Hameister H, Adolph S
Hum Genet. 1986 Mar;72(3):241-4. doi: 10.1007/BF00291886.
None of the up to now localized and expressed oncogenes maps to the mammalian X chromosome. This fact is discussed in the light of a trans-acting regulation mechanism for oncogenes. Such a specific regulation mechanism is demonstrated here for a qualitative change--i.e., varying timing of DNA-replication--at the putative c-myc gene locus in band 15E of murine T-cell leukemia. In intraspecific hybrids between tumor and non-tumor cells this qualitative change spreads over to all chromosomes 15 of the same cell, irrespective of their origin. This effect is thought to reflect a binary trans-acting regulation mechanism between homologous chromosomal loci. In the past specific chromosomal aberrations have been described in various tumors but none of these aberrations involve the X chromosome. For the mammalian X chromosome where there is usually only one gene copy per cell active the described kind of binary trans-acting regulation between homologous gene loci is rendered impossible.
迄今为止,已定位并表达的致癌基因均不在哺乳动物X染色体上。本文根据致癌基因的反式作用调控机制对此事实进行了讨论。本文证明了一种特定的调控机制,即小鼠T细胞白血病15E带中假定的c-myc基因位点发生了定性变化——即DNA复制时间的改变。在肿瘤细胞与非肿瘤细胞的种内杂交中,这种定性变化会扩散到同一细胞的所有15号染色体上,无论其来源如何。这种效应被认为反映了同源染色体位点之间的二元反式作用调控机制。过去在各种肿瘤中描述过特定的染色体畸变,但这些畸变均不涉及X染色体。对于每个细胞通常只有一个活跃基因拷贝的哺乳动物X染色体来说,同源基因位点之间所描述的这种二元反式作用调控是不可能实现的。