A <it>Myc</it>-regulated transcriptional network controls B-cell fate in response to BCR triggering
<p>Abstract</p> <p>Background</p> <p>The B cell antigen receptor (BCR) is a signaling complex that mediates the differentiation of stage-specific cell fate decisions in B lymphocytes. While several studies have shown differences in signal transduction components as bein...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2009-07-01
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| Series: | BMC Genomics |
| Online Access: | http://www.biomedcentral.com/1471-2164/10/323 |
| _version_ | 1818778830066679808 |
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| author | Vaigot Pierre Mlinaric-Rascan Irena Murn Jernej Alibert Olivier Frouin Vincent Gidrol Xavier |
| author_facet | Vaigot Pierre Mlinaric-Rascan Irena Murn Jernej Alibert Olivier Frouin Vincent Gidrol Xavier |
| author_sort | Vaigot Pierre |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>The B cell antigen receptor (BCR) is a signaling complex that mediates the differentiation of stage-specific cell fate decisions in B lymphocytes. While several studies have shown differences in signal transduction components as being key to contrasting phenotypic outcomes, little is known about the differential BCR-triggered gene transcription downstream of the signaling cascades.</p> <p>Results</p> <p>Here we define the transcriptional changes that underlie BCR-induced apoptosis and proliferation of immature and mature B cells, respectively. Comparative genome-wide expression profiling identified 24 genes that discriminated between the early responses of the two cell types to BCR stimulation. Using mice with a conditional <it>Myc</it>-deletion, we validated the microarray data by demonstrating that <it>Myc </it>is critical to promoting BCR-triggered B-cell proliferation. We further investigated the <it>Myc-</it>dependent molecular mechanisms and found that <it>Myc </it>promotes a BCR-dependent clonal expansion of mature B cells by inducing proliferation and inhibiting differentiation.</p> <p>Conclusion</p> <p>This work provides the first comprehensive analysis of the early transcriptional events that lead to either deletion or clonal expansion of B cells upon antigen recognition, and demonstrates that <it>Myc </it>functions as the hub of a transcriptional network that control B-cell fate in the periphery.</p> |
| first_indexed | 2024-12-18T11:50:57Z |
| format | Article |
| id | doaj.art-bfe78c2d78bc41ffb7e21d25631ae057 |
| institution | Directory Open Access Journal |
| issn | 1471-2164 |
| language | English |
| last_indexed | 2024-12-18T11:50:57Z |
| publishDate | 2009-07-01 |
| publisher | BMC |
| record_format | Article |
| series | BMC Genomics |
| spelling | doaj.art-bfe78c2d78bc41ffb7e21d25631ae0572022-12-21T21:09:10ZengBMCBMC Genomics1471-21642009-07-0110132310.1186/1471-2164-10-323A <it>Myc</it>-regulated transcriptional network controls B-cell fate in response to BCR triggeringVaigot PierreMlinaric-Rascan IrenaMurn JernejAlibert OlivierFrouin VincentGidrol Xavier<p>Abstract</p> <p>Background</p> <p>The B cell antigen receptor (BCR) is a signaling complex that mediates the differentiation of stage-specific cell fate decisions in B lymphocytes. While several studies have shown differences in signal transduction components as being key to contrasting phenotypic outcomes, little is known about the differential BCR-triggered gene transcription downstream of the signaling cascades.</p> <p>Results</p> <p>Here we define the transcriptional changes that underlie BCR-induced apoptosis and proliferation of immature and mature B cells, respectively. Comparative genome-wide expression profiling identified 24 genes that discriminated between the early responses of the two cell types to BCR stimulation. Using mice with a conditional <it>Myc</it>-deletion, we validated the microarray data by demonstrating that <it>Myc </it>is critical to promoting BCR-triggered B-cell proliferation. We further investigated the <it>Myc-</it>dependent molecular mechanisms and found that <it>Myc </it>promotes a BCR-dependent clonal expansion of mature B cells by inducing proliferation and inhibiting differentiation.</p> <p>Conclusion</p> <p>This work provides the first comprehensive analysis of the early transcriptional events that lead to either deletion or clonal expansion of B cells upon antigen recognition, and demonstrates that <it>Myc </it>functions as the hub of a transcriptional network that control B-cell fate in the periphery.</p>http://www.biomedcentral.com/1471-2164/10/323 |
| spellingShingle | Vaigot Pierre Mlinaric-Rascan Irena Murn Jernej Alibert Olivier Frouin Vincent Gidrol Xavier A <it>Myc</it>-regulated transcriptional network controls B-cell fate in response to BCR triggering BMC Genomics |
| title | A <it>Myc</it>-regulated transcriptional network controls B-cell fate in response to BCR triggering |
| title_full | A <it>Myc</it>-regulated transcriptional network controls B-cell fate in response to BCR triggering |
| title_fullStr | A <it>Myc</it>-regulated transcriptional network controls B-cell fate in response to BCR triggering |
| title_full_unstemmed | A <it>Myc</it>-regulated transcriptional network controls B-cell fate in response to BCR triggering |
| title_short | A <it>Myc</it>-regulated transcriptional network controls B-cell fate in response to BCR triggering |
| title_sort | it myc it regulated transcriptional network controls b cell fate in response to bcr triggering |
| url | http://www.biomedcentral.com/1471-2164/10/323 |
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