Direct interaction of Ikaros and Foxp1 modulates expression of the G protein-coupled receptor G2A in B-lymphocytes and acute lymphoblastic leukemia.
Identifieur interne : 001718 ( PubMed/Curation ); précédent : 001717; suivant : 001719Direct interaction of Ikaros and Foxp1 modulates expression of the G protein-coupled receptor G2A in B-lymphocytes and acute lymphoblastic leukemia.
Auteurs : Jonathan Bond [Royaume-Uni] ; Renae Domaschenz [Royaume-Uni] ; M Nica Roman-Trufero [Royaume-Uni] ; Pierangela Sabbattini [Royaume-Uni] ; Isabel Ferreiros-Vidal [Royaume-Uni] ; Gareth Gerrard [Royaume-Uni] ; Vahid Asnafi [France] ; Elizabeth Macintyre [France] ; Matthias Merkenschlager [Royaume-Uni] ; Niall Dillon [Royaume-Uni]Source :
- Oncotarget [ 1949-2553 ] ; 2016.
Abstract
Ikaros and Foxp1 are transcription factors that play key roles in normal lymphopoiesis and lymphoid malignancies. We describe a novel physical and functional interaction between the proteins, which requires the central zinc finger domain of Ikaros. The Ikaros-Foxp1 interaction is abolished by deletion of this region, which corresponds to the IK6 isoform that is commonly associated with high-risk acute lymphoblastic leukemia (ALL). We also identify the Gpr132 gene, which encodes the orphan G protein-coupled receptor G2A, as a novel target for Foxp1. Increased expression of Foxp1 enhanced Gpr132 transcription and caused cell cycle changes, including G2 arrest. Co-expression of wild-type Ikaros, but not IK6, displaced Foxp1 binding from the Gpr132 gene, reversed the increase in Gpr132 expression and inhibited G2 arrest. Analysis of primary ALL samples revealed a significant increase in GPR132 expression in IKZF1-deleted BCR-ABL negative patients, suggesting that levels of wild-type Ikaros may influence the regulation of G2A in B-ALL. Our results reveal a novel effect of Ikaros haploinsufficiency on Foxp1 functioning, and identify G2A as a potential modulator of the cell cycle in Ikaros-deleted B-ALL.
DOI: 10.18632/oncotarget.11688
PubMed: 27588474
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Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN</wicri:regionArea></affiliation></author><author><name sortKey="Domaschenz, Renae" sort="Domaschenz, Renae" uniqKey="Domaschenz R" first="Renae" last="Domaschenz">Renae Domaschenz</name><affiliation wicri:level="1"><nlm:affiliation>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN</wicri:regionArea></affiliation></author><author><name sortKey="Roman Trufero, M Nica" sort="Roman Trufero, M Nica" uniqKey="Roman Trufero M" first="M Nica" last="Roman-Trufero">M Nica Roman-Trufero</name><affiliation wicri:level="1"><nlm:affiliation>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN</wicri:regionArea></affiliation></author><author><name sortKey="Sabbattini, Pierangela" sort="Sabbattini, Pierangela" uniqKey="Sabbattini P" first="Pierangela" last="Sabbattini">Pierangela Sabbattini</name><affiliation wicri:level="1"><nlm:affiliation>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN</wicri:regionArea></affiliation></author><author><name sortKey="Ferreiros Vidal, Isabel" sort="Ferreiros Vidal, Isabel" uniqKey="Ferreiros Vidal I" first="Isabel" last="Ferreiros-Vidal">Isabel Ferreiros-Vidal</name><affiliation wicri:level="1"><nlm:affiliation>Lymphocyte Development Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Lymphocyte Development Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN</wicri:regionArea></affiliation></author><author><name sortKey="Gerrard, Gareth" sort="Gerrard, Gareth" uniqKey="Gerrard G" first="Gareth" last="Gerrard">Gareth Gerrard</name><affiliation wicri:level="1"><nlm:affiliation>Imperial Molecular Pathology, Imperial College Academic Health Sciences Centre, Hammersmith Campus, London W12 0NN, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Imperial Molecular Pathology, Imperial College Academic Health Sciences Centre, Hammersmith Campus, London W12 0NN</wicri:regionArea></affiliation></author><author><name sortKey="Asnafi, Vahid" sort="Asnafi, Vahid" uniqKey="Asnafi V" first="Vahid" last="Asnafi">Vahid Asnafi</name><affiliation wicri:level="1"><nlm:affiliation>Université Paris