ArticlePloS one2013
Innexin 3, a new gene required for dorsal closure in Drosophila embryo.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 37 citations in OpenAlex.
- Genome assembly of a nocturnal butterfly (Macrosoma leucophasiata) reveals convergent adaptation of visual genes.Communications biology · 2024Article
- Innexin expression and localization in the Drosophila antenna indicate gap junction or hemichannel involvement in antennal chemosensory sensilla.Cell and tissue research · 2024Article
- The Enigmas of Tissue Closure: Inspiration fromCurrent issues in molecular biology · 2024Review
- Morphological Observation and Transcriptome Analysis of Ciliogenesis inInternational journal of molecular sciences · 2023Article
- Deciphering the roles of unknown/uncharacterized genes in plant development and stress responses.Frontiers in plant science · 2023Review
- Molecular and morphological approach to study the innexin gap junctions inOpen biology · 2021Article
- βPS-Integrin acts downstream of Innexin 2 in modulating stretched cell morphogenesis in the Drosophila ovary.G3 (Bethesda, Md.) · 2021Article
- Germline soma communication mediated by gap junction proteins regulates epithelial morphogenesis.PLoS genetics · 2021Article
- A Meta-Analysis of Bioelectric Data in Cancer, Embryogenesis, and Regeneration.Bioelectricity · 2021Article
- Autocrine insulin pathway signaling regulates actin dynamics in cell wound repair.PLoS genetics · 2020Article
- Innovation of heterochromatin functions drives rapid evolution of essential ZAD-ZNF genes ineLife · 2020Article
- Integration of Migratory Cells into a New Site In Vivo Requires Channel-Independent Functions of Innexins on Microtubules.Developmental cell · 2020Article
- Innexins: Expression, Regulation, and Functions.Frontiers in physiology · 2018Review
- Molecular basis for asymmetry sensing of siRNAs by the Drosophila Loqs-PD/Dcr-2 complex in RNA interference.Nucleic acids research · 2017Article
- Article
- Homology directed repair is unaffected by the absence of siRNAs in Drosophila melanogaster.Nucleic acids research · 2016Article
- Relating proton pumps with gap junctions: colocalization of ductin, the channel-forming subunit c of V-ATPase, with subunit a and with innexins 2 and 3 during Drosophila oogenesis.BMC developmental biology · 2016Article
- Bi-directional gap junction-mediated soma-germline communication is essential for spermatogenesis.Development (Cambridge, England) · 2015Article
- The molecular and immunochemical expression of innexins in the yellow fever mosquito, Aedes aegypti: insights into putative life stage- and tissue-specific functions of gap junctions.Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology · 2015Article
- Bioelectric patterning during oogenesis: stage-specific distribution of membrane potentials, intracellular pH and ion-transport mechanisms in Drosophila ovarian follicles.BMC developmental biology · 2015Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDorsal closure is a morphogenetic event that occurs during mid-embryogenesis in many insects including Drosophila, during which the ectoderm migrates on the extraembryonic amnioserosa to seal the embryo dorsally. The contribution of the ectoderm in this event has been known for a long time. However, amnioserosa tension and contractibility have recently been shown also to be instrumental to the closure. A critical pre-requisite for dorsal closure is integrity of these tissues that in part is mediated by cell-cell junctions and cell adhesion. In this regard, mutations impairing junction formation and/or adhesion lead to dorsal closure. However, no role for the gap junction proteins Innexins has so far been described. RESULTS AND DISCUSSION: Here, we show that Innexin 1, 2 and 3, are present in the ectoderm but also in the amnioserosa in plaques consistent with gap junctions. However, only the loss of Inx3 leads to dorsal closure defects that are completely rescued by overexpression of inx3::GFP in the whole embryo. Loss of Inx3 leads to the destabilisation of Inx1, Inx2 and DE-cadherin at the plasma membrane, suggesting that these four proteins form a complex. Accordingly, in addition to the known interaction of Inx2 with DE-cadherin, we show that Inx3 can bind to DE-cadherin. Furthermore, Inx3-GFP overexpression recruits DE-cadherin from its wildtype plasma membrane domain to typical Innexin plaques, strengthening the notion that they form a complex. Finally, we show that Inx3 stability is directly dependent on tissue tension. Taken together, we propose that Inx3 is a critical factor for dorsal closure and that it mediates the stability of Inx1, 2 and DE-cadherin by forming a complex.
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