Dyson P J, Littlewood T D, Forster A, Rabbitts T H
EMBO J. 1985 Nov;4(11):2885-91. doi: 10.1002/j.1460-2075.1985.tb04018.x.
To help elucidate the mechanism of regulation of the c-myc gene we have characterised the DNase I hypersensitive sites around this gene in the human promyelocytic leukaemia cell line HL60, which carries amplified c-myc, and in Ramos, a Burkitt's lymphoma cell line with a translocation close to exon 1 of c-myc. Although dividing HL60 cells display a pattern of DNase I hypersensitive sites which is similar to that of previously described c-myc genes in B cells (lymphoblastoid and Burkitt's lymphoma), changes were found in DNase I hypersensitive sites upon differentiation of the HL60 cell line (accompanied by decreased c-myc transcription). Lack of c-myc transcription coincides with the loss of several DNase I hypersensitive sites and the reduction in intensity of a further site. A similar pattern was also seen in the inactive allele of the Burkitt's lymphoma cell line Ramos. A striking feature of both differentiated HL60 cells and of the inactive allele in Ramos is the quantitative maintenance of a DNase I hypersensitive site which occurs approximately 2.5 kb upstream of the c-myc gene promoters.
为了帮助阐明c-myc基因的调控机制，我们对人早幼粒细胞白血病细胞系HL60（该细胞系携带扩增的c-myc基因）以及Ramos（一种伯基特淋巴瘤细胞系，其易位靠近c-myc外显子1）中该基因周围的DNA酶I超敏位点进行了表征。虽然处于分裂状态的HL60细胞呈现出一种DNA酶I超敏位点模式，该模式与先前在B细胞（淋巴母细胞样细胞和伯基特淋巴瘤细胞）中描述的c-myc基因的模式相似，但在HL60细胞系分化时（伴随着c-myc转录减少），发现DNA酶I超敏位点发生了变化。c-myc转录缺失与几个DNA酶I超敏位点的丧失以及另一个位点强度的降低相吻合。在伯基特淋巴瘤细胞系Ramos的无活性等位基因中也观察到了类似的模式。分化的HL60细胞和Ramos中的无活性等位基因的一个显著特征是，在c-myc基因启动子上游约2.5 kb处出现的一个DNA酶I超敏位点在数量上得以维持。