Descartes Sorbonne Cité, Institut Necker-Enfants Malades (INEM), Institut National de Recherche Médicale (INSERM), and Laboratory of Onco-Hematology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Necker Enfants-Malades, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Université Paris Descartes Sorbonne Cité, Institut Necker-Enfants Malades (INEM), Institut National de Recherche Médicale (INSERM), and Laboratory of Onco-Hematology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Necker Enfants-Malades, Paris</wicri:regionArea></affiliation></author><author><name sortKey="Macintyre, Elizabeth" sort="Macintyre, Elizabeth" uniqKey="Macintyre E" first="Elizabeth" last="Macintyre">Elizabeth Macintyre</name><affiliation wicri:level="1"><nlm:affiliation>Université Paris Descartes Sorbonne Cité, Institut Necker-Enfants Malades (INEM), Institut National de Recherche Médicale (INSERM), and Laboratory of Onco-Hematology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Necker Enfants-Malades, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Université Paris Descartes Sorbonne Cité, Institut Necker-Enfants Malades (INEM), Institut National de Recherche Médicale (INSERM), and Laboratory of Onco-Hematology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Necker Enfants-Malades, Paris</wicri:regionArea></affiliation></author><author><name sortKey="Merkenschlager, Matthias" sort="Merkenschlager, Matthias" uniqKey="Merkenschlager M" first="Matthias" last="Merkenschlager">Matthias Merkenschlager</name><affiliation wicri:level="1"><nlm:affiliation>Lymphocyte Development Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Lymphocyte Development Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN</wicri:regionArea></affiliation></author><author><name sortKey="Dillon, Niall" sort="Dillon, Niall" uniqKey="Dillon N" first="Niall" last="Dillon">Niall Dillon</name><affiliation wicri:level="1"><nlm:affiliation>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN</wicri:regionArea></affiliation></author></analytic><series><title level="j">Oncotarget</title><idno type="eISSN">1949-2553</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Ikaros and Foxp1 are transcription factors that play key roles in normal lymphopoiesis and lymphoid malignancies. We describe a novel physical and functional interaction between the proteins, which requires the central zinc finger domain of Ikaros. The Ikaros-Foxp1 interaction is abolished by deletion of this region, which corresponds to the IK6 isoform that is commonly associated with high-risk acute lymphoblastic leukemia (ALL). We also identify the Gpr132 gene, which encodes the orphan G protein-coupled receptor G2A, as a novel target for Foxp1. Increased expression of Foxp1 enhanced Gpr132 transcription and caused cell cycle changes, including G2 arrest. Co-expression of wild-type Ikaros, but not IK6, displaced Foxp1 binding from the Gpr132 gene, reversed the increase in Gpr132 expression and inhibited G2 arrest. Analysis of primary ALL samples revealed a significant increase in GPR132 expression in IKZF1-deleted BCR-ABL negative patients, suggesting that levels of wild-type Ikaros may influence the regulation of G2A in B-ALL. Our results reveal a novel effect of Ikaros haploinsufficiency on Foxp1 functioning, and identify G2A as a potential modulator of the cell cycle in Ikaros-deleted B-ALL.</div></front></TEI><pubmed><MedlineCitation Status="In-Process" Owner="NLM"><PMID Version="1">27588474</PMID><DateCreated><Year>2016</Year><Month>09</Month><Day>02</Day></DateCreated><DateRevised><Year>2017</Year><Month>09</Month><Day>22</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1949-2553</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>40</Issue><PubDate><Year>2016</Year><Month>10</Month><Day>04</Day></PubDate></JournalIssue><Title>Oncotarget</Title><ISOAbbreviation>Oncotarget</ISOAbbreviation></Journal><ArticleTitle>Direct interaction of Ikaros and Foxp1 modulates expression of the G protein-coupled receptor G2A in B-lymphocytes and acute lymphoblastic leukemia.