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Incomplete sex chromosome pairing in oligospermic male hybrids of Mus musculus and M. musculus molossinus in relation to the source of the Y chromosome and the presence or absence of a reciprocal translocation

Summary. A series of backcrosses of T70H/+ F_, Mus musculus x Mus m. molossinus females x T70H/T70H Mus musculus males and of a +/+ F₁ Mus musculus x M. m. molossinus male x T70H/T70H and +/+ Mus musculus females were set up to produce T70H/+ B₁ males with a Y chromosome of the 'musculus' (Y) or 'molossinus' (Y*) type, and males with T70H/T70H Y and +/+ Y* karyotypes. Observations of late diplotene—metaphase 1 meiosis were carried out, besides estimates of the number of spermatozoa in the caput epididymidis and the frequency of abnormal sperm mophology. From two T70H/+ F₁ sterile males, 114 pachytene spermatocytes were scored through the electron microscope after whole mount spreading on copper grids. It was concluded that: (1) the T70H/+ F_, and B_, mice showed higher chiasma frequencies than did T70H/+ mice on a random-bred Swiss genetic background; (2) despite this effect, X,Y univalence frequently occurred in all karyotypes and there was a significant correlation (0·81) between the sperm count and the fraction of primary spermatocytes with X,Y univalents; (3) within the T70H/+ F_, males, the sex chromosomes were unpaired in 36·8% of the pachytene spermatocytes scored, and when paired, the pairing segment was generally half the value of that for control spermatocytes; (4) the frequency of X,Y univalence was influenced by the source of the Y chromosome but not by the presence of translocation heterozygosity. Within the B_, karyotypes, autosomal genetic factors must also be important for regulating pairing behaviour; (5) the presence of a reciprocal translocation, independent of X,Y chromosome pairing, also affected the reduced sperm production in the hybrids; (6) spermatozoa of abnormal morphology were frequently produced, especially in the B_, groups with translocation heterozygosity or homozygosity. The deviant shapes were associated with these factors and with the hybrid genetic background but not directly with the numbers of spermatozoa produced.

From these results and others in the literature it appears that insufficient X,Y pairing can lead to sterility in male mice. Such insufficiency then acts as a cell lethal in primary spermatocytes, leading to degeneration mainly during the diplotene– metaphase 1 stages of the first meiotic division, thus preventing the development of secondary spermatocytes.