Atypical protein kinase C (aPKCζ and aPKCλ) is dispensable for mammalian hematopoietic stem cell activity and blood formation
The stem-cell pool is considered to be maintained by a balance between symmetric and asymmetric division of stem cells. The cell polarity model proposes that the facultative use of symmetric and asymmetric cell division is orchestrated by a polarity complex consisting of partitioning-defective prote...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2011-06, Vol.108 (24), p.9957-9962 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
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| creator | Sengupta, Amitava Duran, Angeles Ishikawa, Eri Florian, Maria Carolina Dunn, Susan K Ficker, Ashley M Leitges, Michael Geiger, Hartmut Diaz-Meco, Maria Moscat, Jorge Cancelas, Jose A |
| description | The stem-cell pool is considered to be maintained by a balance between symmetric and asymmetric division of stem cells. The cell polarity model proposes that the facultative use of symmetric and asymmetric cell division is orchestrated by a polarity complex consisting of partitioning-defective proteins Par3 and Par6, and atypical protein kinase C (aPKCζ and aPKCλ), which regulates planar symmetry of dividing stem cells with respect to the signaling microenvironment. However, the role of the polarity complex is unexplored in mammalian adult stem-cell functions. Here we report that, in contrast to accepted paradigms, polarization and activity of adult hematopoietic stem cell (HSC) do not depend on either aPKCζ or aPKCλ or both in vivo. Mice, having constitutive and hematopoietic-specific (Vav1-Cre) deletion of aPKCζ and aPKCλ, respectively, have normal hematopoiesis, including normal HSC self-renewal, engraftment, differentiation, and interaction with the bone marrow microenvironment. Furthermore, inducible complete deletion of aPKCλ (Mx1-Cre) in aPKCζâ»/â» HSC does not affect HSC polarization, self-renewal, engraftment, or lineage repopulation. In addition, aPKCζ- and aPKCλ-deficient HSCs elicited a normal pattern of hematopoietic recovery secondary to myeloablative stress. Taken together, the expression of aPKCζ, aPKCλ, or both are dispensable for primitive and adult HSC fate determination in steady-state and stress hematopoiesis, contrary to the hypothesis of a unique, evolutionary conserved aPKCζ/λ-directed cell polarity signaling mechanism in mammalian HSC fate determination. |
| doi_str_mv | 10.1073/pnas.1103132108 |
| format | Article |
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The cell polarity model proposes that the facultative use of symmetric and asymmetric cell division is orchestrated by a polarity complex consisting of partitioning-defective proteins Par3 and Par6, and atypical protein kinase C (aPKCζ and aPKCλ), which regulates planar symmetry of dividing stem cells with respect to the signaling microenvironment. However, the role of the polarity complex is unexplored in mammalian adult stem-cell functions. Here we report that, in contrast to accepted paradigms, polarization and activity of adult hematopoietic stem cell (HSC) do not depend on either aPKCζ or aPKCλ or both in vivo. Mice, having constitutive and hematopoietic-specific (Vav1-Cre) deletion of aPKCζ and aPKCλ, respectively, have normal hematopoiesis, including normal HSC self-renewal, engraftment, differentiation, and interaction with the bone marrow microenvironment. Furthermore, inducible complete deletion of aPKCλ (Mx1-Cre) in aPKCζâ»/â» HSC does not affect HSC polarization, self-renewal, engraftment, or lineage repopulation. In addition, aPKCζ- and aPKCλ-deficient HSCs elicited a normal pattern of hematopoietic recovery secondary to myeloablative stress. Taken together, the expression of aPKCζ, aPKCλ, or both are dispensable for primitive and adult HSC fate determination in steady-state and stress hematopoiesis, contrary to the hypothesis of a unique, evolutionary conserved aPKCζ/λ-directed cell polarity signaling mechanism in mammalian HSC fate determination.