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dc.contributor.authorHall, Lisa L.
dc.contributor.authorByron, Meg
dc.contributor.authorSakai, Kosuke
dc.contributor.authorCarrel, Laura
dc.contributor.authorWillard, Huntington F.
dc.contributor.authorLawrence, Jeanne B.
dc.date2022-08-11T08:09:36.000
dc.date.accessioned2022-08-23T16:37:08Z
dc.date.available2022-08-23T16:37:08Z
dc.date.issued2002-06-20
dc.date.submitted2009-04-02
dc.identifier.citationProc Natl Acad Sci U S A. 2002 Jun 25;99(13):8677-82. Epub 2002 Jun 18. <a href="http://dx.doi.org/10.1073/pnas.132468999">Link to article on publisher's site</a>
dc.identifier.issn0027-8424 (Print)
dc.identifier.doi10.1073/pnas.132468999
dc.identifier.pmid12072569
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38946
dc.description.abstractIt has been believed that XIST RNA requires a discrete window in early development to initiate the series of chromatin-remodeling events that form the heterochromatic inactive X chromosome. Here we investigate four adult male HT-1080 fibrosarcoma cell lines expressing ectopic human XIST and demonstrate that these postdifferentiation cells can undergo chromosomal inactivation outside of any normal developmental context. All four clonal lines inactivated the transgene-containing autosome to varying degrees and with variable stability. One clone in particular consistently localized the ectopic XIST RNA to a discrete chromosome territory that exhibited striking hallmarks of inactivation, including long-range transcriptional inactivation. Results suggest that some postdifferentiation cell lines are capable of de novo chromosomal inactivation; however, long-term retention of autosomal inactivation was less common, which suggests that autosomal inactivation may confer a selective disadvantage. These results have fundamental significance for understanding genomic programming in early development.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=12072569&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC124357/pdf/pq1302008677.pdf
dc.subjectAcetylation
dc.subjectCell Differentiation
dc.subject*Chromosomes, Human
dc.subjectGene Silencing
dc.subjectHumans
dc.subjectIn Situ Hybridization, Fluorescence
dc.subjectMale
dc.subjectMicroscopy, Fluorescence
dc.subjectRNA
dc.subjectRNA, Untranslated
dc.subjectTranscription Factors
dc.subjectTranscription, Genetic
dc.subjectTumor Cells, Cultured
dc.subjectCell Biology
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleAn ectopic human XIST gene can induce chromosome inactivation in postdifferentiation human HT-1080 cells
dc.typeJournal Article
dc.source.journaltitleProceedings of the National Academy of Sciences of the United States of America
dc.source.volume99
dc.source.issue13
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1776
dc.identifier.contextkey808541
html.description.abstract<p>It has been believed that XIST RNA requires a discrete window in early development to initiate the series of chromatin-remodeling events that form the heterochromatic inactive X chromosome. Here we investigate four adult male HT-1080 fibrosarcoma cell lines expressing ectopic human XIST and demonstrate that these postdifferentiation cells can undergo chromosomal inactivation outside of any normal developmental context. All four clonal lines inactivated the transgene-containing autosome to varying degrees and with variable stability. One clone in particular consistently localized the ectopic XIST RNA to a discrete chromosome territory that exhibited striking hallmarks of inactivation, including long-range transcriptional inactivation. Results suggest that some postdifferentiation cell lines are capable of de novo chromosomal inactivation; however, long-term retention of autosomal inactivation was less common, which suggests that autosomal inactivation may confer a selective disadvantage. These results have fundamental significance for understanding genomic programming in early development.</p>
dc.identifier.submissionpathoapubs/1776
dc.contributor.departmentDepartment of Cell Biology
dc.source.pages8677-82


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