ArticleJournal of cell science2012
Transcriptional regulation of Profilin during wound closure in Drosophila larvae.
Article in Journal of cell science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
29 citing papers in PubMed, 45 citations in OpenAlex.
- A Pvr-AP-1-Mmp1 signaling pathway is activated in astrocytes upon traumatic brain injury.eLife · 2024Article
- Bilateral JNK activation is a hallmark of interface surveillance and promotes elimination of aberrant cells.eLife · 2023Article
- JNK signaling and integrins cooperate to maintain cell adhesion during epithelial fusion inFrontiers in cell and developmental biology · 2023Article
- Fos regulates macrophage infiltration against surrounding tissue resistance by a cortical actin-based mechanism in Drosophila.PLoS biology · 2022Article
- Autocrine insulin pathway signaling regulates actin dynamics in cell wound repair.PLoS genetics · 2020Article
- Injury Activates a Dynamic Cytoprotective Network to Confer Stress Resilience and Drive Repair.Current biology : CB · 2019Article
- Casein kinase 1α decreases β-catenin levels at adherens junctions to facilitate wound closure inDevelopment (Cambridge, England) · 2019Article
- Article
- Jumu is required for circulating hemocyte differentiation and phagocytosis in Drosophila.Cell communication and signaling : CCS · 2018Article
- A scar-like lesion is apparent in basement membrane after wound repair in vivo.Matrix biology : journal of the International Society for Matrix Biology · 2018Article
- Requirement for and polarized localization of integrin proteins during Drosophila wound closure.Molecular biology of the cell · 2018Article
- Septin-dependent remodeling of cortical microtubule drives cell reshaping during epithelial wound healing.Journal of cell science · 2018Article
- Long-term In Vivo Tracking of Inflammatory Cell Dynamics Within Drosophila Pupae.Journal of visualized experiments : JoVE · 2018Article
- Crawling wounded: molecular genetic insights into wound healing from Drosophila larvae.The International journal of developmental biology · 2018Review
- Proteomic analysis of trochophore and veliger larvae development in the small abalone Haliotis diversicolor.BMC genomics · 2017Article
- Yorkie regulates epidermal wound healing in Drosophila larvae independently of cell proliferation and apoptosis.Developmental biology · 2017Article
- Toll pathway is required for wound-induced expression of barrier repair genes in theProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Article
- Insulin and TOR signal in parallel through FOXO and S6K to promote epithelial wound healing.Nature communications · 2016Article
- Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Injury is an inevitable part of life, making wound healing essential for survival. In postembryonic skin, wound closure requires that epidermal cells recognize the presence of a gap and change their behavior to migrate across it. In Drosophila larvae, wound closure requires two signaling pathways [the Jun N-terminal kinase (JNK) pathway and the Pvr receptor tyrosine kinase signaling pathway] and regulation of the actin cytoskeleton. In this and other systems, it remains unclear how the signaling pathways that initiate wound closure connect to the actin regulators that help execute wound-induced cell migrations. Here, we show that chickadee, which encodes the Drosophila Profilin, a protein important for actin filament recycling and cell migration during development, is required for the physiological process of larval epidermal wound closure. After injury, chickadee is transcriptionally upregulated in cells proximal to the wound. We found that JNK, but not Pvr, mediates the increase in chic transcription through the Jun and Fos transcription factors. Finally, we show that chic-deficient larvae fail to form a robust actin cable along the wound edge and also fail to form normal filopodial and lamellipodial extensions into the wound gap. Our results thus connect a factor that regulates actin monomer recycling to the JNK signaling pathway during wound closure. They also reveal a physiological function for an important developmental regulator of actin and begin to tease out the logic of how the wound repair response is organized.
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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.