Polarised cell intercalation during Drosophila axis extension is robust to an orthogonal pull by the invaginating mesoderm

Abstract

As tissues grow and change shape during animal development, they physically pull and push on each other, and these mechanical interactions can be important for morphogenesis. During Drosophila gastrulation, mesoderm invagination temporally overlaps with the convergence and extension of the ectodermal germband; the latter is caused primarily by Myosin II–driven polarised cell intercalation. Here, we investigate the impact of mesoderm invagination on ectoderm extension, examining possible mechanical and mechanotransductive effects on Myosin II recruitment and polarised cell intercalation. We find that the germband ectoderm is deformed by the mesoderm pulling in the orthogonal direction to germband extension (GBE), showing mechanical coupling between these tissues. However, we do not find a significant change in Myosin II planar polarisation in response to mesoderm invagination, nor in the rate of junction shrinkage leading to neighbour exchange events. We conclude that the main cellular mechanism of axis extension, polarised cell intercalation, is robust to the mesoderm invagination pull. We find, however, that mesoderm invagination slows down the rate of anterior-posterior cell elongation that contributes to axis extension, counteracting the tension from the endoderm invagination, which pulls along the direction of GBE.

Mechanical stress combines with planar polarised patterning during metaphase to orient embryonic epithelial cell divisions

“…To remove antero-posterior patterning in the embryo trunk, we used the double mutant kni 10 , hb 4 (null mutants for the gap genes knirps and hunchback ), for which we have evidence that polarised cell intercalation is abolished throughout the trunk [figure S3G in Butler et al (2009) ]. To visualise Myosin-II and cell contours in this double mutant, we used a sqh-EGFP 29B , Gap43-mCherry recombinant on the X chromosome ( Lye et al, 2024 ). Sqh-EGFP 29B ( Ambrosini et al, 2019 ) is a knocked-in tagged version of the endogenous sqh gene, so all MRLC molecules are labelled with GFP.…”

“…The NE was broken down into three domains, VNE, INE and LNE, that from cell counts of in situ images of ind expression ( Lye et al, 2024 ) map approximately to vnd , ind and msh expression domains ( Cornell and Von Ohlen, 2000 ; Reeves and Stathopoulos, 2009 ). vnd cells are unique in becoming progressively elongated in DV and larger, occupying a band between the border with the ME at 12 µm and 30 µm.…”