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dc.contributor.authorTakaku, Yasuharu
dc.contributor.authorHwang, Jung Shan
dc.contributor.authorWolf, Alexander
dc.contributor.authorBöttger, Angelika
dc.contributor.authorShimizu, Hiroshi
dc.contributor.authorDavid, Charles N.
dc.contributor.authorGojobori, Takashi
dc.date.accessioned2014-08-27T09:50:38Z
dc.date.available2014-08-27T09:50:38Z
dc.date.issued2014-01-07
dc.identifier.citationTakaku Y, Hwang JS, Wolf A, Böttger A, Shimizu H, et al. (2014) Innexin gap junctions in nerve cells coordinate spontaneous contractile behavior in Hydra polyps. Sci Rep 4. doi:10.1038/srep03573.
dc.identifier.issn20452322
dc.identifier.pmid24394722
dc.identifier.doi10.1038/srep03573
dc.identifier.urihttp://hdl.handle.net/10754/325397
dc.description.abstractNerve cells and spontaneous coordinated behavior first appeared near the base of animal evolution in the common ancestor of cnidarians and bilaterians. Experiments on the cnidarian Hydra have demonstrated that nerve cells are essential for this behavior, although nerve cells in Hydra are organized in a diffuse network and do not form ganglia. Here we show that the gap junction protein innexin-2 is expressed in a small group of nerve cells in the lower body column of Hydra and that an anti-innexin-2 antibody binds to gap junctions in the same region. Treatment of live animals with innexin-2 antibody eliminates gap junction staining and reduces spontaneous body column contractions. We conclude that a small subset of nerve cells, connected by gap junctions and capable of synchronous firing, act as a pacemaker to coordinate the contraction of the body column in the absence of ganglia.
dc.language.isoen
dc.publisherNature Publishing Group
dc.rightsThis work is licensed under a Creative Commons Attribution 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/
dc.titleInnexin gap junctions in nerve cells coordinate spontaneous contractile behavior in Hydra polyps
dc.typeArticle
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.contributor.departmentComputational Bioscience Research Center (CBRC)
dc.identifier.journalScientific Reports
dc.identifier.pmcidPMC3882753
dc.eprint.versionPublisher's Version/PDF
dc.contributor.institutionHamamatsu University School of Medicine, Department of Biology, 1-20-1 Handayama, Higashi-ku, Hamamatsu, 431-3192, Japan
dc.contributor.institutionCenter for Information Biology-DNA Data Bank of Japan, National Institute of Genetics, Mishima 411-8540, Japan
dc.contributor.institutionHelmholtz Zentrum Mun?chen, German Research Center of Environmental Health, Institute of Molecular Toxicology and Pharmacology, Ingolstdter Landstr. 1, 85764 Neuherberg, Germany
dc.contributor.institutionDepartment Biologie II, Ludwig Maximilians University, Munich 80539, Germany
dc.contributor.institutionDepartment of Developmental Genetics, National Institute of Genetics, Mishima 411-8540, Japan
dc.contributor.affiliationKing Abdullah University of Science and Technology (KAUST)
kaust.personGojobori, Takashi
refterms.dateFOA2018-06-14T07:13:03Z


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This work is licensed under a Creative Commons Attribution 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/
Except where otherwise noted, this item's license is described as This work is licensed under a Creative Commons Attribution 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by/3.0/