Onishi T, Berglund C, Reeder R H
Proc Natl Acad Sci U S A. 1984 Jan;81(2):484-7. doi: 10.1073/pnas.81.2.484.
The mechanism of nucleolar dominance was studied in two lines of mouse-human somatic hybrids. Both lines had preferentially lost human chromosomes but had retained significant amounts of both mouse and human ribosomal genes (genes coding for the 18S, 5.8S, and 28S RNAs of ribosomes). However, the human ribosomal genes were repressed, and only mouse ribosomal genes were expressed. Soluble transcription extracts from the hybrids were able to initiate RNA synthesis accurately on a cloned mouse ribosomal gene but were unable to initiate accurately on a human ribosomal gene. This suggests that nucleolar dominance in these hybrids is due to the loss or inactivation of the gene for a specificity factor required to recognize the human ribosomal gene promoter.
在两株小鼠 - 人类体细胞杂种中研究了核仁显性的机制。两株杂种细胞系都优先丢失了人类染色体，但保留了大量的小鼠和人类核糖体基因（编码核糖体18S、5.8S和28S RNA的基因）。然而，人类核糖体基因被抑制，只有小鼠核糖体基因表达。杂种细胞系的可溶性转录提取物能够在克隆的小鼠核糖体基因上准确起始RNA合成，但不能在人类核糖体基因上准确起始。这表明这些杂种中的核仁显性是由于识别人类核糖体基因启动子所需的特异性因子基因的缺失或失活。
