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dc.contributor.authorWang, Jian
dc.contributor.authorLee, Ching-Hsien J.
dc.contributor.authorLin, Suewei
dc.contributor.authorLee, Tzumin
dc.date2022-08-11T08:09:30.000
dc.date.accessioned2022-08-23T16:33:06Z
dc.date.available2022-08-23T16:33:06Z
dc.date.issued2006-04-01
dc.date.submitted2012-05-24
dc.identifier.citationDevelopment. 2006 Apr;133(7):1231-40. Epub 2006 Feb 22. <a href="http://dx.doi.org/10.1242/dev.02299" target="_blank">Link to article on publisher's site</a>
dc.identifier.issn0950-1991 (Linking)
dc.identifier.doi10.1242/dev.02299
dc.identifier.pmid16495309
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38025
dc.description<p>Co-author Suewei Lin is a student in the Neuroscience program in the Graduate School of Biomedical Sciences (GSBS) at UMass Medical School.</p>
dc.description.abstractPolyhomeotic (Ph), which forms complexes with other Polycomb-group (PcG) proteins, is widely required for maintenance of cell identity by ensuring differential gene expression patterns in distinct types of cells. Genetic mosaic screens in adult fly brains allow for recovery of a mutation that simultaneously disrupts the tandemly duplicated Drosophila ph transcriptional units. Distinct clones of neurons normally acquire different characteristic projection patterns and can be differentially labeled using various subtype-specific drivers in mosaic brains. Such neuronal diversity is lost without Ph. In response to ecdysone, ph mutant neurons are transformed into cells with unidentifiable projection patterns and indistinguishable gene expression profiles during early metamorphosis. Some subtype-specific neuronal drivers become constitutively activated, while others are constantly suppressed. By contrast, loss of other PcG proteins, including Pc and E(z), causes different neuronal developmental defects; and, consistent with these phenomena, distinct Hox genes are differentially misexpressed in different PcG mutant clones. Taken together, Drosophila Ph is essential for governing neuronal diversity, especially during steroid hormone signaling.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=16495309&dopt=Abstract">Link to Article in PubMed</a>
dc.rightsPublisher PDF posted as allowed by the publisher's author rights policy athttp://dev.biologists.org/site/misc/rights_permissions.xhtml#author.
dc.subjectAnimals
dc.subjectBrain
dc.subjectChromosome Mapping
dc.subjectChromosomes
dc.subjectClone Cells
dc.subjectCrosses, Genetic
dc.subjectDNA-Binding Proteins
dc.subjectDrosophila
dc.subjectDrosophila Proteins
dc.subjectEcdysone
dc.subjectFemale
dc.subjectGene Expression
dc.subjectGenes, Homeobox
dc.subjectGenes, Insect
dc.subjectGenetic Complementation Test
dc.subjectImmunohistochemistry
dc.subjectInsect Proteins
dc.subjectLarva
dc.subjectMale
dc.subjectMetamorphosis, Biological
dc.subject*Mutation
dc.subjectNeurons
dc.subjectNucleoproteins
dc.subjectOrgan Culture Techniques
dc.subjectRecombination, Genetic
dc.subjectDevelopmental Neuroscience
dc.titleSteroid hormone-dependent transformation of polyhomeotic mutant neurons in the Drosophila brain
dc.typeJournal Article
dc.source.journaltitleDevelopment (Cambridge, England)
dc.source.volume133
dc.source.issue7
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1058&amp;context=neurobiology_pp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/neurobiology_pp/59
dc.identifier.contextkey2911174
refterms.dateFOA2022-08-23T16:33:06Z
html.description.abstract<p>Polyhomeotic (Ph), which forms complexes with other Polycomb-group (PcG) proteins, is widely required for maintenance of cell identity by ensuring differential gene expression patterns in distinct types of cells. Genetic mosaic screens in adult fly brains allow for recovery of a mutation that simultaneously disrupts the tandemly duplicated Drosophila ph transcriptional units. Distinct clones of neurons normally acquire different characteristic projection patterns and can be differentially labeled using various subtype-specific drivers in mosaic brains. Such neuronal diversity is lost without Ph. In response to ecdysone, ph mutant neurons are transformed into cells with unidentifiable projection patterns and indistinguishable gene expression profiles during early metamorphosis. Some subtype-specific neuronal drivers become constitutively activated, while others are constantly suppressed. By contrast, loss of other PcG proteins, including Pc and E(z), causes different neuronal developmental defects; and, consistent with these phenomena, distinct Hox genes are differentially misexpressed in different PcG mutant clones. Taken together, Drosophila Ph is essential for governing neuronal diversity, especially during steroid hormone signaling.</p>
dc.identifier.submissionpathneurobiology_pp/59
dc.contributor.departmentMedicine, Division of Hematology/Oncology
dc.contributor.departmentGraduate School of Biomedical Sciences, Neuroscience Program
dc.contributor.departmentLee Lab
dc.contributor.departmentNeurobiology
dc.source.pages1231-40
dc.contributor.studentSuewei Lin
dc.description.thesisprogramNeuroscience


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