ArticlePloS one2014
Mechanisms of regulating tissue elongation in Drosophila wing: impact of oriented cell divisions, oriented mechanical forces, and reduced cell size.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Programming the elongation of mammalian cell aggregates with synthetic gene circuits.bioRxiv : the preprint server for biology · 2024Article
- How dynamic prestress governs the shape of living systems, from the subcellular to tissue scale.Interface focus · 2022Review
- Apical Constriction Reversal upon Mitotic Entry Underlies Different Morphogenetic Outcomes of Cell Division.Molecular biology of the cell · 2020Article
- Self-sustained planar intercalations due to mechanosignaling feedbacks lead to robust axis extension during morphogenesis.Scientific reports · 2020Article
- Neuronal differentiation influences progenitor arrangement in the vertebrate neuroepithelium.Development (Cambridge, England) · 2019Article
- Dynamic cellular finite-element method for modelling large-scale cell migration and proliferation under the control of mechanical and biochemical cues: a study of re-epithelialization.Journal of the Royal Society, Interface · 2017Article
- Patterning of wound-induced intercellular Ca(2+) flashes in a developing epithelium.Physical biology · 2015Article
- Colloquium: Mechanical formalisms for tissue dynamics.The European physical journal. E, Soft matter · 2015Article
- Multiscale Modeling of Cellular Epigenetic States: Stochasticity in Molecular Networks, Chromatin Folding in Cell Nuclei, and Tissue Pattern Formation of Cells.Critical reviews in biomedical engineering · 2015Article
- Article
- Effects of mechanical properties on tumor invasion: insights from a cellular model.Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE Engineering in Medicine and Biology Society. Annual International Conference · 2014Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Regulation of cell growth and cell division plays fundamental roles in tissue morphogenesis. However, the mechanisms of regulating tissue elongation through cell growth and cell division are still not well understood. The wing imaginal disc of Drosophila provides a model system that has been widely used to study tissue morphogenesis. Here we use a recently developed two-dimensional cellular model to study the mechanisms of regulating tissue elongation in Drosophila wing. We simulate the effects of directional cues on tissue elongation. We also computationally analyze the role of reduced cell size. Our simulation results indicate that oriented cell divisions, oriented mechanical forces, and reduced cell size can all mediate tissue elongation, but they function differently. We show that oriented cell divisions and oriented mechanical forces act as directional cues during tissue elongation. Between these two directional cues, oriented mechanical forces have a stronger influence than oriented cell divisions. In addition, we raise the novel hypothesis that reduced cell size may significantly promote tissue elongation. We find that reduced cell size alone cannot drive tissue elongation. However, when combined with directional cues, such as oriented cell divisions or oriented mechanical forces, reduced cell size can significantly enhance tissue elongation in Drosophila wing. Furthermore, our simulation results suggest that reduced cell size has a short-term effect on cell topology by decreasing the frequency of hexagonal cells, which is consistent with experimental observations. Our simulation results suggest that cell divisions without cell growth play essential roles in tissue elongation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.