English
 
User Manual Privacy Policy Disclaimer Contact us
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Transcriptional repression by PRC1 in the absence of H2A monoubiquitylation

MPS-Authors
/persons/resource/persons82503

Pengelly,  Ana Raquel
Müller, Jürg / Chromatin Biology, Max Planck Institute of Biochemistry, Max Planck Society;

/persons/resource/persons132143

Kalb,  Reinhard
Müller, Jürg / Chromatin Biology, Max Planck Institute of Biochemistry, Max Planck Society;

/persons/resource/persons181439

Finkl,  Katja
Müller, Jürg / Chromatin Biology, Max Planck Institute of Biochemistry, Max Planck Society;

/persons/resource/persons78423

Müller,  Jürg
Müller, Jürg / Chromatin Biology, Max Planck Institute of Biochemistry, Max Planck Society;

External Ressource
No external resources are shared
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Pengelly, A. R., Kalb, R., Finkl, K., & Müller, J. (2015). Transcriptional repression by PRC1 in the absence of H2A monoubiquitylation. GENES & DEVELOPMENT, 29(14), 1487-1492. doi:10.1101/gad.265439.115.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0028-45D9-F
Abstract
Histone H2A monoubiquitylation (H2Aub) is considered to be a key effector in transcriptional repression by Polycomb-repressive complex 1 (PRC1). We analyzed Drosophila with a point mutation in the PRC1 subunit Sce that abolishes its H2A ubiquitylase activity or with point mutations in the H2A and H2Av residues ubiquitylated by PRC1. H2Aub is essential for viability and required for efficient histone H3 Lys27 trimethylation by PRC2 early in embryogenesis. However, H2Aub-deficient animals fully maintain repression of PRC1 target genes and do not show phenotypes characteristic of Polycomb group mutants. PRC1 thus represses canonical target genes independently of H2Aub.