Reisman D, Rotter V
Department of Cell Biology, Weizmann Institute of Science, Rehovot, Israel.
Mol Cell Biol. 1989 Aug;9(8):3571-5. doi: 10.1128/mcb.9.8.3571-3575.1989.
Transcription from the Moloney murine leukemia virus (Mo-MuLV) long terminal repeat (LTR) is inhibited in murine stem cells and induced during maturation of these cells. We have investigated whether alterations in the activity of this viral regulatory element also occur during differentiation of human myeloid leukemia cells. The Mo-MuLV LTR and the simian virus 40 (SV40) early promoter were introduced into HL-60 promyelocytes on Epstein-Barr virus-derived chloramphenicol acetyltransferase expression vectors. When these cells were induced to terminally differentiate, transcription from the Mo-MuLV LTR was induced approximately 10-fold. Expression from the SV40 promoter remained constant during differentiation of these cells. Replacing the SV40 transcriptional enhancer with the Mo-MuLV LTR transcriptional enhancer rendered the SV40 promoter inducible during differentiation. We conclude that sequences within the transcriptional enhancer of the Mo-MuLV LTR contain cis-acting elements responsible for induction of gene expression during differentiation of human myeloid cells.
莫洛尼鼠白血病病毒（Mo-MuLV）长末端重复序列（LTR）的转录在小鼠干细胞中受到抑制，并在这些细胞成熟过程中被诱导。我们研究了在人髓系白血病细胞分化过程中，这种病毒调节元件的活性是否也会发生改变。将Mo-MuLV LTR和猿猴病毒40（SV40）早期启动子导入基于爱泼斯坦-巴尔病毒的氯霉素乙酰转移酶表达载体上的HL-60早幼粒细胞中。当这些细胞被诱导终末分化时，来自Mo-MuLV LTR的转录被诱导了约10倍。在这些细胞分化过程中，SV40启动子的表达保持恒定。用Mo-MuLV LTR转录增强子取代SV40转录增强子，使得SV40启动子在分化过程中可被诱导。我们得出结论，Mo-MuLV LTR转录增强子内的序列包含负责在人髓系细胞分化过程中诱导基因表达的顺式作用元件。
