Migrating cells control morphogenesis of substratum serving as track to promote directional movement of the collective
- Creators
- Macabenta, Frank
- Stathopoulos, Angelike
Abstract
In Drosophila embryos, caudal visceral mesoderm (CVM) cells undergo bilateral migration along the trunk visceral mesoderm (TVM) in order to form midgut muscles. Mutation of FGF receptor Heartless (Htl) has been shown to cause CVM migration defects, particularly midline crossing of the bilateral groups. Here, we show that htl mutants also exhibit TVM defects including contralateral merging. Both CVM mismigration and TVM contralateral merging are attenuated by restoring FGF signaling specifically in the CVM, suggesting that migrating CVM cells influence TVM morphogenesis; however, the inverse, supplying FGF to the TVM, does not rescue CVM mismigration. In addition, we show that FGF regulates integrin expression in both tissues, but only providing a source of integrin specifically to the TVM attenuates the contralateral merging phenotype. Finally, we demonstrate that the CVM influences cell shape in the TVM, and a loss of CVM results in TVM morphological defects. In summary, this study provides insight into how a migrating collective of cells can influence their tissue substrate and supports the view that morphogenesis of tissues during development is interdependent.
Additional Information
© 2019 Published by The Company of Biologists Ltd. Received 21 February 2019; Accepted 17 June 2019. We thank M. Frasch, R. Lehmann, A. Michelson and J. Skeath for sharing fly stocks and antibodies, and are grateful to V. Stepanik, Z. Ákos, J. Sun, H. L. Curtis and J. Irizarry for assistance and helpful discussions. The authors declare no competing or financial interests. Author contributions: Conceptualization: F.M., A.S.; Methodology: F.M., A.S.; Validation: F.M.; Investigation: F.M.; Resources: A.S.; Data curation: F.M.; Writing - original draft: F.M.; Writing - review & editing: F.M., A.S.; Visualization: F.M.; Supervision: A.S.; Project administration: A.S.; Funding acquisition: F.M., A.S. This work was funded by National Institutes of Health grants R35GM118146 to A.S. and F32GM119395 to F.M. Deposited in PMC for release after 12 months.Attached Files
Published - dev177295.full.pdf
Supplemental Material - DEV177295supp.pdf
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Additional details
- PMCID
- PMC6679368
- Eprint ID
- 97913
- Resolver ID
- CaltechAUTHORS:20190815-093628766
- R35GM118146
- NIH
- F32GM119395
- NIH Postdoctoral Fellowship
- Created
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2019-08-15Created from EPrint's datestamp field
- Updated
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2021-11-16Created from EPrint's last_modified field