ArticleThe Journal of biological chemistry2013
The Drosophila platelet-derived growth factor and vascular endothelial growth factor-receptor related (Pvr) protein ligands Pvf2 and Pvf3 control hemocyte viability and invasive migration.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 69 citations in OpenAlex.
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- Growth deregulation and interaction with host hemocytes contribute to tumor progression in a Drosophila brain tumor model.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
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- Haemocyte-mediated immunity in insects: Cells, processes and associated components in the fight against pathogens and parasites.Immunology · 2021Review
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- Coordination among multiple receptor tyrosine kinase signals controls Drosophila developmental timing and body size.Cell reports · 2021Article
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- Receptor Tyrosine Kinases in Development: Insights fromInternational journal of molecular sciences · 2019Review
- Growth Factor Signaling Regulates Mechanical Nociception in Flies and Vertebrates.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- A Large Scale Systemic RNAi Screen in the Red Flour BeetleG3 (Bethesda, Md.) · 2019Article
- Review
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2 authors at 1 institution in 1 country.
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Abstract
Vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) family members are essential and evolutionary conserved determinants of blood cell development and dispersal. In addition, VEGFs are integral to vascular growth and permeability with detrimental contributions to ischemic diseases and metastatic cancers. The PDGF/VEGF-receptor related (Pvr) protein is implicated in the migration and trophic maintenance of macrophage-like hemocytes in Drosophila melanogaster embryos. pvr mutants have a depleted hemocyte population and a breakdown in hemocyte distribution. Previous studies suggested redundant functions for the Pvr ligands, Pvf2 and Pvf3 in the regulation of hemocyte migration, proliferation, and size. However, the precise roles that Pvf2 and Pvf3 play in hematopoiesis remain unclear due to the lack of available mutants. To determine Pvf2 and Pvf3 functions in vivo, we generated a genomic deletion that simultaneously disrupts Pvf2 and Pvf3. From our studies, we identified contributions of Pvf2 and Pvf3 to the Pvr trophic maintenance of hemocytes. Furthermore, we uncovered a novel role for Pvfs in invasive migrations. We showed that Pvf2 and Pvf3 are not required for the directed migration of hemocytes, but act locally in epithelial cells to coordinate trans-epithelial migration of hemocytes. Our findings redefine Pvf roles in hemocyte migration and highlight novel Pvf roles in hemocyte invasive migration. These new parallels between the Pvr and PDGF/VEGF pathways extend the utility of the Drosophila embryonic system to dissect physiological and pathological roles of PDGF/VEGF-like growth factors.
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Registered trials
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