Monocytic leukemia zinc finger protein is essential for the development of long-term reconstituting hematopoietic stem cells
Monocytic leukemia zinc finger protein (MOZ), a transcriptional coactivator and member of the MYST family of histone acetyltransferases, is the target of recurrent translocations in acute myeloid leukemia. Since genes associated with translocations in leukemia are typically important regulators of b...
Gespeichert in:
| Veröffentlicht in: | Genes & development 2006-05, Vol.20 (9), p.1175-1186 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1186 |
|---|---|
| container_issue | 9 |
| container_start_page | 1175 |
| container_title | Genes & development |
| container_volume | 20 |
| creator | Thomas, Tim Corcoran, Lynn M Gugasyan, Raffi Dixon, Mathew P Brodnicki, Thomas Nutt, Stephen L Metcalf, Donald Voss, Anne K |
| description | Monocytic leukemia zinc finger protein (MOZ), a transcriptional coactivator and member of the MYST family of histone acetyltransferases, is the target of recurrent translocations in acute myeloid leukemia. Since genes associated with translocations in leukemia are typically important regulators of blood formation, we investigated if Moz has a role in normal hematopoiesis. We generated mice carrying a mutation in the Moz gene. Homozygous Moz mutant mice died at birth. Moz mutant fetal liver hematopoietic cells were incapable of contributing to the hematopoietic system of recipients after transplantation. We observed profound defects in the stem cell compartment of Moz-deficient mice. Progenitors of all lineages were reduced in number. However, blood cell lineage commitment was unaffected. Together, these results show that Moz is essential for a fundamental property of hematopoietic stem cells, the ability to reconstitute the hematopoietic system of a recipient after transplantation and that Moz is specifically required in the stem cell compartment. |
| doi_str_mv | 10.1101/gad.1382606 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1472476</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>19967164</sourcerecordid><originalsourceid>FETCH-LOGICAL-c476t-77f67f5a0b8beb3201371aa5eab92fb5c5c95017a1f1e5fac94c7cc66a1688493</originalsourceid><addsrcrecordid>eNqFkUFv1DAQhS0EotvCiTvyiQtK60liO74goQooUhEXOFuOd7xrSOxgO5WK-uPxqiugp55Gmvn05j09Ql4BOwdgcLEz23PohlYw8YRsgPeq4b2UT8mGDYo1qhPqhJzm_IMxVhnxnJyAEBwEHzbk7ksM0d4Wb-mE60-cvaG_fbDU-bDDRJcUC_pAfaaYM4bizURdTLTskW7xBqe4zHVNo6NTDLumYJppQhtDLr6spcrQPc6mxCV6PPzJBWdqcZryC_LMmSnjy-M8I98_fvh2edVcf_30-fL9dWN7KUojpRPSccPGYcSxaxl0EozhaEbVupFbbhVnIA04QO6MVb2V1gphQAxDr7oz8u5ed1nHGbe2-k1m0kvys0m3OhqvH16C3-tdvNHQy7ZaqAJvjgIp_loxFz37fIhgAsY1ayFV2wvRPQqCUkKC6Cv49h60Keac0P11A0wfatW1Vn2stdKv_w_wjz322P0BYBOilQ</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>19967164</pqid></control><display><type>article</type><title>Monocytic leukemia zinc finger protein is essential for the development of long-term reconstituting hematopoietic stem cells</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><creator>Thomas, Tim ; Corcoran, Lynn M ; Gugasyan, Raffi ; Dixon, Mathew P ; Brodnicki, Thomas ; Nutt, Stephen L ; Metcalf, Donald ; Voss, Anne K</creator><creatorcontrib>Thomas, Tim ; Corcoran, Lynn M ; Gugasyan, Raffi ; Dixon, Mathew P ; Brodnicki, Thomas ; Nutt, Stephen L ; Metcalf, Donald ; Voss, Anne K</creatorcontrib><description>Monocytic leukemia zinc finger protein (MOZ), a transcriptional coactivator and member of the MYST family of histone acetyltransferases, is the target of recurrent translocations in acute myeloid leukemia. Since genes associated with translocations in leukemia are typically important regulators of blood formation, we investigated if Moz has a role in normal hematopoiesis. We generated mice carrying a mutation in the Moz gene. Homozygous Moz mutant mice died at birth. Moz mutant fetal liver hematopoietic cells were incapable of contributing to the hematopoietic system of recipients after transplantation. We observed profound defects in the stem cell compartment of Moz-deficient mice. Progenitors of all lineages were reduced in number. However, blood cell lineage commitment was unaffected. Together, these results show that Moz is essential for a fundamental property of hematopoietic stem cells, the ability to reconstitute the hematopoietic system of a recipient after transplantation and that Moz is specifically required in the stem cell compartment.