Anton Wutz

Summary

Affiliation: University of Vienna
Country: Austria

Publications

  1. ncbi Xist function: bridging chromatin and stem cells
    Anton Wutz
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria
    Trends Genet 23:457-64. 2007
  2. ncbi A chromosomal memory triggered by Xist regulates histone methylation in X inactivation
    Alexander Kohlmaier
    Research Institute of Molecular Pathology, Vienna, Austria
    PLoS Biol 2:E171. 2004
  3. ncbi X inactivation Xplained
    Anton Wutz
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria
    Curr Opin Genet Dev 17:387-93. 2007
  4. ncbi The Trithorax group protein Ash2l and Saf-A are recruited to the inactive X chromosome at the onset of stable X inactivation
    Dieter Pullirsch
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria
    Development 137:935-43. 2010
  5. ncbi Recruitment of PRC1 function at the initiation of X inactivation independent of PRC2 and silencing
    Stefan Schoeftner
    Research Institute of Molecular Pathology, Vienna, Austria
    EMBO J 25:3110-22. 2006
  6. ncbi Cancer progenitors and epigenetic contexts: an Xisting connection
    Ruben Agrelo
    Research Institute of Molecular Pathology, Vienna, Austria
    Epigenetics 4:568-70. 2009
  7. ncbi Hematopoietic precursor cells transiently reestablish permissiveness for X inactivation
    Fabio Savarese
    Research Institute of Molecular Pathology, Vienna Biocenter, Dr Bohr Gasse 7, 1030 Vienna, Austria
    Mol Cell Biol 26:7167-77. 2006
  8. ncbi ConteXt of change--X inactivation and disease
    Ruben Agrelo
    Research Institute of Molecular Pathology, Vienna, Austria
    EMBO Mol Med 2:6-15. 2010
  9. ncbi Xist and the order of silencing
    Karen Ng
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria
    EMBO Rep 8:34-9. 2007
  10. ncbi Polycomb complexes act redundantly to repress genomic repeats and genes
    Martin Leeb
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria
    Genes Dev 24:265-76. 2010