</ArticleTitle><Pagination><MedlinePgn>65923-65936</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.18632/oncotarget.11688</ELocationID><Abstract><AbstractText>Ikaros and Foxp1 are transcription factors that play key roles in normal lymphopoiesis and lymphoid malignancies. We describe a novel physical and functional interaction between the proteins, which requires the central zinc finger domain of Ikaros. The Ikaros-Foxp1 interaction is abolished by deletion of this region, which corresponds to the IK6 isoform that is commonly associated with high-risk acute lymphoblastic leukemia (ALL). We also identify the Gpr132 gene, which encodes the orphan G protein-coupled receptor G2A, as a novel target for Foxp1. Increased expression of Foxp1 enhanced Gpr132 transcription and caused cell cycle changes, including G2 arrest. Co-expression of wild-type Ikaros, but not IK6, displaced Foxp1 binding from the Gpr132 gene, reversed the increase in Gpr132 expression and inhibited G2 arrest. Analysis of primary ALL samples revealed a significant increase in GPR132 expression in IKZF1-deleted BCR-ABL negative patients, suggesting that levels of wild-type Ikaros may influence the regulation of G2A in B-ALL. Our results reveal a novel effect of Ikaros haploinsufficiency on Foxp1 functioning, and identify G2A as a potential modulator of the cell cycle in Ikaros-deleted B-ALL.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Bond</LastName><ForeName>Jonathan</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Université Paris Descartes Sorbonne Cité, Institut Necker-Enfants Malades (INEM), Institut National de Recherche Médicale (INSERM), and Laboratory of Onco-Hematology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Necker Enfants-Malades, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Domaschenz</LastName><ForeName>Renae</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Present address: Chromatin and Transcriptional Regulation Group, John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Roman-Trufero</LastName><ForeName>Mónica</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sabbattini</LastName><ForeName>Pierangela</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ferreiros-Vidal</LastName><ForeName>Isabel</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Lymphocyte Development Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gerrard</LastName><ForeName>Gareth</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>Imperial Molecular Pathology, Imperial College Academic Health Sciences Centre, Hammersmith Campus, London W12 0NN, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Asnafi</LastName><ForeName>Vahid</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Université Paris Descartes Sorbonne Cité, Institut Necker-Enfants Malades (INEM), Institut National de Recherche Médicale (INSERM), and Laboratory of Onco-Hematology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Necker Enfants-Malades, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Macintyre</LastName><ForeName>Elizabeth</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Université Paris Descartes Sorbonne Cité, Institut Necker-Enfants Malades (INEM), Institut National de Recherche Médicale (INSERM), and Laboratory of Onco-Hematology, Assistance Publique-Hôpitaux de Paris (AP-HP), Hôpital Necker Enfants-Malades, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Merkenschlager</LastName><ForeName>Matthias</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Lymphocyte Development Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Dillon</LastName><ForeName>Niall</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Gene Regulation and Chromatin Group, MRC Clinical Sciences Centre, Imperial College Faculty of Medicine, Hammersmith Campus, London W12 0NN, United Kingdom.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>MC_U120027516</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant><Grant><GrantID>MC_U120036884</GrantID><Agency>Medical Research Council</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Oncotarget</MedlineTA><NlmUniqueID>101532965</NlmUniqueID><ISSNLinking>1949-2553</ISSNLinking></MedlineJournalInfo><CommentsCorrectionsList><CommentsCorrections 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