Differential effects on gene transcription and hematopoietic differentiation correlate with GATA2 mutant disease phenotypes.
Identifieur interne : 000630 ( Main/Exploration ); précédent : 000629; suivant : 000631Differential effects on gene transcription and hematopoietic differentiation correlate with GATA2 mutant disease phenotypes.
Auteurs : C-E Chong [Australie] ; P. Venugopal [Australie] ; P H Stokes [Australie] ; Y K Lee [Australie] ; P J Brautigan [Australie] ; D T O. Yeung [Australie] ; M. Babic [Australie] ; G A Engler [Australie] ; S W Lane [Australie] ; M. Klingler-Hoffmann [Australie] ; J M Matthews [Australie] ; R J D'Andrea [Australie] ; A L Brown [Australie] ; C N Hahn [Australie] ; H S Scott [Australie]Source :
- Leukemia [ 1476-5551 ] ; 2017.
Abstract
Heterozygous GATA2 mutations underlie an array of complex hematopoietic and lymphatic diseases. Analysis of the literature reporting three recurrent GATA2 germline (g) mutations (gT354M, gR396Q and gR398W) revealed different phenotype tendencies. Although all three mutants differentially predispose to myeloid malignancies, there was no difference in leukemia-free survival for GATA2 patients. Despite intense interest, the molecular pathogenesis of GATA2 mutation is poorly understood. We functionally characterized a GATA2 mutant allelic series representing major disease phenotypes caused by germline and somatic (s) mutations in zinc finger 2 (ZF2). All GATA2 mutants, except for sL359V, displayed reduced DNA-binding affinity and transactivation compared with wild type (WT), which could be attributed to mutations of arginines critical for DNA binding or amino acids required for ZF2 domain structural integrity. Two GATA2 mutants (gT354M and gC373R) bound the key hematopoietic differentiation factor PU.1 more strongly than WT potentially perturbing differentiation via sequestration of PU.1. Unlike WT, all mutants failed to suppress colony formation and some mutants skewed cell fate to granulocytes, consistent with the monocytopenia phenotype seen in GATA2-related immunodeficiency disorders. These findings implicate perturbations of GATA2 function shaping the course of development of myeloid malignancy subtypes and strengthen complete or nearly complete haploinsufficiency for predisposition to lymphedema.Leukemia advance online publication, 11 July 2017; doi:10.1038/leu.2017.196.
DOI: 10.1038/leu.2017.196
PubMed: 28642594
Affiliations:
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Yeung</name><affiliation wicri:level="1"><nlm:affiliation>Department of Genetics and Molecular Pathology, SA Pathology and University of South Australia Alliance, Adelaide, South Australia, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Genetics and Molecular Pathology, SA Pathology and University of South Australia Alliance, Adelaide, South Australia</wicri:regionArea><wicri:noRegion>South Australia</wicri:noRegion></affiliation></author><author><name sortKey="Babic, M" sort="Babic, M" uniqKey="Babic M" first="M" last="Babic">M. Babic</name><affiliation wicri:level="1"><nlm:affiliation>Department of Genetics and Molecular Pathology, SA Pathology and University of South Australia Alliance, Adelaide, South Australia, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Genetics and Molecular Pathology, SA Pathology and University of South Australia Alliance, Adelaide, South Australia</wicri:regionArea><wicri:noRegion>South Australia</wicri:noRegion></affiliation></author><author><name sortKey="Engler, G A" sort="Engler, G A" uniqKey="Engler G" first="G A" last="Engler">G A Engler</name><affiliation wicri:level="1"><nlm:affiliation>Division of Hematology, SA Pathology, Adelaide, South Australia, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Division of Hematology, SA Pathology, Adelaide, South Australia</wicri:regionArea><wicri:noRegion>South Australia</wicri:noRegion></affiliation></author><author><name sortKey="Lane, S W" sort="Lane, S W" uniqKey="Lane S" first="S W" last="Lane">S W Lane</name><affiliation wicri:level="1"><nlm:affiliation>QIMR Berghofer Medical Research Institute and University of Queensland, Brisbane, Queensland, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>QIMR Berghofer Medical Research Institute and University of Queensland, Brisbane, Queensland</wicri:regionArea><wicri:noRegion>Queensland</wicri:noRegion></affiliation></author><author><name sortKey="Klingler Hoffmann, M" sort="Klingler Hoffmann, M" uniqKey="Klingler Hoffmann M" first="M" last="Klingler-Hoffmann">M. Klingler-Hoffmann</name><affiliation wicri:level="1"><nlm:affiliation>School of Biological Sciences, University of Adelaide, Adelaide, South Australia, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Biological Sciences, University of Adelaide, Adelaide, South Australia</wicri:regionArea><wicri:noRegion>South Australia</wicri:noRegion></affiliation></author><author><name sortKey="Matthews, J M" sort="Matthews, J M" uniqKey="Matthews J" first="J M" last="Matthews">J M Matthews</name><affiliation wicri:level="1"><nlm:affiliation>School of Molecular Bioscience, University of Sydney, Sydney, New South Wales, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>School of Molecular Bioscience, University of Sydney, Sydney, New South Wales</wicri:regionArea><wicri:noRegion>New South Wales</wicri:noRegion></affiliation></author><author><name sortKey="D Andrea, R J" sort="D Andrea, R J" uniqKey="D Andrea R" first="R J" last="D'Andrea">R J D'Andrea</name><affiliation