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Genome-wide analysis of the binding pattern of the transcriptional co-activator Cbp.

ABSTRACT: The transcriptional coactivator Cbp is critical for hematopoietic stem cell (HSC) development. However, its role in adult HSC and the mechanistic detail of Cbp control of HSC function remain unknown. Using conditional deletion of Cbp in the adult HSC compartment, we demonstrate an altered balance between differentiation and self-renewal with gradual loss of phenotypic HSC, differentiation defects in lower compartments and the development of myeloid malignancies. In addition, we demonstrate that Cbp -/- HSCs reconstitute hematopoiesis with lower efficiency than their wild type counterparts and readily exhaust over time when placed under the replicative stress of serial transplantation. Furthermore, we demonstrate abnormal cell cycle (re)entry and apoptosis in HSC which, with preferential differentiation, also contribute to stem cell exhaustion. Finally we demonstrate global transcriptional abnormalities predicted to alter cell cycle control, balanced differentiation and HSC function upon Cbp deletion and link Cbp to a critical HSC transcriptional regulatory network through genome-wide analysis of Cbp binding. 1 sample (Cbp) and 1 control, all prepared from a hematopoietic progenitor/stem cell line (BM-HPC)

ORGANISM(S): Mus musculus

SUBMITTER: Wai-In Chan 

PROVIDER: E-GEOD-25265 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The transcriptional coactivator Cbp regulates self-renewal and differentiation in adult hematopoietic stem cells.

Chan Wai-In WI   Hannah Rebecca L RL   Dawson Mark A MA   Pridans Clare C   Foster Donna D   Joshi Anagha A   Göttgens Berthold B   Van Deursen Jan M JM   Huntly Brian J P BJ  

Molecular and cellular biology 20111017 24

The transcriptional coactivator Cbp plays an important role in a wide range of cellular processes, including proliferation, differentiation, and apoptosis. Although studies have shown its requirement for hematopoietic stem cell (HSC) development, its role in adult HSC maintenance, as well as the cellular and molecular mechanisms underlying Cbp function, is not clear. Here, we demonstrate a gradual loss of phenotypic HSCs and differentiation defects following conditional ablation of Cbp during ad  ...[more]

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