Widespread Failure of Hematolymphoid Differentiation Caused by a Recessive Niche-Filling Allele of the Ikaros Transcription Factor
A central issue in understanding the hematolymphoid system is the generation of appropriate mutant alleles in mice to reveal the function of regulatory genes. Here we describe a mouse strain, Plastic, with a point mutation in a zinc finger of Ikaros that disrupts DNA binding but preserves efficient...
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| Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 2003-07, Vol.19 (1), p.131-144 |
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| creator | Papathanasiou, Peter Perkins, Andrew C. Cobb, Bradley S. Ferrini, Roger Sridharan, Rupa Hoyne, Gerard F. Nelms, Keats A. Smale, Stephen T. Goodnow, Christopher C. |
| description | A central issue in understanding the hematolymphoid system is the generation of appropriate mutant alleles in mice to reveal the function of regulatory genes. Here we describe a mouse strain,
Plastic, with a point mutation in a zinc finger of Ikaros that disrupts DNA binding but preserves efficient assembly of the full-length protein into higher order complexes.
Ikaros
Plastic
homozygosity is embryonically lethal with severe defects in terminal erythrocyte and granulocyte differentiation, excessive macrophage formation, and blocked lymphopoiesis, while heterozygotes display a partial block in lymphocyte differentiation. The contrast with more circumscribed effects of
Ikaros alleles that ablate the full-length protein highlights the importance in mammals of generating recessive niche-filling alleles that inactivate function without creating a void in multimolecular assemblies. |
| doi_str_mv | 10.1016/S1074-7613(03)00168-7 |
| format | Article |
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Plastic, with a point mutation in a zinc finger of Ikaros that disrupts DNA binding but preserves efficient assembly of the full-length protein into higher order complexes.
Ikaros
Plastic
homozygosity is embryonically lethal with severe defects in terminal erythrocyte and granulocyte differentiation, excessive macrophage formation, and blocked lymphopoiesis, while heterozygotes display a partial block in lymphocyte differentiation. The contrast with more circumscribed effects of
Ikaros alleles that ablate the full-length protein highlights the importance in mammals of generating recessive niche-filling alleles that inactivate function without creating a void in multimolecular assemblies.</description><identifier>ISSN: 1074-7613</identifier><identifier>EISSN: 1097-4180</identifier><identifier>DOI: 10.1016/S1074-7613(03)00168-7</identifier><identifier>PMID: 12871645</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Alleles ; Anemia - etiology ; Animals ; Cell Differentiation ; Deoxyribonucleic acid ; Dimerization ; DNA ; DNA - metabolism ; DNA-Binding Proteins ; Erythrocytes - physiology ; Ethylnitrosourea ; Gene expression ; Genomes ; Hematopoiesis - physiology ; Hepatocytes - physiology ; Ikaros Transcription Factor ; Lymphocytes - physiology ; Lymphoma - etiology ; Mice ; Mice, Inbred C57BL ; Mutation ; Myeloid Cells - physiology ; Point Mutation ; Proteins ; Stem cells ; Transcription factors ; Transcription Factors - chemistry ; Transcription Factors - genetics ; Transcription Factors - physiology</subject><ispartof>Immunity (Cambridge, Mass.), 2003-07, Vol.19 (1), p.131-144</ispartof><rights>2003 Cell Press</rights><rights>Copyright Elsevier Limited Jul 2003</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c585t-3e5194e232ec819262465f2d8b6d3b79d40864606ad0deb7e0971eedd1661f2d3</citedby><cites>FETCH-LOGICAL-c585t-3e5194e232ec819262465f2d8b6d3b79d40864606ad0deb7e0971eedd1661f2d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1074761303001687$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12871645$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Papathanasiou, Peter</creatorcontrib><creatorcontrib>Perkins, Andrew C.</creatorcontrib><creatorcontrib>Cobb, Bradley S.</creatorcontrib><creatorcontrib>Ferrini, Roger</creatorcontrib><creatorcontrib>Sridharan, Rupa</creatorcontrib><creatorcontrib>Hoyne, Gerard F.</creatorcontrib><creatorcontrib>Nelms, Keats A.</creatorcontrib><creatorcontrib>Smale, Stephen T.</creatorcontrib><creatorcontrib>Goodnow, Christopher C.</creatorcontrib><title>Widespread Failure of Hematolymphoid Differentiation Caused by a Recessive Niche-Filling Allele of the Ikaros Transcription Factor</title><title>Immunity (Cambridge, Mass.)</title><addtitle>Immunity</addtitle><description>A central issue in understanding the hematolymphoid system is the generation of appropriate mutant alleles in mice to reveal the function of regulatory genes. Here we describe a mouse strain,
Plastic, with a point mutation in a zinc finger of Ikaros that disrupts DNA binding but preserves efficient assembly of the full-length protein into higher order complexes.
