Analysis of the autosomal mutation abo and its interaction with the ribosomal DNA or Drosophila melanogaster: the role of X-chromosome heterochromatin.

Abstract

The autosomal recessive, maternal-effect mutation abnormal oocyte (abo: 2-38) preferentially lowers the viability os 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, Xhabo and cr+, wer 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)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 baetween In(1)Wm4 and Canton-S males to attached-X abo females show significant, though reuduced, 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.