| First Author | Balter BB | Year | 2012 |
| Journal | Mol Immunol | Volume | 52 |
| Issue | 1 | Pages | 1-8 |
| PubMed ID | 22580346 | Mgi Jnum | J:188170 |
| Mgi Id | MGI:5439258 | Doi | 10.1016/j.molimm.2012.04.006 |
| Citation | Balter BB, et al. (2012) Mice lacking Smu tandem repeats maintain RNA polymerase patterns but exhibit histone modification pattern shifts linked to class switch site locations. Mol Immunol 52(1):1-8 |
| abstractText | Antibody switching involves class switch recombination (CSR) events between switch (S) regions located upstream of heavy chain constant (C) genes. Mechanisms targeting CSR to S-regions are not clear. Deletion of Smu tandem repeat (SmuTR) sequences causes CSR to shift into downstream regions that do not undergo CSR in WT B-cells, including the Cmu-region. We now find that, in SmuTR(-/-) B cells, Smu chromatin histone modification patterns also shift downstream relative to WT and coincide with SmuTR(-/-) CSR locations. Our results suggest that histone H3 acetylation and methylation are involved in accessibility of switch regions and that these modifications are not dependent on the underlying sequence, but may be controlled by the location of upstream promoter or regulatory elements. Our studies also show RNA polymerase II (RNAPII) loading increases in the Emu/Imu region in stimulated B cells; these increases are independent of SmuTR sequences. Longer Smu deletions have been reported to eliminate increases in RNAPII density, therefore we suggest that sequences between Imu and Smu (possibly the Imu splicing region as well as G-tracts that are involved in stable RNA:DNA complex formation during transcription) might control the RNAPII density increases. |
