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Many translocations between the Y chromosome and a major autosome have no effect on the fertility of Drosophila melanogaster males. However, when such translocation-bearing males also carry an X chromosome deficient for a large portion of the centric heterochromatin, they are generally sterile. This has been interpreted to be the result of an interaction between the deficiency and the subterminally capped autosome. Using this observation as a starting point, we have developed a selection scheme for radiation-induced translocation resealings that depends on the prediction that fertility in the presence of such a deficient X is restored whenever the displaced autosomal tip is brought back in association with an autosomal centromere. The observation and the prediction form the basis for what is referred to as the autosomal continuity model for male fertility.—Such a mutagenesis scheme offers several advantages. (1) It is efficient, producing upward of 1% resealings in some cases. (2) It is simple; since fertility is the basis for the selective screen, many males can be tested in a single vial. (3) It can be used to simultaneously generate both duplications and deficiencies specific for chromosomal material adjacent to the original translocation breakpoints. (4) The target for mutagenesis can be mature sperm.—Analysis of the pattern of male-fertile rearrangements obtained from several translocation lines using this protocol indicates that continuity of the autosomal tips and their centromeres is neither a necessary nor sufficient condition for male fertility in the presence of a bobbed-deficient X. Thus, the simple autosomal continuity model is not adequate to explain this complicated mechanism of chromosomal control of fertility and will have to be revised accordingly. Potential future lines of inquiry toward this goal are discussed.

genetics

CHROMOSOMAL CONTROL OF FERTILITY IN DROSOPHILA MELANOGASTER. I. RESCUE OF T(Y;A)/bb l-158 MALE STERILITY BY CHROMOSOME REARRANGEMENT