English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

MEIS homeodomain proteins facilitate PARP1/ARTD1-mediated eviction of histone H1

MPS-Authors
/persons/resource/persons137770

Langer,  Julian David       
Department of Molecular Membrane Biology, Max Planck Institute of Biophysics, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Hau, A.-C., Grebbin, B. M., Agoston, Z., Anders-Maurer, M., Müller, T., Groß, A., et al. (2017). MEIS homeodomain proteins facilitate PARP1/ARTD1-mediated eviction of histone H1. The Journal of Cell Biology: JCB, 216(9), 2715-2729. doi:10.1083/jcb.201701154.


Cite as: https://hdl.handle.net/21.11116/0000-0001-27EB-B
Abstract
Pre–B-cell leukemia homeobox (PBX) and myeloid ecotropic viral integration site (MEIS) proteins control cell fate decisions in many physiological and pathophysiological contexts, but how these proteins function mechanistically remains poorly defined. Focusing on the first hours of neuronal differentiation of adult subventricular zone–derived stem/progenitor cells, we describe a sequence of events by which PBX-MEIS facilitates chromatin accessibility of transcriptionally inactive genes: In undifferentiated cells, PBX1 is bound to the H1-compacted promoter/proximal enhancer of the neuron-specific gene doublecortin (Dcx). Once differentiation is induced, MEIS associates with chromatin-bound PBX1, recruits PARP1/ARTD1, and initiates PARP1-mediated eviction of H1 from the chromatin fiber. These results for the first time link MEIS proteins to PARP-regulated chromatin dynamics and provide a mechanistic basis to explain the profound cellular changes elicited by these proteins.