| First Author | Roundy KM | Year | 2009 |
| Journal | Mol Immunol | Volume | 47 |
| Issue | 2-3 | Pages | 517-25 |
| PubMed ID | 19740539 | Mgi Jnum | J:155241 |
| Mgi Id | MGI:4413387 | Doi | 10.1016/j.molimm.2009.08.016 |
| Citation | Roundy KM, et al. (2009) Deletion of putative intronic control sequences does not alter cell or stage specific expression of Cr2. Mol Immunol 47(2-3):517-25 |
| abstractText | The expression of the mouse Cr2 gene has been shown to be restricted to mature B cells, follicular dendritic cells and, in some reports, to a minor population of activated T cells. In this report, we demonstrate that the expression of antigen(s) recognized by the anti-CR2 antibody on the surface of T cells is co-incident with T cell apoptotic death. Two distinct regions of the Cr2 gene have been implicated as critical for specific expression, the promoter region at the transcription start site and a control region within the first intron of the gene, approximately 1500 bp from the transcription start site. We have created a mouse that is lacking this intronic control sequence which, in the wild type (WT) mouse, contains multiple known binding sites for RBP-jkappa, Oct, NFAT and YY1 proteins. The analysis of this mouse named Cr2iDelta (Cr2 intron deletion) demonstrated normal tissue specific expression of the Cr2 gene including a lack of expression in mouse T cells. B cell expression of the Cr2 gene products, CR1 and CR2, is normal compared to WT, and the FDC of these mice continue to express Cr2 gene products. Therefore the intronic control region of the Cr2 gene, defined in transfection-based reporter gene assays as instrumental in controlling the cell specific expression profile of Cr2, does not influence the expression of the Cr2 gene in vivo nor alter the relative production of the CR1 and CR2 proteins via alternative slicing of Cr2 gene products. |