</description><identifier>ISSN: 0890-9369</identifier><identifier>EISSN: 1549-5477</identifier><identifier>DOI: 10.1101/gad.1382606</identifier><identifier>PMID: 16651658</identifier><language>eng</language><publisher>United States: Cold Spring Harbor Laboratory Press</publisher><subject>Animals ; Cell Differentiation ; Cell Lineage ; Embryo Loss ; Hematopoietic Stem Cells - cytology ; Hematopoietic Stem Cells - physiology ; Histone Acetyltransferases - genetics ; Histone Acetyltransferases - physiology ; Liver - cytology ; Liver - embryology ; Mice ; Mice, Mutant Strains ; Organ Specificity ; Research Paper ; T-Lymphocytes - cytology ; T-Lymphocytes - physiology ; Thymus Gland - cytology ; Thymus Gland - embryology ; Zinc Fingers</subject><ispartof>Genes & development, 2006-05, Vol.20 (9), p.1175-1186</ispartof><rights>Copyright © 2006, Cold Spring Harbor Laboratory Press 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-77f67f5a0b8beb3201371aa5eab92fb5c5c95017a1f1e5fac94c7cc66a1688493</citedby><cites>FETCH-LOGICAL-c476t-77f67f5a0b8beb3201371aa5eab92fb5c5c95017a1f1e5fac94c7cc66a1688493</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472476/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1472476/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16651658$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Thomas, Tim</creatorcontrib><creatorcontrib>Corcoran, Lynn M</creatorcontrib><creatorcontrib>Gugasyan, Raffi</creatorcontrib><creatorcontrib>Dixon, Mathew P</creatorcontrib><creatorcontrib>Brodnicki, Thomas</creatorcontrib><creatorcontrib>Nutt, Stephen L</creatorcontrib><creatorcontrib>Metcalf, Donald</creatorcontrib><creatorcontrib>Voss, Anne K</creatorcontrib><title>Monocytic leukemia zinc finger protein is essential for the development of long-term reconstituting hematopoietic stem cells</title><title>Genes & development</title><addtitle>Genes Dev</addtitle><description>Monocytic leukemia zinc finger protein (MOZ), a transcriptional coactivator and member of the MYST family of histone acetyltransferases, is the target of recurrent translocations in acute myeloid leukemia. Since genes associated with translocations in leukemia are typically important regulators of blood formation, we investigated if Moz has a role in normal hematopoiesis. We generated mice carrying a mutation in the Moz gene. Homozygous Moz mutant mice died at birth. Moz mutant fetal liver hematopoietic cells were incapable of contributing to the hematopoietic system of recipients after transplantation. We observed profound defects in the stem cell compartment of Moz-deficient mice. Progenitors of all lineages were reduced in number. However, blood cell lineage commitment was unaffected. Together, these results show that Moz is essential for a fundamental property of hematopoietic stem cells, the ability to reconstitute the hematopoietic system of a recipient after transplantation and that Moz is specifically required in the stem cell compartment.</description><subject>Animals</subject><subject>Cell Differentiation</subject><subject>Cell Lineage</subject><subject>Embryo Loss</subject><subject>Hematopoietic Stem Cells - cytology</subject><subject>Hematopoietic Stem Cells - physiology</subject><subject>Histone Acetyltransferases - genetics</subject><subject>Histone Acetyltransferases - physiology</subject><subject>Liver - cytology</subject><subject>Liver - embryology</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Organ Specificity</subject><subject>Research Paper</subject><subject>T-Lymphocytes - cytology</subject><subject>T-Lymphocytes - physiology</subject><subject>Thymus Gland - cytology</subject><subject>Thymus Gland - embryology</subject><subject>Zinc Fingers</subject><issn>0890-9369</issn><issn>1549-5477</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUFv1DAQhS0EotvCiTvyiQtK60liO74goQooUhEXOFuOd7xrSOxgO5WK-uPxqiugp55Gmvn05j09Ql4BOwdgcLEz23PohlYw8YRsgPeq4b2UT8mGDYo1qhPqhJzm_IMxVhnxnJyAEBwEHzbk7ksM0d4Wb-mE60-cvaG_fbDU-bDDRJcUC_pAfaaYM4bizURdTLTskW7xBqe4zHVNo6NTDLumYJppQhtDLr6spcrQPc6mxCV6PPzJBWdqcZryC_LMmSnjy-M8I98_fvh2edVcf_30-fL9dWN7KUojpRPSccPGYcSxaxl0EozhaEbVupFbbhVnIA04QO6MVb2V1gphQAxDr7oz8u5ed1nHGbe2-k1m0kvys0m3OhqvH16C3-tdvNHQy7ZaqAJvjgIp_loxFz37fIhgAsY1ayFV2wvRPQqCUkKC6Cv49h60Keac0P11A0wfatW1Vn2stdKv_w_wjz322P0BYBOilQ</recordid><startdate>20060501</startdate><enddate>20060501</enddate><creator>Thomas, Tim</creator><creator>Corcoran, Lynn M</creator><creator>Gugasyan, Raffi</creator><creator>Dixon, Mathew P</creator><creator>Brodnicki, Thomas</creator><creator>Nutt, Stephen L</creator><creator>Metcalf, Donald</creator><creator>Voss, Anne K</creator><general>Cold Spring Harbor Laboratory Press</general><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>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20060501</creationdate><title>Monocytic leukemia zinc finger protein is essential for the development of long-term reconstituting hematopoietic stem cells</title><author>Thomas, Tim ; Corcoran, Lynn M ; Gugasyan, Raffi ; Dixon, Mathew P ; Brodnicki, Thomas ; Nutt, Stephen L ; Metcalf, Donald ; Voss, Anne K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-77f67f5a0b8beb3201371aa5eab92fb5c5c95017a1f1e5fac94c7cc66a1688493</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Cell Differentiation</topic><topic>Cell Lineage</topic><topic>Embryo Loss</topic><topic>Hematopoietic Stem Cells - cytology</topic><topic>Hematopoietic Stem Cells - physiology</topic><topic>Histone Acetyltransferases - genetics</topic><topic>Histone Acetyltransferases - physiology</topic><topic>Liver - cytology</topic><topic>Liver - embryology</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Organ Specificity</topic><topic>Research Paper</topic><topic>T-Lymphocytes - cytology</topic><topic>T-Lymphocytes - physiology</topic><topic>Thymus Gland - cytology</topic><topic>Thymus Gland - embryology</topic><topic>Zinc Fingers</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Thomas, Tim</creatorcontrib><creatorcontrib>Corcoran, Lynn M</creatorcontrib><creatorcontrib>Gugasyan, Raffi</creatorcontrib><creatorcontrib>Dixon, Mathew P</creatorcontrib><creatorcontrib>Brodnicki, Thomas</creatorcontrib><creatorcontrib>Nutt, Stephen L</creatorcontrib><creatorcontrib>Metcalf, Donald</creatorcontrib><creatorcontrib>Voss, Anne K</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Genes & development</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Thomas, Tim</au><au>Corcoran, Lynn M</au><au>Gugasyan, Raffi</au><au>Dixon, Mathew P</au><au>Brodnicki, Thomas</au><au>Nutt, Stephen L</au><au>Metcalf, Donald</au><au>Voss, Anne K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Monocytic leukemia zinc finger protein is essential for the development of long-term reconstituting hematopoietic stem cells</atitle><jtitle>Genes & development</jtitle><addtitle>Genes Dev</addtitle><date>2006-05-01</date><risdate>2006</risdate><volume>20</volume><issue>9</issue><spage>1175</spage><epage>1186</epage><pages>1175-1186</pages><issn>0890-9369</issn><eissn>1549-5477</eissn><abstract>Monocytic leukemia zinc finger protein (MOZ), a transcriptional coactivator and member of the MYST family of histone acetyltransferases, is the target of recurrent translocations in acute myeloid leukemia. Since genes associated with translocations in leukemia are typically important regulators of blood formation, we investigated if Moz has a role in normal hematopoiesis. We generated mice carrying a mutation in the Moz gene. Homozygous Moz mutant mice died at birth. Moz mutant fetal liver hematopoietic cells were incapable of contributing to the hematopoietic system of recipients after transplantation. We observed profound defects in the stem cell compartment of Moz-deficient mice. Progenitors of all lineages were reduced in number. However, blood cell lineage commitment was unaffected. Together, these results show that Moz is essential for a fundamental property of hematopoietic stem cells, the ability to reconstitute the hematopoietic system of a recipient after transplantation and that Moz is specifically required in the stem cell compartment.</abstract><cop>United States</cop><pub>Cold Spring Harbor Laboratory Press</pub><pmid>16651658</pmid><doi>10.1101/gad.1382606</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0890-9369 |
| ispartof | Genes & development, 2006-05, Vol.20 (9), p.1175-1186 |
| issn | 0890-9369 1549-5477 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_1472476 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central |
| subjects | Animals Cell Differentiation Cell Lineage Embryo Loss Hematopoietic Stem Cells - cytology Hematopoietic Stem Cells - physiology Histone Acetyltransferases - genetics Histone Acetyltransferases - physiology Liver - cytology Liver - embryology Mice Mice, Mutant Strains Organ Specificity Research Paper T-Lymphocytes - cytology T-Lymphocytes - physiology Thymus Gland - cytology Thymus Gland - embryology Zinc Fingers |
| title | Monocytic leukemia zinc finger protein is essential for the development of long-term reconstituting hematopoietic stem cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-05T08%3A11%3A33IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Monocytic%20leukemia%20zinc%20finger%20protein%20is%20essential%20for%20the%20development%20of%20long-term%20reconstituting%20hematopoietic%20stem%20cells&rft.jtitle=Genes%20&%20development&rft.au=Thomas,%20Tim&rft.date=2006-05-01&rft.volume=20&rft.issue=9&rft.spage=1175&rft.epage=1186&rft.pages=1175-1186&rft.issn=0890-9369&rft.eissn=1549-5477&rft_id=info:doi/10.1101/gad.1382606&rft_dat=%3Cproquest_pubme%3E19967164%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=19967164&rft_id=info:pmid/16651658&rfr_iscdi=true |