ArticlePLoS genetics2018
The transcription factor Dysfusion promotes fold and joint morphogenesis through regulation of Rho1.
Article in PLoS genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Single-cell sequencing reveals potential novel insights into appendage-patterning and joint-development in a spider.Developmental dynamics : an official publication of the American Association of Anatomists · 2026Article
- Single-cell transcriptomics of X-ray irradiatedeLife · 2026Article
- Unveiling the cell dynamics during the final shape formation of the tarsus in Drosophila adult leg by live imaging.Development genes and evolution · 2024Article
- Cell proliferation and Notch signaling coordinate the formation of epithelial folds in the Drosophila leg.Development (Cambridge, England) · 2024Article
- Genetical control of 2D pattern and depth of the primordial furrow that prefigures 3D shape of the rhinoceros beetle horn.Scientific reports · 2020Article
- Using Nanobodies to Study Protein Function in Developing Organisms.Antibodies (Basel, Switzerland) · 2019Review
- I Spy in the Developing Fly a Multitude of Ways to Die.Journal of developmental biology · 2018Review
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2 authors.
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Abstract
The mechanisms that control tissue patterning and cell behavior are extensively studied separately, but much less is known about how these two processes are coordinated. Here we show that the Drosophila transcription factor Dysfusion (Dysf) directs leg epithelial folding and joint formation through the regulation of Rho1 activity. We found that Dysf-induced Rho1 activity promotes apical constriction specifically in folding epithelial cells. Here we show that downregulation of Rho1 or its downstream effectors cause defects in fold and joint formation. In addition, Rho1 and its effectors are sufficient to induce the formation of epithelial folds when misexpressed in a flat epithelium. Furthermore, as apoptotic cells can actively control tissue remodeling, we analyzed the role of cell death in the formation of tarsal folds and its relation to Rho1 activity. Surprisingly, we found no defects in this process when apoptosis is inhibited. Our results highlight the coordination between a patterning transcription factor and the cellular processes that cause the cell shape changes necessary to sculpt a flat epithelium into a three dimensional structure.
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