| First Author | Yao X | Year | 2010 |
| Journal | Mol Immunol | Volume | 48 |
| Issue | 1-3 | Pages | 153-63 |
| PubMed ID | 20884053 | Mgi Jnum | J:167090 |
| Mgi Id | MGI:4867143 | Doi | 10.1016/j.molimm.2010.08.014 |
| Citation | Yao X, et al. (2010) The L2a element is a mouse CD8 silencer that interacts with MAR-binding proteins SATB1 and CDP. Mol Immunol 48(1-3):153-63 |
| abstractText | Previous transgenic-reporter and targeted-deletion studies indicate that the subset-specific expression of CD8alphabeta heterodimers is controlled by multiple enhancer activities, since no silencer elements had been found within the locus. We have identified such a silencer as L2a, a previously characterized approximately 220 bp nuclear matrix associating region (MAR) located approximately 4.5 kb upstream of CD8alpha. L2a transgenes driven by the E8(I) enhancer showed no reporter expression in thymic subsets or T cells in splenic, inguinal and mesenteric lymph node peripheral T cells. Deletion of L2a resulted in significant reporter de-repression, even in the CD4(+)CD8(+) double positive (DP) thymocyte population. L2a contains binding sites for two MAR-interacting proteins, SATB1 and CDP. We found that that binding of these factors was markedly influenced by the content and spacing of L2a sub-motifs (L and S) and that SATB1 binds preferentially to the L motif both in vitro and in vivo. A small fraction of the transgenic CD8 single positive (SP) thymocytes and peripheral CD8(+) T cells bypassed L2a-silencing to give rise to variegated expression of the transgenic reporter. Crossing the L2a-containing transgene onto a SATB1 knockdown background enhanced variegated expression, suggesting that SATB1 is critical in overcoming L2a-silenced transcription. |
