Nishikura K, Murray J M
Wistar Institute, Philadelphia, Pennsylvania 19104.
Oncogene. 1988 May;2(5):493-8.
In human Burkitt lymphoma, the expression of the c-myc allele that has been translocated to the immunoglobulin gene locus is constitutively elevated, whereas transcription from the normal untranslocated allele on chromosome 8 is usually undetectable. Our experiments were carried out to check several plausible mechanisms proposed to explain this selective inactivation. By examining the c-myc transcripts in the presence of cycloheximide and/or actinomycin D and using differential S1 mapping, which distinguishes the c-myc transcripts of the translocated from the untranslocated allele, we found that the selective inactivation of the normal c-myc gene locus is not by a post-transcriptional regulatory mechanism, by autorepression from the constitutive expression of c-myc protein derived from the translocated locus, nor by suppression due to the previously proposed labile protein repressor. Our results are accommodated most easily by an inactivation mechanism that stably modifies the structure of the untranslocated c-myc gene.
在人类伯基特淋巴瘤中，已易位至免疫球蛋白基因位点的c-myc等位基因的表达持续升高，而8号染色体上正常未易位等位基因的转录通常无法检测到。我们开展实验以检验为解释这种选择性失活而提出的几种合理机制。通过在放线菌酮和/或放线菌素D存在的情况下检测c-myc转录本，并使用能区分易位和未易位等位基因的c-myc转录本的差异S1作图，我们发现正常c-myc基因位点的选择性失活并非通过转录后调控机制，并非通过源自易位位点的c-myc蛋白的组成型表达的自抑制作用，也不是由于先前提出的不稳定蛋白阻遏物导致的抑制作用。我们的结果最容易用一种稳定修饰未易位c-myc基因结构的失活机制来解释。
