Document Detail


Developmentally regulated expression of MEF2C limits the response to BCR engagement in transitional B cells.
MedLine Citation:
PMID:  22311635     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Transitional and naïve mature peripheral B cells respond very differently to B-cell receptor (BCR) cross-linking. While transitional B cells undergo apoptosis upon BCR engagement, mature B cells survive and proliferate. This differential response correlates with the capacity of mature, but not transitional B cells to transcribe genes that promote cell survival and proliferation, including those encoding c-Myc and the Bcl-2 family members Bcl-xL and A1. We recently demonstrated that transitional B cells fail to assemble transcriptional machinery at the promoter region of these target genes despite equivalent cytoplasmic signaling and nuclear translocation of key transcription factors including NF-κB and nuclear factor of activated T cells (NFAT). The transcription factor myocyte enhancer factor-2C (MEF2C) is regulated by both calcineurin and mitogen-activated protein kinase signaling pathways, and is essential for proliferation and survival downstream of BCR engagement in mature B cells. In this work, we demonstrate that transitional B cells have intrinsically low levels of MEF2C protein and DNA-binding activity, and that this developmental difference in MEF2C expression is functionally significant. Forced expression of MEF2C in transitional B cells promoted cell survival, proliferation, and upregulation of pro-survival genes. Thus, low MEF2C expression limits transitional B-cell responsiveness to BCR engagement before these cells reach maturity.
Authors:
Sarah F Andrews; Xuezhi Dai; Byoung Y Ryu; Tod Gulick; Bindu Ramachandran; David J Rawlings
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  European journal of immunology     Volume:  42     ISSN:  1521-4141     ISO Abbreviation:  Eur. J. Immunol.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-04-27     Completed Date:  2012-07-06     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  1273201     Medline TA:  Eur J Immunol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  1327-36     Citation Subset:  IM    
Copyright Information:
© 2012 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
Affiliation:
Center for Immunity and Immunotherapies, Seattle Children's Research Institute, Seattle, WA, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis Regulatory Proteins / genetics
Cell Proliferation
Cell Survival
Gene Expression Regulation, Developmental*
Membrane Proteins / genetics
Mice
Mice, Inbred C57BL
Mice, Knockout
Myogenic Regulatory Factors / analysis,  genetics*
Precursor Cells, B-Lymphoid / metabolism*
Proto-Oncogene Proteins / genetics
Receptors, Antigen, B-Cell / metabolism*
Up-Regulation
Grant Support
ID/Acronym/Agency:
AI071163/AI/NIAID NIH HHS; HD037091/HD/NICHD NIH HHS; P01 HL073104/HL/NHLBI NIH HHS; R01 AI084457/AI/NIAID NIH HHS; R01 HD037091/HD/NICHD NIH HHS; R56 AI084457/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Apoptosis Regulatory Proteins; 0/Bcl-2-like protein 11; 0/Mef2c protein, mouse; 0/Membrane Proteins; 0/Myogenic Regulatory Factors; 0/Proto-Oncogene Proteins; 0/Receptors, Antigen, B-Cell
Comments/Corrections

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