wicri:level="1"><nlm:affiliation>Centre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Centre for Cancer Biology, University of South Australia and SA Pathology, Adelaide, South Australia</wicri:regionArea><wicri:noRegion>South Australia</wicri:noRegion></affiliation></author><author><name sortKey="Brown, A L" sort="Brown, A L" uniqKey="Brown A" first="A L" last="Brown">A L Brown</name><affiliation wicri:level="1"><nlm:affiliation>Department of Genetics and Molecular Pathology, SA Pathology and University of South Australia Alliance, Adelaide, South Australia, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Genetics and Molecular Pathology, SA Pathology and University of South Australia Alliance, Adelaide, South Australia</wicri:regionArea><wicri:noRegion>South Australia</wicri:noRegion></affiliation></author><author><name sortKey="Hahn, C N" sort="Hahn, C N" uniqKey="Hahn C" first="C N" last="Hahn">C N Hahn</name><affiliation wicri:level="1"><nlm:affiliation>Department of Genetics and Molecular Pathology, SA Pathology and University of South Australia Alliance, Adelaide, South Australia, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Genetics and Molecular Pathology, SA Pathology and University of South Australia Alliance, Adelaide, South Australia</wicri:regionArea><wicri:noRegion>South Australia</wicri:noRegion></affiliation></author><author><name sortKey="Scott, H S" sort="Scott, H S" uniqKey="Scott H" first="H S" last="Scott">H S Scott</name><affiliation wicri:level="1"><nlm:affiliation>Department of Genetics and Molecular Pathology, SA Pathology and University of South Australia Alliance, Adelaide, South Australia, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Department of Genetics and Molecular Pathology, SA Pathology and University of South Australia Alliance, Adelaide, South Australia</wicri:regionArea><wicri:noRegion>South Australia</wicri:noRegion></affiliation></author></analytic><series><title level="j">Leukemia</title><idno type="eISSN">1476-5551</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Heterozygous GATA2 mutations underlie an array of complex hematopoietic and lymphatic diseases. Analysis of the literature reporting three recurrent GATA2 germline (g) mutations (gT354M, gR396Q and gR398W) revealed different phenotype tendencies. Although all three mutants differentially predispose to myeloid malignancies, there was no difference in leukemia-free survival for GATA2 patients. Despite intense interest, the molecular pathogenesis of GATA2 mutation is poorly understood. We functionally characterized a GATA2 mutant allelic series representing major disease phenotypes caused by germline and somatic (s) mutations in zinc finger 2 (ZF2). All GATA2 mutants, except for sL359V, displayed reduced DNA-binding affinity and transactivation compared with wild type (WT), which could be attributed to mutations of arginines critical for DNA binding or amino acids required for ZF2 domain structural integrity. Two GATA2 mutants (gT354M and gC373R) bound the key hematopoietic differentiation factor PU.1 more strongly than WT potentially perturbing differentiation via sequestration of PU.1. Unlike WT, all mutants failed to suppress colony formation and some mutants skewed cell fate to granulocytes, consistent with the monocytopenia phenotype seen in GATA2-related immunodeficiency disorders. These findings implicate perturbations of GATA2 function shaping the course of development of myeloid malignancy subtypes and strengthen complete or nearly complete haploinsufficiency for predisposition to lymphedema.Leukemia advance online publication, 11 July 2017; doi:10.1038/leu.2017.196.</div></front></TEI><affiliations><list><country><li>Australie</li></country></list><tree><country name="Australie"><noRegion><name sortKey="Chong, C E" sort="Chong, C E" uniqKey="Chong C" first="C-E" last="Chong">C-E Chong</name></noRegion><name sortKey="Babic, M" sort="Babic, M" uniqKey="Babic M" first="M" last="Babic">M. Babic</name><name sortKey="Brautigan, P J" sort="Brautigan, P J" uniqKey="Brautigan P" first="P J" last="Brautigan">P J Brautigan</name><name sortKey="Brown, A L" sort="Brown, A L" uniqKey="Brown A" first="A L" last="Brown">A L Brown</name><name sortKey="D Andrea, R J" sort="D Andrea, R J" uniqKey="D Andrea R" first="R J" last="D'Andrea">R J D'Andrea</name><name sortKey="Engler, G A" sort="Engler, G A" uniqKey="Engler G" first="G A" last="Engler">G A Engler</name><name sortKey="Hahn, C N" sort="Hahn, C N" uniqKey="Hahn C" first="C N" last="Hahn">C N Hahn</name><name sortKey="Klingler Hoffmann, M" sort="Klingler Hoffmann, M" uniqKey="Klingler Hoffmann M" first="M" last="Klingler-Hoffmann">M. Klingler-Hoffmann</name><name sortKey="Lane, S W" sort="Lane, S W" uniqKey="Lane S" first="S W" last="Lane">S W Lane</name><name sortKey="Lee, Y K" sort="Lee, Y K" uniqKey="Lee Y" first="Y K" last="Lee">Y K Lee</name><name sortKey="Matthews, J M" sort="Matthews, J M" uniqKey="Matthews J" first="J M" last="Matthews">J M Matthews</name><name sortKey="Scott, H S" sort="Scott, H S" uniqKey="Scott H" first="H S" last="Scott">H S Scott</name><name sortKey="Stokes, P H" sort="Stokes, P H" uniqKey="Stokes P" first="P H" last="Stokes">P H Stokes</name><name sortKey="Venugopal, P" sort="Venugopal, P" uniqKey="Venugopal P" first="P" last="Venugopal">P. Venugopal</name><name sortKey="Yeung, D T O" sort="Yeung, D T O" uniqKey="Yeung D" first="D T O" last="Yeung">D T O. Yeung</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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