Collaborators

Detail Information

Publications22

  1. ncbi Xist function: bridging chromatin and stem cells
    Anton Wutz
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria
    Trends Genet 23:457-64. 2007
    ..This review emphasizes the opportunity that Xist provides to functionally define epigenetic transitions in development, to understand cell identity, pluripotency and stem cell differentiation...
  2. ncbi A chromosomal memory triggered by Xist regulates histone methylation in X inactivation
    Alexander Kohlmaier
    Research Institute of Molecular Pathology, Vienna, Austria
    PLoS Biol 2:E171. 2004
    ....
  3. ncbi X inactivation Xplained
    Anton Wutz
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria
    Curr Opin Genet Dev 17:387-93. 2007
    ..Chromosome-wide silencing is then initiated by the noncoding Xist RNA, which evolved with the mammalian Xic and covers the inactive X chromosome...
  4. ncbi The Trithorax group protein Ash2l and Saf-A are recruited to the inactive X chromosome at the onset of stable X inactivation
    Dieter Pullirsch
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria
    Development 137:935-43. 2010
    ..This observation highlights a crucial role for spatial organization of chromatin changes in the maintenance of X inactivation...
  5. ncbi Recruitment of PRC1 function at the initiation of X inactivation independent of PRC2 and silencing
    Stefan Schoeftner
    Research Institute of Molecular Pathology, Vienna, Austria
    EMBO J 25:3110-22. 2006
    ..Our data show that Xist recruits PRC1 components by both PRC2 dependent and independent modes and in the absence of PRC2 function is sufficient for the establishment of Polycomb-based memory systems in X inactivation...
  6. ncbi Cancer progenitors and epigenetic contexts: an Xisting connection
    Ruben Agrelo
    Research Institute of Molecular Pathology, Vienna, Austria
    Epigenetics 4:568-70. 2009
    ..It has been demonstrated that Xist is functional in tumor cells, where SATB1 was identified as the first silencing factor for Xist mediated chromosome silencing...
  7. ncbi Hematopoietic precursor cells transiently reestablish permissiveness for X inactivation
    Fabio Savarese
    Research Institute of Molecular Pathology, Vienna Biocenter, Dr Bohr Gasse 7, 1030 Vienna, Austria
    Mol Cell Biol 26:7167-77. 2006
    ..This suggests that Xist function is restricted in development by the limited activity of epigenetic pathways rather than by a change in the responsiveness of chromatin between embryonic and differentiated cell types...
  8. ncbi ConteXt of change--X inactivation and disease
    Ruben Agrelo
    Research Institute of Molecular Pathology, Vienna, Austria
    EMBO Mol Med 2:6-15. 2010
    ..Understanding their reactivation will deepen our understanding of tumourigenesis and may be exploited for cancer therapy...
  9. ncbi Xist and the order of silencing
    Karen Ng
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria
    EMBO Rep 8:34-9. 2007
    ..Here, we critically review our understanding of dosage compensation in placental mammals and place these findings in the context of other cellular processes that intersect with mammalian dosage compensation...
  10. ncbi Polycomb complexes act redundantly to repress genomic repeats and genes
    Martin Leeb
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria
    Genes Dev 24:265-76. 2010
    ..This indicates a contribution of the Polycomb group system to the defense against parasitic DNA, and a potential role of genomic repeats in Polycomb-mediated gene regulation...
  11. ncbi Ring1B is crucial for the regulation of developmental control genes and PRC1 proteins but not X inactivation in embryonic cells
    Martin Leeb
    Research Institute of Molecular Pathology, Vienna, Austria
    J Cell Biol 178:219-29. 2007
    ..Other chromatin marks associated with the initiation of X inactivation are not affected in Ring1B-deficient cells, suggesting compensation for the loss of Ring1B in X inactivation in contrast to the repression of lineage genes...
  12. ncbi SATB1 defines the developmental context for gene silencing by Xist in lymphoma and embryonic cells
    Ruben Agrelo
    Research Institute of Molecular Pathology, Vienna, Austria
    Dev Cell 16:507-16. 2009
    ..Thus, our data establish SATB1 as a crucial silencing factor contributing to the initiation of X inactivation...
  13. ncbi RNAs templating chromatin structure for dosage compensation in animals
    Anton Wutz
    Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria
    Bioessays 25:434-42. 2003
    ..They do not appear to act in a sequence-specific manner but might provide scaffolds for co-operative binding of chromatin-associated complexes that enable spreading of chromatin modifications...
  14. ncbi X chromosome inactivation sparked by non-coding RNAs
    Martin Leeb
    Institute of Molecular Pathology, Vienna, Austria
    RNA Biol 6:94-9. 2009
    ..Here, we review non-coding RNAs that have been implicated in X chromosome inactivation. Focusing on the best studied transcripts Xist and Tsix we portray a current perspective on chromosome wide gene regulation by non-coding RNAs...
  15. ncbi X inactivation and disease
    Ruben Agrelo
    Research Institute of Molecular Pathology, Dr Bohr Gasse 7, 1030 Vienna, Austria
    Semin Cell Dev Biol 21:194-200. 2010
    ..This dosage-compensation mechanism is based on the long functional Xist RNA. Here, we review our understanding of dosage compensation and Xist function in the context of disease...
  16. ncbi A system for imaging the regulatory noncoding Xist RNA in living mouse embryonic stem cells
    Karen Ng
    Research Institute of Molecular Pathology, 1030 Vienna, Austria
    Mol Biol Cell 22:2634-45. 2011
    ..Our data reveal a strategy for visualizing Xist and indicate that spreading over the chromosome might involve dynamic binding and displacement...
  17. ncbi Synergy of Eed and Tsix in the repression of Xist gene and X-chromosome inactivation
    Shinwa Shibata
    Department of Stem Cell Biology, Graduate School of Medicine, Kanazawa University, Takara machi, Kanazawa, Ishikawa, Japan
    EMBO J 27:1816-26. 2008
    ..The synergy of Polycomb group proteins and antisense Tsix transcription in Xist gene regulation explains why males can repress Xist without Tsix...
  18. ncbi A novel role for Xist RNA in the formation of a repressive nuclear compartment into which genes are recruited when silenced
    Julie Chaumeil
    Mammalian Developmental Epigenetic Group, UMR 218, Curie Institute, 75248 Paris Cedex 05, France
    Genes Dev 20:2223-37. 2006
    ....
  19. ncbi Chromosomal silencing and localization are mediated by different domains of Xist RNA
    Anton Wutz
    Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, Massachusetts 02142, USA
    Nat Genet 30:167-74. 2002
    ..Association of Xist RNA with chromatin is mediated by functionally redundant sequences that act cooperatively and are dispersed throughout the remainder of Xist but show little or no homology...
  20. ncbi HOXA10 is a critical regulator for hematopoietic stem cells and erythroid/megakaryocyte development
    Mattias Magnusson
    Molecular Medicine and Gene Therapy, Institute of Laboratory Medicine, Lund University Hospital, 221 84 Lund, Sweden
    Blood 109:3687-96. 2007
    ..These findings reveal novel molecular pathways that act downstream of HOXA10 and identify HOXA10 as a master regulator of postnatal hematopoietic development...
  21. ncbi Efficient method to generate single-copy transgenic mice by site-specific integration in embryonic stem cells
    Caroline Beard
    Whitehead Institute for Biomedical Research, Cambridge, Massachusetts 02142, USA
    Genesis 44:23-8. 2006
    ..This strategy and the vectors described here are generally applicable to any locus in ES cells and should allow for the rapid production of mice with transgenes efficiently targeted to a defined site...
  22. ncbi Hypoxic induction of Ctgf is directly mediated by Hif-1
    Debra F Higgins
    Department of Medicine, University of Pennsylvania, Philadelphia, PA 19104 6144, USA
    Am J Physiol Renal Physiol 287:F1223-32. 2004
    ..Our findings have important implications for a number of fibrotic disorders in which hypoxia, CTGF, and TGF-beta(1) are involved, including renal, dermal, hepatic, and pulmonary fibrosis...