Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Mtg16 regulates E protein activity and lineage specification in dendritic cell development (ChIP-seq)

ABSTRACT: E protein transcription factors specify major immune cell lineages including lymphocytes and interferon-producing plasmacytoid dendritic cells (pDCs). Corepressors of the ETO family can bind to and block transactivation by E proteins, but the physiological role of these interactions remained unclear. We report that ETO protein Mtg16 binds chromatin primarily through the pDC-specific E protein E2-2 in human pDCs. Mtg16-deficient mice showed impaired pDC development and functionality, whereas the specification of the classical dendritic cells (cDCs) was enhanced. The deletion of Mtg16 caused aberrant expression of E protein antagonist Id2 in pDCs. Thus, Mtg16 acts as a cofactor of E2-2 to promote pDC differentiation and restrict cDC development, revealing an unexpected positive role of ETO proteins in E protein activity. Analysis of E2-2 and Mtg16 immunoprecipitated chromatin from CAL-1 cell line.

ORGANISM(S): Homo sapiens

SUBMITTER: Hiyaa Ghosh 

PROVIDER: E-GEOD-43876 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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ETO family protein Mtg16 regulates the balance of dendritic cell subsets by repressing Id2.

Ghosh Hiyaa S HS   Ceribelli Michele M   Matos Ines I   Lazarovici Allan A   Bussemaker Harmen J HJ   Lasorella Anna A   Hiebert Scott W SW   Liu Kang K   Staudt Louis M LM   Reizis Boris B  

The Journal of experimental medicine 20140630 8

Dendritic cells (DCs) comprise two major subsets, the interferon (IFN)-producing plasmacytoid DCs (pDCs) and antigen-presenting classical DCs (cDCs). The development of pDCs is promoted by E protein transcription factor E2-2, whereas E protein antagonist Id2 is specifically absent from pDCs. Conversely, Id2 is prominently expressed in cDCs and promotes CD8(+) cDC development. The mechanisms that control the balance between E and Id proteins during DC subset specification remain unknown. We found  ...[more]

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