Abstract
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.
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Jaafar, H., Gabriel-Robez, O. & Rumpler, Y. Pattern of ribonucleic acid synthesis in vitro in primary spermatocytes from mouse testis carrying an X-autosome translocation. Chromosoma 98, 330–334 (1989). https://doi.org/10.1007/BF00292385
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DOI: https://doi.org/10.1007/BF00292385