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Dual role for the zeste-white3/shaggy -encoded kinase in mesoderm and heart development of Drosophila

dc.contributor.authorPark, Maiyonen_US
dc.contributor.authorVenkatesh, Tyamagondlu V.en_US
dc.contributor.authorBodmer, Rolfen_US
dc.date.accessioned2006-04-19T13:45:43Z
dc.date.available2006-04-19T13:45:43Z
dc.date.issued1998en_US
dc.identifier.citationPark, Maiyon; Venkatesh, Tyamagondlu V.; Bodmer, Rolf (1998)."Dual role for the zeste-white3/shaggy -encoded kinase in mesoderm and heart development of Drosophila ." Developmental Genetics 22(3): 201-211. <http://hdl.handle.net/2027.42/34686>en_US
dc.identifier.issn0192-253Xen_US
dc.identifier.issn1520-6408en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/34686
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=9621428&dopt=citationen_US
dc.description.abstractA Drosophila homolog of the serine/threonine kinase GSK-3β, encoded by the zest-white3/shaggy gene ( zw3 ), has been implicated as a maternally provided antagonist of zygotic signaling by the secreted segmentation gene wingless ( wg ). The wg signal apparently causes a spatially localized inhibition of the ubiquitous repressor function of zw3. This double negative mechanism of signal transduction has been shown to mediate the patterning function of Wg in a number of developmental processes. Although wg is absolutely required for specifying the heart progenitors within the mesoderm of Drosophila, the role of zw3 in this process has been unclear. Here, we present evidence that zw3 has a dual role in mesoderm development: (1) zw3 acts as an antagonist in cardiogenic wg signal transduction, and (2) zw3 also seems to be required to promote positively the formation of a larger mesodermal region, the tinman - and dpp -dependent “dorsal mesoderm,” which is a prerequisite not only for cardiogenesis, but also for visceral mesoderm formation. We also demonstrate that a recently identified proximal component of the wg cascade, which is a transcription factor encoded by pangolin/dTCF ( dTCF ), also seems to mediate wg -dependent cardiogenesis. Further, we present evidence that Notch ( N ), which opposes wg signaling in other situations, is unlikely to be directly involved in the cardiogenic wg pathway, but seems to have multiple other myogenic functions, one of which is to inhibit mesoderm differentiation altogether, when overexpressed as a constitutively active form. Dev. Genet. 22:201–211, 1998. © 1998 Wiley-Liss, Inc.en_US
dc.format.extent904220 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherJohn Wiley & Sons, Inc.en_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherGeneticsen_US
dc.titleDual role for the zeste-white3/shaggy -encoded kinase in mesoderm and heart development of Drosophilaen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelBiological Chemistryen_US
dc.subject.hlbsecondlevelGeneticsen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.subject.hlbtoplevelScienceen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Biology, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationumDepartment of Biology, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationumDepartment of Biology, University of Michigan, Ann Arbor, Michigan ; who is now at IBDM, (until July 1998), Campus de Luminy, case 907, F-13288 Marseille, France.-mrs.fr After July 1998: Dr. Rolf Bodmer, Dept. of Biology, University of Michigan, 830 N. University, Ann Arbor, MI 48109–1048. E-mail:rolf@umich.eduen_US
dc.identifier.pmid9621428en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/34686/1/3_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/(SICI)1520-6408(1998)22:3<201::AID-DVG3>3.0.CO;2-Aen_US
dc.identifier.sourceDevelopmental Geneticsen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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