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dc.contributor.authorLiu, Qian
dc.contributor.authorJones, Takako I.
dc.contributor.authorBachmann, Rebecca A.
dc.contributor.authorMeghpara, Mitchell
dc.contributor.authorRogowski, Lauren
dc.contributor.authorWilliams, Benjamin D.
dc.contributor.authorJones, Peter L.
dc.date2022-08-11T08:10:14.000
dc.date.accessioned2022-08-23T17:00:50Z
dc.date.available2022-08-23T17:00:50Z
dc.date.issued2012-05-22
dc.date.submitted2014-12-04
dc.identifier.citationCell Biosci. 2012 May 22;2(1):18. doi: 10.1186/2045-3701-2-18. <a href="http://dx.doi.org/10.1186/2045-3701-2-18">Link to article on publisher's site</a>
dc.identifier.issn2045-3701 (Linking)
dc.identifier.doi10.1186/2045-3701-2-18
dc.identifier.pmid22616817
dc.identifier.urihttp://hdl.handle.net/20.500.14038/43878
dc.description<p>At the time of publication, Peter Jones and Takako Jones were not yet affiliated with the University of Massachusetts Medical School.</p>
dc.description.abstractBACKGROUND: Caenorhabditis elegans sarcomeres have been studied extensively utilizing both forward and reverse genetic techniques to provide insight into muscle development and the mechanisms behind muscle contraction. A previous genetic screen investigating early muscle development produced 13 independent mutant genes exhibiting a Pat (paralyzed and arrested elongation at the two-fold length of embryonic development) muscle phenotype. This study reports the identification and characterization of one of those genes, pat-9. RESULTS: Positional cloning, reverse genetics, and plasmid rescue experiments were used to identify the predicted C. elegans gene T27B1.2 (recently named ztf-19) as the pat-9 gene. Analysis of pat-9 showed it is expressed early in development and within body wall muscle lineages, consistent with a role in muscle development and producing a Pat phenotype. However, unlike most of the other known Pat gene family members, which encode structural components of muscle attachment sites, PAT-9 is an exclusively nuclear protein. Analysis of the predicted PAT-9 amino acid sequence identified one putative nuclear localization domain and three C2H2 zinc finger domains. Both immunocytochemistry and PAT-9::GFP fusion expression confirm that PAT-9 is primarily a nuclear protein and chromatin immunoprecipitation (ChIP) experiments showed that PAT-9 is present on certain gene promoters. CONCLUSIONS: We have shown that the T27B1.2 gene is pat-9. Considering the Pat-9 mutant phenotype shows severely disrupted muscle attachment sites despite PAT-9 being a nuclear zinc finger protein and not a structural component of muscle attachment sites, we propose that PAT-9 likely functions in the regulation of gene expression for some necessary structural or regulatory component(s) of the muscle attachment sites.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=22616817&dopt=Abstract">Link to Article in PubMed</a>
dc.rights<p>Copyright ©2012 Liu et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<a href="http://creativecommons.org/licenses/by/2.0">http://creativecommons.org/licenses/by/2.0</a>), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p>
dc.subjectSarcomere
dc.subjectMuscle
dc.subjectZinc finger
dc.subjectPat
dc.subjectCell Biology
dc.subjectDevelopmental Biology
dc.subjectMolecular Biology
dc.subjectMolecular Genetics
dc.subjectMusculoskeletal Diseases
dc.subjectNervous System Diseases
dc.titleC. elegans PAT-9 is a nuclear zinc finger protein critical for the assembly of muscle attachments
dc.typeJournal Article
dc.source.journaltitleCell and bioscience
dc.source.volume2
dc.source.issue1
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1017&amp;context=peterjones&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/peterjones/18
dc.legacy.embargo2014-12-11T00:00:00-08:00
dc.identifier.contextkey6422502
refterms.dateFOA2022-08-23T17:00:50Z
html.description.abstract<p>BACKGROUND: Caenorhabditis elegans sarcomeres have been studied extensively utilizing both forward and reverse genetic techniques to provide insight into muscle development and the mechanisms behind muscle contraction. A previous genetic screen investigating early muscle development produced 13 independent mutant genes exhibiting a Pat (paralyzed and arrested elongation at the two-fold length of embryonic development) muscle phenotype. This study reports the identification and characterization of one of those genes, pat-9.</p> <p>RESULTS: Positional cloning, reverse genetics, and plasmid rescue experiments were used to identify the predicted C. elegans gene T27B1.2 (recently named ztf-19) as the pat-9 gene. Analysis of pat-9 showed it is expressed early in development and within body wall muscle lineages, consistent with a role in muscle development and producing a Pat phenotype. However, unlike most of the other known Pat gene family members, which encode structural components of muscle attachment sites, PAT-9 is an exclusively nuclear protein. Analysis of the predicted PAT-9 amino acid sequence identified one putative nuclear localization domain and three C2H2 zinc finger domains. Both immunocytochemistry and PAT-9::GFP fusion expression confirm that PAT-9 is primarily a nuclear protein and chromatin immunoprecipitation (ChIP) experiments showed that PAT-9 is present on certain gene promoters.</p> <p>CONCLUSIONS: We have shown that the T27B1.2 gene is pat-9. Considering the Pat-9 mutant phenotype shows severely disrupted muscle attachment sites despite PAT-9 being a nuclear zinc finger protein and not a structural component of muscle attachment sites, we propose that PAT-9 likely functions in the regulation of gene expression for some necessary structural or regulatory component(s) of the muscle attachment sites.</p>
dc.identifier.submissionpathpeterjones/18
dc.contributor.departmentDepartment of Cell and Developmental Biology
dc.source.pages18


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