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Mechanical coupling between endoderm invagination and axis extension in Drosophila

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How genetic programs generate cell-intrinsic forces to shape embryos is actively studied, but less so how tissue-scale physical forces impact morphogenesis. I will discuss the role of tissue-scale forces during Drosophila germband extension (GBE). Previous work in our lab had shown that cells elongate in the anteroposterior (AP) axis in the extending germband, suggesting that an extrinsic tensile force contributed to body axis extension. {Butler LC et al. 2009. Nat Cell Biol 11: 859-864}.

To identify the morphogenetic movements that could be the source of this extrinsic force, we mapped gastrulation movements temporally using light sheet microscopy to image whole Drosophila embryos. We found that both mesoderm and endoderm invaginations are synchronous with the onset of GBE . AP cell elongation remains when mesoderm invagination is blocked, but is abolished in the absence of endoderm invagination. This suggested that endoderm invagination is the source of the tensile force.

We next looked for evidence of this force in acellular embryos, which lack polarized cell intercalation but in which endoderm invagination still occurs. We used laser ablation to show that tension is increased in the AP orientation compared to DV orientation in the posterior germband of these mutants. We propose that endoderm invagination is the source of the extrinsic force contributing to germband extension. This highlights the importance of physical interactions between tissues during morphogenesis.

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