is fine-tuned by a balance of both positive and negative regulation. Cells are mechanically linked through adherens junctions, allowing forces that are generated by cells to be integrated across the tissue, ensuring coordinated cell behavior during tissue invagination. The transmission of force between cells also enables mechanical feedback whereby force generation influences both cell and cytoskeletal behavior. Finally, after tissue invagination, mesoderm cells undergo an epithelial-to-mesenchymal transition and cell spreading. We highlight studies that have utilized this model system to uncover fundamental principles at molecular-, cell-, and tissue-levels, which have contributed to our understanding of similar tissue morphogenetic processes across different organisms.