ANALYSIS OF THE AUTOSOMAL MUTATION abo AND ITS INTERACTION WITH THE RIBOSOMAL DNA OF DROSOPHILA MELANOGASTER: THE ROLE OF X-CHROMOSOME HETEROCHROMATIN

Barry Yedvobnick ¹, Hallie M. Krider ¹, and Bryan I. Levine ¹

¹ Biological Sciences Group, Genetics and Cell Biology Section, University of Connecticut, Storrs, Connecticut 06268

The autosomal recessive, maternal-effect mutation abnormal oocyte (abo: 2–38) preferentially lowers the viability of XO progeny. The severity of the sex-ratio distortion is reduced by duplications of maternal or zygotic heterochromatin (Sandler 1970, 1977; Parry and Sandler 1974). Utilizing X-chromosome inversions that contain modifications in the quantity and arrangement of the heterochromatic functions, Xh^abo and cr⁺, we have extended our investigations of abo's influence on XO male recovery and rDNA redundancy (Krider, Yedvobnick and Levine 1979).——XO males bearing In(1)sc^S1Lsc^4R or In(1)w^m4Lsc^4R are recovered twice as frequently as X chromosomes containing a single Xh region, implying that these inversions possess a duplication of Xh^abo. abo mutant females heterozygous for In(1)sc^S1Lsc^4R and wild-type X chromosomes generate XO progeny that do not contain elevated rDNA redundancies. XO males containing In(1)w^m4 exhibit male recoveries and rDNA elevations similar to those of males bearing a wild-type X chromosome, when both derive from a common abo/abo mother. Reciprocal crosses between In(1)w^m4 and Canton-S males to attached-X abo females show significant, though reduced, sex ratios in the absence of an rDNA effect. The observation that abo can elevate the rDNA redundancy of In(1)w^m4, a chromosome that does not compensate, suggests that abo and cr⁺ functions are not directly related.