Identification of a Ctcf Cofactor, Yy1, for the X Chromosome Binary Switch
In mammals, inactivation of one X chromosome in the female equalizes gene dosages between XX females and XY males. Two noncoding loci, Tsix and Xite, together regulate X chromosome fate by controlling homologous chromosome pairing, counting, and mutually exclusive choice. Following choice, the asymm...
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| Veröffentlicht in: | Molecular cell 2007-01, Vol.25 (1), p.43-56 |
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| creator | Donohoe, Mary E. Zhang, Li-Feng Xu, Na Shi, Yang Lee, Jeannie T. |
| description | In mammals, inactivation of one X chromosome in the female equalizes gene dosages between XX females and XY males. Two noncoding loci,
Tsix and
Xite, together regulate X chromosome fate by controlling homologous chromosome pairing, counting, and mutually exclusive choice. Following choice, the asymmetry of
Xite and
Tsix expression drives divergent chromosome fates, but how this pattern becomes established is currently unknown. Although no proven
trans-acting factors have been identified, a likely candidate is Ctcf, a chromatin insulator with essential function in autosomal imprinting. Here, we search for
trans-factors and identify Yy1 as a required cofactor for Ctcf. Paired Ctcf-Yy1 elements are highly clustered within the counting/choice and imprinting domain of
Tsix. A deficiency of Yy1 leads to aberrant
Tsix and
Xist expression, resulting in a deficit of male and female embryos. Yy1 and Ctcf associate through specific protein-protein interactions and together transactivate
Tsix. We propose that the Ctcf-Yy1-Tsix complex functions as a key component of the X chromosome binary switch. |
| doi_str_mv | 10.1016/j.molcel.2006.11.017 |
| format | Article |
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Tsix and
Xite, together regulate X chromosome fate by controlling homologous chromosome pairing, counting, and mutually exclusive choice. Following choice, the asymmetry of
Xite and
Tsix expression drives divergent chromosome fates, but how this pattern becomes established is currently unknown. Although no proven
trans-acting factors have been identified, a likely candidate is Ctcf, a chromatin insulator with essential function in autosomal imprinting. Here, we search for
trans-factors and identify Yy1 as a required cofactor for Ctcf. Paired Ctcf-Yy1 elements are highly clustered within the counting/choice and imprinting domain of
Tsix. A deficiency of Yy1 leads to aberrant
Tsix and
Xist expression, resulting in a deficit of male and female embryos. Yy1 and Ctcf associate through specific protein-protein interactions and together transactivate
Tsix. We propose that the Ctcf-Yy1-Tsix complex functions as a key component of the X chromosome binary switch.</description><identifier>ISSN: 1097-2765</identifier><identifier>EISSN: 1097-4164</identifier><identifier>DOI: 10.1016/j.molcel.2006.11.017</identifier><identifier>PMID: 17218270</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Base Sequence ; Blastocyst - cytology ; CCCTC-Binding Factor ; Chromosomes, Mammalian - genetics ; DEVBIO ; DNA ; DNA - metabolism ; DNA-Binding Proteins - metabolism ; Embryonic Stem Cells - cytology ; Female ; Humans ; Male ; Mice ; Mice, Mutant Strains ; Molecular Sequence Data ; Protein Binding ; Repressor Proteins - metabolism ; RNA, Long Noncoding ; RNA, Untranslated - genetics ; RNA, Untranslated - metabolism ; RNA-Binding Proteins - metabolism ; Trans-Activators - metabolism ; X Chromosome - genetics ; X Chromosome Inactivation ; YY1 Transcription Factor - deficiency ; YY1 Transcription Factor - metabolism</subject><ispartof>Molecular cell, 2007-01, Vol.25 (1), p.43-56</ispartof><rights>2007 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c472t-bc8c6552613de17e37a9049f77d2987060048d9abaa39a797af7e7f93ee3c8883</citedby><cites>FETCH-LOGICAL-c472t-bc8c6552613de17e37a9049f77d2987060048d9abaa39a797af7e7f93ee3c8883</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.molcel.2006.11.017$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17218270$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Donohoe, Mary E.