Dudley Darryll D, Manis John P, Zarrin Ali A, Kaylor Lianne, Tian Ming, Alt Frederick W
Howard Hughes Medical Institute, Children's Hospital, Department of Genetics, Harvard Medical School, and Center for Blood Research, Boston, MA 02115, USA.
Proc Natl Acad Sci U S A. 2002 Jul 23;99(15):9984-9. doi: 10.1073/pnas.152333499. Epub 2002 Jul 11.
Ig heavy chain class switch recombination (CSR) involves a recombination/deletion mechanism that exchanges the expressed C(H) gene with a downstream C(H) gene. CSR is mediated by highly repetitive switch (S) region sequences and requires the activation-induced deaminase (AID). The S region 5' of the C mu gene (S mu) can undergo high-frequency internal deletions in normal B cells and B cell lines activated for CSR, although the relationship of these deletions and CSR has not been elucidated. In this study, we introduced constitutively transcribed S mu or S gamma 2b regions into a pro-B cell line that can be activated for AID expression, CSR, and endogenous S mu deletions. We find that randomly integrated S region transcription units in these cells also undergo increased levels of internal rearrangements after cellular activation, indicating that the deletion process is independent of location within the Ig heavy chain locus and potentially AID-promoted. To test the latter issue, we generated hybridomas from wild-type and AID-deficient activated B cells and assayed them for internal S mu deletions and S region mutations. These studies demonstrated that efficient intra-S region recombination depends on AID expression and that internal S region deletions are accompanied by frequent mutations, indicating that most S region deletions occur by the same mechanism as CSR.
免疫球蛋白重链类别转换重组(CSR)涉及一种重组/缺失机制,该机制可将表达的C(H)基因与下游的C(H)基因进行交换。CSR由高度重复的转换(S)区序列介导,并且需要激活诱导的脱氨酶(AID)。Cμ基因(Sμ)5'端的S区在正常B细胞和被激活以进行CSR的B细胞系中可发生高频内部缺失,尽管这些缺失与CSR之间的关系尚未阐明。在本研究中,我们将持续转录的Sμ或Sγ2b区导入一个前B细胞系,该细胞系可被激活以表达AID、进行CSR和发生内源性Sμ缺失。我们发现,这些细胞中随机整合的S区转录单位在细胞激活后也会经历更高水平的内部重排,这表明缺失过程与免疫球蛋白重链基因座内的位置无关,并且可能是由AID促进的。为了测试后一个问题,我们从野生型和AID缺陷型激活的B细胞中产生杂交瘤,并检测它们的内部Sμ缺失和S区突变。这些研究表明,高效的S区内重组依赖于AID的表达,并且内部S区缺失伴随着频繁的突变,这表明大多数S区缺失与CSR的发生机制相同。