Ikaros
Plastic
homozygosity is embryonically lethal with severe defects in terminal erythrocyte and granulocyte differentiation, excessive macrophage formation, and blocked lymphopoiesis, while heterozygotes display a partial block in lymphocyte differentiation. The contrast with more circumscribed effects of
Ikaros alleles that ablate the full-length protein highlights the importance in mammals of generating recessive niche-filling alleles that inactivate function without creating a void in multimolecular assemblies.</description><subject>Alleles</subject><subject>Anemia - etiology</subject><subject>Animals</subject><subject>Cell Differentiation</subject><subject>Deoxyribonucleic acid</subject><subject>Dimerization</subject><subject>DNA</subject><subject>DNA - metabolism</subject><subject>DNA-Binding Proteins</subject><subject>Erythrocytes - physiology</subject><subject>Ethylnitrosourea</subject><subject>Gene expression</subject><subject>Genomes</subject><subject>Hematopoiesis - physiology</subject><subject>Hepatocytes - physiology</subject><subject>Ikaros Transcription Factor</subject><subject>Lymphocytes - physiology</subject><subject>Lymphoma - etiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mutation</subject><subject>Myeloid Cells - physiology</subject><subject>Point Mutation</subject><subject>Proteins</subject><subject>Stem cells</subject><subject>Transcription factors</subject><subject>Transcription Factors - chemistry</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - physiology</subject><issn>1074-7613</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV2L1DAUhoMo7jr6E5SAIHpRzWnTpL2SZXTchUVBV7wMaXLqZE2bmrQLc-svN_MBgjcLgYTw5E3yPoQ8B_YWGIh334BJXkgB1WtWvWF5qynkA3IOrJUFh4Y93K9PyBl5ktJthnjdssfkDMpGguD1Ofnzw1lMU0Rt6UY7v0SkoaeXOOg5-N0wbYOz9IPre4w4zk7PLox0rZeElnY7qulXNJiSu0P62ZktFhvnvRt_0gvv0R_C5i3Sq186hkRvoh6TiW46xGy0mUN8Sh712id8dppX5Pvm4836srj-8ulqfXFdmLqp56LCGlqOZVWiaaAtRclF3Ze26YStOtlazhrBBRPaMoudxFwEIFoLQkDmqhV5dcydYvi9YJrV4JJB7_WIYUlKVrwVUPN7QZAt5wBlBl_-B96GJY75EwpqxksmWlllqj5SJjeQIvZqim7QcaeAqb1LdXCp9qIUy2PvMr9mRV6c0pduQPvv1EleBt4fAcyt3TmMKhmHo0HrIppZ2eDuueIvFxeuSQ</recordid><startdate>20030701</startdate><enddate>20030701</enddate><creator>Papathanasiou, Peter</creator><creator>Perkins, Andrew C.</creator><creator>Cobb, Bradley S.</creator><creator>Ferrini, Roger</creator><creator>Sridharan, Rupa</creator><creator>Hoyne, Gerard F.</creator><creator>Nelms, Keats A.</creator><creator>Smale, Stephen T.</creator><creator>Goodnow, Christopher C.</creator><general>Elsevier Inc</general><general>Elsevier Limited</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20030701</creationdate><title>Widespread Failure of Hematolymphoid Differentiation Caused by a Recessive Niche-Filling Allele of the Ikaros Transcription Factor</title><author>Papathanasiou, Peter ; 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Here we describe a mouse strain,
Plastic, with a point mutation in a zinc finger of Ikaros that disrupts DNA binding but preserves efficient assembly of the full-length protein into higher order complexes.
Ikaros
Plastic
homozygosity is embryonically lethal with severe defects in terminal erythrocyte and granulocyte differentiation, excessive macrophage formation, and blocked lymphopoiesis, while heterozygotes display a partial block in lymphocyte differentiation. The contrast with more circumscribed effects of
Ikaros alleles that ablate the full-length protein highlights the importance in mammals of generating recessive niche-filling alleles that inactivate function without creating a void in multimolecular assemblies.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>12871645</pmid><doi>10.1016/S1074-7613(03)00168-7</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Cell Press Free Archives; Elsevier ScienceDirect Journals; EZB-FREE-00999 freely available EZB journals |
| subjects | Alleles Anemia - etiology Animals Cell Differentiation Deoxyribonucleic acid Dimerization DNA DNA - metabolism DNA-Binding Proteins Erythrocytes - physiology Ethylnitrosourea Gene expression Genomes Hematopoiesis - physiology Hepatocytes - physiology Ikaros Transcription Factor Lymphocytes - physiology Lymphoma - etiology Mice Mice, Inbred C57BL Mutation Myeloid Cells - physiology Point Mutation Proteins Stem cells Transcription factors Transcription Factors - chemistry Transcription Factors - genetics Transcription Factors - physiology |
| title | Widespread Failure of Hematolymphoid Differentiation Caused by a Recessive Niche-Filling Allele of the Ikaros Transcription Factor |
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