</creatorcontrib><creatorcontrib>Zhang, Li-Feng</creatorcontrib><creatorcontrib>Xu, Na</creatorcontrib><creatorcontrib>Shi, Yang</creatorcontrib><creatorcontrib>Lee, Jeannie T.</creatorcontrib><title>Identification of a Ctcf Cofactor, Yy1, for the X Chromosome Binary Switch</title><title>Molecular cell</title><addtitle>Mol Cell</addtitle><description>In mammals, inactivation of one X chromosome in the female equalizes gene dosages between XX females and XY males. Two noncoding loci,
Tsix and
Xite, together regulate X chromosome fate by controlling homologous chromosome pairing, counting, and mutually exclusive choice. Following choice, the asymmetry of
Xite and
Tsix expression drives divergent chromosome fates, but how this pattern becomes established is currently unknown. Although no proven
trans-acting factors have been identified, a likely candidate is Ctcf, a chromatin insulator with essential function in autosomal imprinting. Here, we search for
trans-factors and identify Yy1 as a required cofactor for Ctcf. Paired Ctcf-Yy1 elements are highly clustered within the counting/choice and imprinting domain of
Tsix. A deficiency of Yy1 leads to aberrant
Tsix and
Xist expression, resulting in a deficit of male and female embryos. Yy1 and Ctcf associate through specific protein-protein interactions and together transactivate
Tsix. We propose that the Ctcf-Yy1-Tsix complex functions as a key component of the X chromosome binary switch.</description><subject>Animals</subject><subject>Base Sequence</subject><subject>Blastocyst - cytology</subject><subject>CCCTC-Binding Factor</subject><subject>Chromosomes, Mammalian - genetics</subject><subject>DEVBIO</subject><subject>DNA</subject><subject>DNA - metabolism</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Embryonic Stem Cells - cytology</subject><subject>Female</subject><subject>Humans</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Molecular Sequence Data</subject><subject>Protein Binding</subject><subject>Repressor Proteins - metabolism</subject><subject>RNA, Long Noncoding</subject><subject>RNA, Untranslated - genetics</subject><subject>RNA, Untranslated - metabolism</subject><subject>RNA-Binding Proteins - metabolism</subject><subject>Trans-Activators - metabolism</subject><subject>X Chromosome - genetics</subject><subject>X Chromosome Inactivation</subject><subject>YY1 Transcription Factor - deficiency</subject><subject>YY1 Transcription Factor - metabolism</subject><issn>1097-2765</issn><issn>1097-4164</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kElPIzEQRi3EiP0fIOQTJ9Lj6na8XJCgxTaKNIcZJDhZjrusOEq3wXYY8e_pKJG4zanq8L5aHiHnwCpgIH4uqz6uHK6qmjFRAVQM5B45AqblhIPg-7u-lmJ6SI5zXjIGfKr0ATkEWYOqJTsiv546HErwwdkS4kCjp5a2xXnaRm9diemKvn7CFfUx0bJA-kLbRYp9zLFHehsGmz7pn3-huMUp-eHtKuPZrp6Q5_u7v-3jZPb74am9mU0cl3WZzJ1yYjqtBTQdgsRGWs249lJ2tVaSCca46rSdW9toK7W0XqL0ukFsnFKqOSGX27lvKb6vMRfThzyKWNkB4zoboXjNuGhGkG9Bl2LOCb15S6EfDzbAzMahWZqtQ7NxaADM6HCMXezmr-c9dt-hnbQRuN4COH75ETCZ7AIODruQ0BXTxfD_DV9GnIKo</recordid><startdate>20070112</startdate><enddate>20070112</enddate><creator>Donohoe, Mary E.</creator><creator>Zhang, Li-Feng</creator><creator>Xu, Na</creator><creator>Shi, Yang</creator><creator>Lee, Jeannie T.