Baldacci P, Transy C, Cochet M, Penit C, Israel A, Kourilsky P
J Exp Med. 1986 Sep 1;164(3):677-94. doi: 10.1084/jem.164.3.677.
We have fused an H-2- thymoma (BM5R.9) with an H-2+ thymoma (BW5147) and have found that many of the resulting hybrids exhibit an H-2- phenotype. In several hybrids that were analyzed in detail, this phenotype is related to the absence of steady-state H-2 mRNA and shows some instability, possibly related to the loss of chromosomes in segregants. We conclude from our studies that BM5R.9 cells display a trans-acting mechanism that can repress the expression of H-2 antigens, and that the gene(s) causing the repression are not located on chromosome 17. This mechanism is not sufficient to explain the H-2- phenotype of BM5R.9, for which an additional, cis-acting process, must be postulated. We discuss these results in the context of the regulation of expression of the major class I transplantation antigens.
我们将一个H-2-胸腺瘤(BM5R.9)与一个H-2+胸腺瘤(BW5147)进行了融合,发现许多由此产生的杂种表现出H-2-表型。在几个经过详细分析的杂种中,这种表型与稳态H-2 mRNA的缺失有关,并表现出一些不稳定性,这可能与分离物中染色体的丢失有关。我们从研究中得出结论,BM5R.9细胞表现出一种反式作用机制,该机制可以抑制H-2抗原的表达,并且导致这种抑制的基因不在17号染色体上。这种机制不足以解释BM5R.9的H-2-表型,为此必须假定存在一个额外的顺式作用过程。我们在主要I类移植抗原表达调控的背景下讨论了这些结果。