These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Analysis of the autosomal mutation abo and its interaction with the ribosomal DNA or Drosophila melanogaster: the role of X-chromosome heterochromatin. Author: Yedvobnick B, Krider HM, Levine BI. Journal: Genetics; 1980 Jul; 95(3):661-72. PubMed ID: 6777245. 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.[Abstract] [Full Text] [Related] [New Search]