</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20070112</creationdate><title>Identification of a Ctcf Cofactor, Yy1, for the X Chromosome Binary Switch</title><author>Donohoe, Mary E. ; Zhang, Li-Feng ; Xu, Na ; Shi, Yang ; Lee, Jeannie T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c472t-bc8c6552613de17e37a9049f77d2987060048d9abaa39a797af7e7f93ee3c8883</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Base Sequence</topic><topic>Blastocyst - cytology</topic><topic>CCCTC-Binding Factor</topic><topic>Chromosomes, Mammalian - genetics</topic><topic>DEVBIO</topic><topic>DNA</topic><topic>DNA - metabolism</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Embryonic Stem Cells - cytology</topic><topic>Female</topic><topic>Humans</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Molecular Sequence Data</topic><topic>Protein Binding</topic><topic>Repressor Proteins - metabolism</topic><topic>RNA, Long Noncoding</topic><topic>RNA, Untranslated - genetics</topic><topic>RNA, Untranslated - metabolism</topic><topic>RNA-Binding Proteins - metabolism</topic><topic>Trans-Activators - metabolism</topic><topic>X Chromosome - genetics</topic><topic>X Chromosome Inactivation</topic><topic>YY1 Transcription Factor - deficiency</topic><topic>YY1 Transcription Factor - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Donohoe, Mary E.</creatorcontrib><creatorcontrib>Zhang, Li-Feng</creatorcontrib><creatorcontrib>Xu, Na</creatorcontrib><creatorcontrib>Shi, Yang</creatorcontrib><creatorcontrib>Lee, Jeannie T.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular cell</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Donohoe, Mary E.</au><au>Zhang, Li-Feng</au><au>Xu, Na</au><au>Shi, Yang</au><au>Lee, Jeannie T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification of a Ctcf Cofactor, Yy1, for the X Chromosome Binary Switch</atitle><jtitle>Molecular cell</jtitle><addtitle>Mol Cell</addtitle><date>2007-01-12</date><risdate>2007</risdate><volume>25</volume><issue>1</issue><spage>43</spage><epage>56</epage><pages>43-56</pages><issn>1097-2765</issn><eissn>1097-4164</eissn><abstract>In mammals, inactivation of one X chromosome in the female equalizes gene dosages between XX females and XY males. Two noncoding loci,
Tsix and
Xite, together regulate X chromosome fate by controlling homologous chromosome pairing, counting, and mutually exclusive choice. Following choice, the asymmetry of
Xite and
Tsix expression drives divergent chromosome fates, but how this pattern becomes established is currently unknown. Although no proven
trans-acting factors have been identified, a likely candidate is Ctcf, a chromatin insulator with essential function in autosomal imprinting. Here, we search for
trans-factors and identify Yy1 as a required cofactor for Ctcf. Paired Ctcf-Yy1 elements are highly clustered within the counting/choice and imprinting domain of
Tsix. A deficiency of Yy1 leads to aberrant
Tsix and
Xist expression, resulting in a deficit of male and female embryos. Yy1 and Ctcf associate through specific protein-protein interactions and together transactivate
Tsix. We propose that the Ctcf-Yy1-Tsix complex functions as a key component of the X chromosome binary switch.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17218270</pmid><doi>10.1016/j.molcel.2006.11.017</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Full-Text Journals in Chemistry (Open access); Open Access: Cell Press Free Archives; ScienceDirect Freedom Collection (Elsevier); EZB Electronic Journals Library |
| subjects | Animals Base Sequence Blastocyst - cytology CCCTC-Binding Factor Chromosomes, Mammalian - genetics DEVBIO DNA DNA - metabolism DNA-Binding Proteins - metabolism Embryonic Stem Cells - cytology Female Humans Male Mice Mice, Mutant Strains Molecular Sequence Data Protein Binding Repressor Proteins - metabolism RNA, Long Noncoding RNA, Untranslated - genetics RNA, Untranslated - metabolism RNA-Binding Proteins - metabolism Trans-Activators - metabolism X Chromosome - genetics X Chromosome Inactivation YY1 Transcription Factor - deficiency YY1 Transcription Factor - metabolism |
| title | Identification of a Ctcf Cofactor, Yy1, for the X Chromosome Binary Switch |
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