| Literature DB >> 15454082 |
Naoyuki Fujita1, David L Jaye, Cissy Geigerman, Adil Akyildiz, Myesha R Mooney, Jeremy M Boss, Paul A Wade.
Abstract
The transcriptional repressor BCL-6 regulates B lymphocyte cell fate during the germinal center reaction by preventing terminal differentiation of B lymphocytes into plasma cells until appropriate signals are received. Here, we report a cofactor, MTA3, a cell type-specific subunit of the corepressor complex Mi-2/NuRD, for BCL-6-dependent cell fate determination. MTA3 is expressed in the same pattern in germinal centers as BCL-6. BCL-6 physically interacts with Mi-2/NuRD and this interaction is sensitive to BCL-6 acetylation status. Depletion of MTA3 by RNAi impairs BCL-6-dependent repression and alters the cell-specific transcriptional pattern characteristic of the B lymphocyte. Remarkably, exogenous expression of BCL-6 in a plasma cell line leads, in an MTA3-dependent manner, to repression of plasma cell-specific transcripts, reactivation of the B cell transcriptional program, expression of B lymphocyte cell surface markers, and reprogramming of cell fate.Entities:
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Year: 2004 PMID： 15454082 DOI： 10.1016/j.cell.2004.09.014
Source DB: PubMed Journal: Cell ISSN： 0092-8674 Impact factor: 41.582