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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 chromatin (SANDLER 1970, 1977; PARRY and SANDLER 1974). Utilizing X-chromosome inversions that contain modifications in the quantity and arrangement of the heterochromatic functions, Xhabo and cr  +, we have extended our investigations of nbo's influence on XO male recovery and rDNA redundancy (KRIDER,YEDVOBNICK and LEVINE 1979).——XO males bearing In(1)scs1Lsc4R or In(1)wm4Lsc4R are recovered twice as frequently as X chromosomes containing a single Xh region, implying that these inversions possess a duplication of Xhabo. abo mutant females heterozygous for In(1)scs1Lsc4R and wild-type X chromosomes generate XO progeny that do not contain elevated rDNA redundancies. XO males containing In(1)wm4 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)wm4 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)wm4, a chromosome that does not compensate, suggests that abo and cr+ functions are not directly related.

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