Tsuji Hideo, Ishii-Ohba Hiroko, Katsube Takanori, Ukai Hideki, Aizawa Shiro, Doi Masahiro, Hioki Kyoji, Ogiu Toshiaki
Low Dose Radiation Effects Research Project Group, Radiation Hazards Research Group, and Environmental and Toxicological Science Research Group, National Institute of Radiological Sciences, Chiba, Japan.
Cancer Res. 2004 Dec 15;64(24):8882-90. doi: 10.1158/0008-5472.CAN-03-1163.
Deregulated V(D)J recombination-mediated chromosomal rearrangements are implicated in the etiology of B- and T-cell lymphomagenesis. We describe three pathways for the formation of 5'-deletions of the Notch1 gene in thymic lymphomas of wild-type or V(D)J recombination-defective severe combined immune deficiency (scid) mice. A pair of recombination signal sequence-like sequences composed of heptamer- and nonamer-like motifs separated by 12- or 23-bp spacers (12- and 23-recombination signal sequence) were present in the vicinity of the deletion breakpoints in wild-type thymic lymphomas, accompanied by palindromic or nontemplated nucleotides at the junctions. In scid thymic lymphomas, the deletions at the recombination signal sequence-like sequences occurred at a significantly lower frequency than in wild-type mice, whereas the deletions did not occur in Rag2(-/-) thymocytes. These results show that the 5'-deletions are formed by Rag-mediated V(D)J recombination machinery at cryptic recombination signal sequences in the Notch1 locus. In contrast, one third of the deletions in radiation-induced scid thymic lymphomas had microhomology at both ends, indicating that in the absence of DNA-dependent protein kinase-dependent nonhomologous end-joining, the microhomology-mediated nonhomologous end-joining pathway functions as the main mechanism to produce deletions. Furthermore, the deletions were induced via a coupled pathway between Rag-mediated cleavage at a cryptic recombination signal sequence and microhomology-mediated end-joining in radiation-induced scid thymic lymphomas. As the deletions at cryptic recombination signal sequences occur spontaneously, microhomology-mediated pathways might participate mainly in radiation-induced lymphomagenesis. Recombination signal sequence-mediated deletions were present clonally in the thymocyte population, suggesting that thymocytes with a 5'-deletion of the Notch1 gene have a growth advantage and are involved in lymphomagenesis.
失调的V(D)J重组介导的染色体重排与B细胞和T细胞淋巴瘤发生的病因学有关。我们描述了野生型或V(D)J重组缺陷型严重联合免疫缺陷(scid)小鼠胸腺淋巴瘤中Notch1基因5'端缺失形成的三种途径。在野生型胸腺淋巴瘤的缺失断点附近存在一对由七聚体和九聚体样基序组成、间隔12或23个碱基对间隔序列(12和23重组信号序列)的重组信号序列样序列,连接处伴有回文或非模板化核苷酸。在scid胸腺淋巴瘤中,重组信号序列样序列处的缺失发生频率明显低于野生型小鼠,而在Rag2(-/-)胸腺细胞中未发生缺失。这些结果表明,5'端缺失是由Rag介导的V(D)J重组机制在Notch1基因座的隐蔽重组信号序列处形成的。相比之下,辐射诱导的scid胸腺淋巴瘤中三分之一的缺失两端具有微同源性,这表明在缺乏DNA依赖性蛋白激酶依赖性非同源末端连接的情况下,微同源性介导的非同源末端连接途径是产生缺失的主要机制。此外,在辐射诱导的scid胸腺淋巴瘤中,缺失是通过隐蔽重组信号序列处Rag介导的切割与微同源性介导的末端连接之间的耦合途径诱导的。由于隐蔽重组信号序列处的缺失是自发发生的,微同源性介导的途径可能主要参与辐射诱导的淋巴瘤发生。重组信号序列介导的缺失在胸腺细胞群体中呈克隆性存在,这表明Notch1基因5'端缺失的胸腺细胞具有生长优势并参与淋巴瘤发生。