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dc.contributor.authorAshraf, Shovon Imtiaz
dc.contributor.authorGanguly, Atish
dc.contributor.authorRoote, John
dc.contributor.authorIp, Y. Tony
dc.date2022-08-11T08:08:59.000
dc.date.accessioned2022-08-23T16:14:37Z
dc.date.available2022-08-23T16:14:37Z
dc.date.issued2004-09-15
dc.date.submitted2008-07-02
dc.identifier.citationDev Dyn. 2004 Oct;231(2):379-86. <a href="http://dx.doi.org/10.1002/dvdy.20130">Link to article on publisher's site</a>
dc.identifier.issn1058-8388 (Print)
dc.identifier.doi10.1002/dvdy.20130
dc.identifier.pmid15366015
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33904
dc.description.abstractThe Snail family of zinc-finger transcriptional repressors is essential for morphogenetic cell movements, mesoderm formation, and neurogenesis during embryonic development. These proteins also control cell cycle, cell death, and cancer progression. In Drosophila, three members of this protein family, Snail, Escargot, and Worniu, have essential but redundant functions in asymmetric cell division of neuroblasts. In addition, Snail is critical for early mesoderm formation and Escargot is required for maintaining diploidy in wing imaginal disc cells. In this report, we demonstrate that Worniu plays a role in brain development. We show that alleles of the l(2)35Da complementation group are mutants of worniu. The developing larvae of these mutant alleles fail to shorten their brainstems. The brain phenotype, as well as the lethality, of these mutants can be rescued by worniu transgenes. Moreover, RNAi experiments targeting the worniu transcript show the same nonshortening phenotype in larval brains. worniu is expressed in the neuroblasts of brain hemispheres and ventral ganglions. The results suggest that the loss of Worniu function within the neuroblasts ultimately causes the larval brainstem to fail to go through shortening during development.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15366015&dopt=Abstract ">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1002/dvdy.20130
dc.subjectAnimals; Animals, Genetically Modified; Brain; Drosophila Proteins; Drosophila melanogaster; In Situ Hybridization; Larva; Phenotype; RNA Interference; Transcription Factors; Transgenes; Zinc Fingers
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleWorniu, a Snail family zinc-finger protein, is required for brain development in Drosophila
dc.typeJournal Article
dc.source.journaltitleDevelopmental dynamics : an official publication of the American Association of Anatomists
dc.source.volume231
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/56
dc.identifier.contextkey542468
html.description.abstract<p>The Snail family of zinc-finger transcriptional repressors is essential for morphogenetic cell movements, mesoderm formation, and neurogenesis during embryonic development. These proteins also control cell cycle, cell death, and cancer progression. In Drosophila, three members of this protein family, Snail, Escargot, and Worniu, have essential but redundant functions in asymmetric cell division of neuroblasts. In addition, Snail is critical for early mesoderm formation and Escargot is required for maintaining diploidy in wing imaginal disc cells. In this report, we demonstrate that Worniu plays a role in brain development. We show that alleles of the l(2)35Da complementation group are mutants of worniu. The developing larvae of these mutant alleles fail to shorten their brainstems. The brain phenotype, as well as the lethality, of these mutants can be rescued by worniu transgenes. Moreover, RNAi experiments targeting the worniu transcript show the same nonshortening phenotype in larval brains. worniu is expressed in the neuroblasts of brain hemispheres and ventral ganglions. The results suggest that the loss of Worniu function within the neuroblasts ultimately causes the larval brainstem to fail to go through shortening during development.</p>
dc.identifier.submissionpathgsbs_sp/56
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages379-86


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