A disruption of pachytene DNA metabolism in male mice with chromosomally-derived sterility.
DNA metabolism was analyzed in spermatocytes of mice that were sterile either because of X-autosome or autosome-autosome translocations, or because of trisomy. In the strains analyzed, spermatogenic development is arrested by metaphase I or soon thereafter. In all such strains a disruption of the normal pattern of pachytene DNA metabolism occurred. Prepachytene metabolism appeared normal. Disruption was manifest in both the level of endogenously generated nicks during pachytene and in the distribution of nicks among the different DNA sequence classes. Nicking was more intense in the steriles and tended to be randomized in distribution. Satellite DNA underwent pachytene nick-repair in the steriles but not in fertile controls. The repair capacity of spermatocytes from steriles was equal to that of the fertiles; the higher frequency of nicks in the steriles was due to a persistence of nicking activity.
D000818:Animals; D002875:Chromosomes; D004247:DNA / Q000378:metabolism*; D004260:DNA Repair; D004264:DNA Topoisomerases, Type I / Q000378:metabolism; D004276:DNA, Satellite / Q000378:metabolism; D005260:Female; D007248:Infertility, Male / Q000235:genetics* / Q000378:metabolism; D008297:Male; D051379:Mice; D013094:Spermatozoa / Q000378:metabolism; D014178:Translocation, Genetic; D014314:Trisomy; D014960:X Chromosome
D004276:DNA, Satellite; D004247:DNA; D004264:DNA Topoisomerases, Type I