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拓扑异构酶I缺陷导致RNA聚合酶II积累,并增加免疫球蛋白可变基因中激活诱导胞嘧啶脱氨酶(AID)的丰度。

Topoisomerase I deficiency causes RNA polymerase II accumulation and increases AID abundance in immunoglobulin variable genes.

作者信息

Maul Robert W, Saribasak Huseyin, Cao Zheng, Gearhart Patricia J

机构信息

Laboratory of Molecular Biology and Immunology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, United States.

Laboratory of Molecular Biology and Immunology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, United States.

出版信息

DNA Repair (Amst). 2015 Jun;30:46-52. doi: 10.1016/j.dnarep.2015.03.004. Epub 2015 Mar 18.

Abstract

Activation-induced deaminase (AID) is a DNA cytosine deaminase that diversifies immunoglobulin genes in B cells. Recent work has shown that RNA polymerase II (Pol II) accumulation correlates with AID recruitment. However, a direct link between Pol II and AID abundance has not been tested. We used the DT40 B-cell line to manipulate levels of Pol II by decreasing topoisomerase I (Top1), which relaxes DNA supercoiling in front of the transcription complex. Top1 was decreased by stable transfection of a short hairpin RNA against Top1, which produced an accumulation of Pol II in transcribed genes, compared to cells transfected with sh-control RNA. The increased Pol II density enhanced AID recruitment to variable genes in the λ light chain locus, and resulted in higher levels of somatic hypermutation and gene conversion. It has been proposed by another lab that AID itself might directly suppress Top1 to increase somatic hypermutation. However, we found that in both AID(+/+) and AID(-/-) B cells from DT40 and mice, Top1 protein levels were identical, indicating that the presence or absence of AID did not decrease Top1 expression. Rather, our results suggest that the mechanism for increased diversity when Top1 is reduced is that Pol II accumulates and recruits AID to variable genes.

摘要

激活诱导的胞苷脱氨酶(AID)是一种DNA胞嘧啶脱氨酶,可使B细胞中的免疫球蛋白基因多样化。最近的研究表明,RNA聚合酶II(Pol II)的积累与AID的募集相关。然而,Pol II与AID丰度之间的直接联系尚未得到验证。我们使用DT40 B细胞系,通过降低拓扑异构酶I(Top1)来调控Pol II的水平,Top1可缓解转录复合物前方的DNA超螺旋。通过稳定转染针对Top1的短发夹RNA来降低Top1,与转染对照短发夹RNA的细胞相比,这导致转录基因中Pol II的积累。增加的Pol II密度增强了AID向λ轻链基因座可变基因的募集,并导致更高水平的体细胞高频突变和基因转换。另一个实验室提出,AID本身可能直接抑制Top1以增加体细胞高频突变。然而,我们发现,在来自DT40和小鼠的AID(+/+)和AID(-/-) B细胞中,Top1蛋白水平相同,这表明AID的存在与否并不会降低Top1的表达。相反,我们的结果表明,当Top1减少时多样性增加的机制是Pol II积累并将AID募集到可变基因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9461/4425579/509bdb244213/nihms673297f1.jpg

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