Antagonistic function of Lmd and Zfh1 fine tunes cell fate decisions in the Twi and Tin positive mesoderm of Drosophila melanogaster

DC FieldValueLanguage
dc.contributor.authorSellin, Julia
dc.contributor.authorDrechsler, Maik
dc.contributor.authorNguyen, Hanh T.
dc.contributor.authorPaululat, Achim
dc.date.accessioned2021-12-23T16:18:28Z-
dc.date.available2021-12-23T16:18:28Z-
dc.date.issued2009
dc.identifier.issn00121606
dc.identifier.urihttps://osnascholar.ub.uni-osnabrueck.de/handle/unios/12703-
dc.description.abstractIn this study we show that cell fate decisions in the dorsal and lateral mesoderm of Drosophila melanogaster depend on the antagonistic action of the Gli-like transcription factor Lame duck (Lmd) and the zinc finger homeodomain factor Zfh1. Lmd expression leads to the reduction of Zfh1 positive cell types, thereby restricting the number of Odd-skipped (Odd) positive and Tinman (Tin) positive pericardial cells in the dorsal mesoderm. In more lateral regions, ectopic activation of Zfh1 or loss of Lmd leads to an excess of adult muscle precursor (AMP) like cells. We also observed that Lmd is co-expressed with Tin in the early dorsal mesoderm and leads to a reduction of Tin expression in cells destined to become dorsal fusion competent myoblasts (FCMs). In the absence of Lmd function, these cells remain Tin positive and develop as Tin positive pericardial cells although they do not express Zfh1. We show further that Tin repression and pericardial restriction in the dorsal mesoderm facilitated by Lmd is instructed by a late Decapentaplegic (Dpp) signal that is abolished in embryos carrying the disk region mutation dpp(d6). (c) 2008 Elsevier Inc. All rights reserved.
dc.description.sponsorshipDFGGerman Research Foundation (DFG)European Commission [DFG Pa 517/10-1, SFB 431]; NIHUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [RO1-AR4628]; We thank Stuart Newfeld for the fruitful discussions and help with general questions, and Martina Biedermann and Mechthild Krabusch for the excellent technical assistance. We also thank C. Klambt, Z. C. Lai, M. Leptin, M. Fraschj Skeath, R. M. Cripps, H. A. Muller, Kjagla, R. Renkawitz-Pohl, R. Lehmann, M. Taylor, the Bloomington Stock Center and the Developmental Studies Hybridoma Bank for antibodies, fly stocks and cloned materials. This research was supported by the European Program of Excellence MYORES and grants from the DFG to A.P. (European PhD program 767: Transcriptional Control in Development, DFG Pa 517/10-1 and the SFB 431: Membranproteine - Funktionelle Dynamik und Kopplung an Reaktionsketten) and the NIH to H.T.N. (RO1-AR4628).
dc.language.isoen
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE
dc.relation.ispartofDEVELOPMENTAL BIOLOGY
dc.subjectADULT MUSCLES
dc.subjectCARDIAC DEVELOPMENT
dc.subjectCardiogenesis
dc.subjectDevelopmental Biology
dc.subjectDORSAL ECTODERM
dc.subjectDorsal vessel
dc.subjectDpp
dc.subjectEXPRESSION
dc.subjectHeart
dc.subjectHEART DEVELOPMENT
dc.subjectMesoderm
dc.subjectMUSCLE DIFFERENTIATION
dc.subjectMYOGENESIS
dc.subjectNEUROGENIC GENES
dc.subjectNOTCH
dc.subjectOdd-skipped
dc.subjectPERICARDIAL CELLS
dc.subjectSomatic musculature
dc.titleAntagonistic function of Lmd and Zfh1 fine tunes cell fate decisions in the Twi and Tin positive mesoderm of Drosophila melanogaster
dc.typejournal article
dc.identifier.doi10.1016/j.ydbio.2008.10.041
dc.identifier.isiISI:000263285200016
dc.description.volume326
dc.description.issue2
dc.description.startpage444
dc.description.endpage455
dc.contributor.orcid0000-0001-5354-2872
dc.contributor.orcid0000-0002-8845-6859
dc.contributor.researcheridJ-6435-2019
dc.identifier.eissn1095564X
dc.publisher.place525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA
dcterms.isPartOf.abbreviationDev. Biol.
dcterms.oaStatusBronze
crisitem.author.deptFB 05 - Biologie/Chemie-
crisitem.author.deptidfb05-
crisitem.author.orcid0000-0002-8845-6859-
crisitem.author.parentorgUniversität Osnabrück-
crisitem.author.netidPaAc947-
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