Jaafar H, Gabriel-Robez O, Rumpler Y
Institut d'Embryologie, Faculté de Médecine, Strasbourg, France.
Chromosoma. 1989 Nov;98(5):330-4. doi: 10.1007/BF00292385.
In an attempt to elucidate the mechanism of sterility of X-autosome translocations in the mouse, we studied the distribution of [3H]-uridine incorporation in sterile males carrying the balanced X-16 reciprocal translocation. The results failed to show an overall reactivation of the X as has been postulated by Lifschytz and Lindsley (1972) but there was some spreading of X inactivation along the translocated and normal chromosome 16 in those regions that were close to the X breakpoint. We feel that this process could be responsible for metabolic disturbances leading to degeneration of primary spermatocytes and, therefore, to sterility.
为了阐明小鼠中X-常染色体易位导致不育的机制，我们研究了携带平衡的X-16相互易位的不育雄性小鼠中[3H]-尿苷掺入的分布情况。结果并未显示出如Lifschytz和Lindsley（1972年）所假设的X染色体的全面重新激活，但在靠近X染色体断点的区域，X染色体失活沿着易位的和正常的16号染色体有一定程度的扩展。我们认为，这一过程可能是导致初级精母细胞退化进而导致不育的代谢紊乱的原因。