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.1103132108</identifier><identifier>PMID: 21653884</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>adults ; Animals ; Biological Sciences ; Blood ; bone marrow ; Cell Differentiation ; cell division ; Cell Lineage ; Cell Polarity ; Cell Proliferation ; Chimeras ; Daughter cells ; Female ; Flow Cytometry ; Gene Expression ; Gene expression regulation ; Hematopoiesis ; Hematopoietic Stem Cell Transplantation - methods ; Hematopoietic stem cells ; Hematopoietic Stem Cells - cytology ; Hematopoietic Stem Cells - metabolism ; Hematopoietic system ; Isoenzymes - deficiency ; Isoenzymes - genetics ; Kinases ; Male ; Mammals ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Mice, Transgenic ; Progenitor cells ; protein kinase C ; Protein Kinase C - deficiency ; Protein Kinase C - genetics ; Proteins ; Reverse Transcriptase Polymerase Chain Reaction ; Rodents ; Signal Transduction ; Stem cells</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2011-06, Vol.108 (24), p.9957-9962</ispartof><rights>Copyright 2011 The National Academy of Sciences of the United States of America</rights><rights>Copyright National Academy of Sciences Jun 14, 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c489t-1f2dc1c7b6f560757524a6ec092e1c6557d8e74fe8cf711532098f759fc9fae63</citedby><cites>FETCH-LOGICAL-c489t-1f2dc1c7b6f560757524a6ec092e1c6557d8e74fe8cf711532098f759fc9fae63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/108/24.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/25831342$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/25831342$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27924,27925,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21653884$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sengupta, Amitava</creatorcontrib><creatorcontrib>Duran, Angeles</creatorcontrib><creatorcontrib>Ishikawa, Eri</creatorcontrib><creatorcontrib>Florian, Maria Carolina</creatorcontrib><creatorcontrib>Dunn, Susan K</creatorcontrib><creatorcontrib>Ficker, Ashley M</creatorcontrib><creatorcontrib>Leitges, Michael</creatorcontrib><creatorcontrib>Geiger, Hartmut</creatorcontrib><creatorcontrib>Diaz-Meco, Maria</creatorcontrib><creatorcontrib>Moscat, Jorge</creatorcontrib><creatorcontrib>Cancelas, Jose A</creatorcontrib><title>Atypical protein kinase C (aPKCζ and aPKCλ) is dispensable for mammalian hematopoietic stem cell activity and blood formation</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>The stem-cell pool is considered to be maintained by a balance between symmetric and asymmetric division of stem cells. The cell polarity model proposes that the facultative use of symmetric and asymmetric cell division is orchestrated by a polarity complex consisting of partitioning-defective proteins Par3 and Par6, and atypical protein kinase C (aPKCζ and aPKCλ), which regulates planar symmetry of dividing stem cells with respect to the signaling microenvironment. However, the role of the polarity complex is unexplored in mammalian adult stem-cell functions. Here we report that, in contrast to accepted paradigms, polarization and activity of adult hematopoietic stem cell (HSC) do not depend on either aPKCζ or aPKCλ or both in vivo. Mice, having constitutive and hematopoietic-specific (Vav1-Cre) deletion of aPKCζ and aPKCλ, respectively, have normal hematopoiesis, including normal HSC self-renewal, engraftment, differentiation, and interaction with the bone marrow microenvironment. Furthermore, inducible complete deletion of aPKCλ (Mx1-Cre) in aPKCζâ»/â» HSC does not affect HSC polarization, self-renewal, engraftment, or lineage repopulation. In addition, aPKCζ- and aPKCλ-deficient HSCs elicited a normal pattern of hematopoietic recovery secondary to myeloablative stress. Taken together, the expression of aPKCζ, aPKCλ, or both are dispensable for primitive and adult HSC fate determination in steady-state and stress hematopoiesis, contrary to the hypothesis of a unique, evolutionary conserved aPKCζ/λ-directed cell polarity signaling mechanism in mammalian HSC fate determination.</description><subject>adults</subject><subject>Animals</subject><subject>Biological Sciences</subject><subject>Blood</subject><subject>bone marrow</subject><subject>Cell Differentiation</subject><subject>cell division</subject><subject>Cell Lineage</subject><subject>Cell Polarity</subject><subject>Cell Proliferation</subject><subject>Chimeras</subject><subject>Daughter cells</subject><subject>Female</subject><subject>Flow Cytometry</subject><subject>Gene Expression</subject><subject>Gene expression regulation</subject><subject>Hematopoiesis</subject><subject>Hematopoietic Stem Cell Transplantation - methods</subject><subject>Hematopoietic stem cells</subject><subject>Hematopoietic Stem Cells - cytology</subject><subject>Hematopoietic Stem Cells - metabolism</subject><subject>Hematopoietic system</subject><subject>Isoenzymes - deficiency</subject><subject>Isoenzymes - genetics</subject><subject>Kinases</subject><subject>Male</subject><subject>Mammals</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic</subject><subject>Progenitor cells</subject><subject>protein kinase C</subject><subject>Protein Kinase C - deficiency</subject><subject>Protein Kinase C - genetics</subject><subject>Proteins</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Stem cells</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkT1vFDEQhi0EIkegpgIsGqC4xOO113aDFJ34EpFAgtSWz2snPnbXi-2LdHX6_BwaOvhj7HJHDqiskZ95ZkYvQg-BHAER1fHQm3wEQCqoKBB5C82AKJjXTJHbaEYIFXPJKDtA93JeEUIUl-QuOqBQ80pKNkNXJ2UzBGtaPKRYXOjxlzA6HV7g5-bj-8XP6x_fsOkbvCu-v8Ah4ybkwfXZLFuHfUy4M11n2mB6fOE6U-IQgyvB4lxch61rW2xsCZehbH67lm2MzdQ4siH299Edb9rsHuzeQ3T2-tXnxdv56Yc37xYnp3PLpCpz8LSxYMWy9rwmggtOmamdJYo6sDXnopFOMO-k9QKAV5Qo6QVX3ipvXF0dopdb77Bedq6xri_JtHpIoTNpo6MJ-t-fPlzo83ipK4CaET4Knu0EKX5du1x0F_J0nuldXGctBYWKE5Aj-fQ_chXXqR-vmyDGq0qIETreQjbFnJPzN6sA0VO8eopX7-MdOx7_fcEN_yfPEXiyA6bOvU5qyrRSfBr6aEuscolpb-ByHMLo3uBN1OY8hazPPlECNSGgQI1r_wImWsH1</recordid><startdate>20110614</startdate><enddate>20110614</enddate><creator>Sengupta, Amitava</creator><creator>Duran, Angeles</creator><creator>Ishikawa, Eri</creator><creator>Florian, Maria Carolina</creator><creator>Dunn, Susan K</creator><creator>Ficker, Ashley M</creator><creator>Leitges, Michael</creator><creator>Geiger, Hartmut</creator><creator>Diaz-Meco, Maria</creator><creator>Moscat, Jorge</creator><creator>Cancelas, Jose A</creator><general>National Academy of Sciences</general><general>National Acad Sciences</general><scope>FBQ</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>7QG</scope><scope>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20110614</creationdate><title>Atypical protein kinase C (aPKCζ and aPKCλ) is dispensable for mammalian hematopoietic stem cell activity and blood formation</title><author>Sengupta, Amitava ; 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The cell polarity model proposes that the facultative use of symmetric and asymmetric cell division is orchestrated by a polarity complex consisting of partitioning-defective proteins Par3 and Par6, and atypical protein kinase C (aPKCζ and aPKCλ), which regulates planar symmetry of dividing stem cells with respect to the signaling microenvironment. However, the role of the polarity complex is unexplored in mammalian adult stem-cell functions. Here we report that, in contrast to accepted paradigms, polarization and activity of adult hematopoietic stem cell (HSC) do not depend on either aPKCζ or aPKCλ or both in vivo. Mice, having constitutive and hematopoietic-specific (Vav1-Cre) deletion of aPKCζ and aPKCλ, respectively, have normal hematopoiesis, including normal HSC self-renewal, engraftment, differentiation, and interaction with the bone marrow microenvironment. Furthermore, inducible complete deletion of aPKCλ (Mx1-Cre) in aPKCζâ»/â» HSC does not affect HSC polarization, self-renewal, engraftment, or lineage repopulation. In addition, aPKCζ- and aPKCλ-deficient HSCs elicited a normal pattern of hematopoietic recovery secondary to myeloablative stress. Taken together, the expression of aPKCζ, aPKCλ, or both are dispensable for primitive and adult HSC fate determination in steady-state and stress hematopoiesis, contrary to the hypothesis of a unique, evolutionary conserved aPKCζ/λ-directed cell polarity signaling mechanism in mammalian HSC fate determination.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>21653884</pmid><doi>10.1073/pnas.1103132108</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | adults Animals Biological Sciences Blood bone marrow Cell Differentiation cell division Cell Lineage Cell Polarity Cell Proliferation Chimeras Daughter cells Female Flow Cytometry Gene Expression Gene expression regulation Hematopoiesis Hematopoietic Stem Cell Transplantation - methods Hematopoietic stem cells Hematopoietic Stem Cells - cytology Hematopoietic Stem Cells - metabolism Hematopoietic system Isoenzymes - deficiency Isoenzymes - genetics Kinases Male Mammals Mice Mice, Inbred Strains Mice, Knockout Mice, Transgenic Progenitor cells protein kinase C Protein Kinase C - deficiency Protein Kinase C - genetics Proteins Reverse Transcriptase Polymerase Chain Reaction Rodents Signal Transduction Stem cells |
| title | Atypical protein kinase C (aPKCζ and aPKCλ) is dispensable for mammalian hematopoietic stem cell activity and blood formation |
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