STUDIES ON THE MUTATION ABNORMAL OOCYTE AND ITS INTERACTION WITH THE RIBOSOMAL DNA OF DROSOPHILA MELANOGASTER

Hallie M Krider; Bryan I Levine

doi:10.1093/genetics/81.3.501

STUDIES ON THE MUTATION ABNORMAL OOCYTE AND ITS INTERACTION WITH THE RIBOSOMAL DNA OF DROSOPHILA MELANOGASTER

Genetics ◽

10.1093/genetics/81.3.501 ◽

1975 ◽

Vol 81 (3) ◽

pp. 501-513

Author(s):

Hallie M Krider ◽

Bryan I Levine

Keyword(s):

Drosophila Melanogaster ◽

Ribosomal Rna ◽

Ribosomal Dna ◽

Phenotypic Expression ◽

Functional Interaction ◽

Ribosomal Cistrons

ABSTRACT Sandler (1970) suggested that mutation, abnormal oocyte (abo:2–38), may influence the function of the ribosomal RNA cistrons. We have examined the abo mutation and its interaction with the ribosomal DNA of Drosophila melanogaster. We observed that the expression of the abo phenotype is unstable under the appropriate conditions, a behavior which paralleled changes in the phenotypic expression of bobbed mutations during the magnification of the ribosomal DNA. The change in the expression of the abo phenotype is correlated with an increase in the redundancy of the ribosomal cistrons, further suggesting a functional interaction of the abo and bobbed regions.

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DIFFERENTIATION OF DROSOPHILA CELLS LACKING RIBOSOMAL DNA, IN VITRO

Genetics ◽

10.1093/genetics/73.3.429 ◽

1973 ◽

Vol 73 (3) ◽

pp. 429-434

Author(s):

J James Donady ◽

R L Seecof ◽

M A Fox

Keyword(s):

Drosophila Melanogaster ◽

Ribosomal Rna ◽

Ribosomal Dna ◽

Rna Synthesis ◽

Wild Type ◽

Drosophila Cells

ABSTRACT Drosophila melanogaster embryos that lacked ribosomal DNA were obtained from appropriate crosses. Cells were taken from such embryos before overt differentiation took place and were cultured in vitro. These cells differentiated into neurons and myocytes with the same success as did wild-type controls. Therefore, ribosomal RNA synthesis is not necessary for the differentiation of neurons and myocytes in vitro.

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THE EFFECT OF ABO PHENOTYPIC EXPRESSION ON RIBOSOMAL DNA INSTABILITIES IN DROSOPHILA MELANOGASTER

Genetics ◽

10.1093/genetics/92.3.879 ◽

1979 ◽

Vol 92 (3) ◽

pp. 879-889

Author(s):

Hallie M Krider ◽

Barry Yedvobnick ◽

Bryan I Levine

Keyword(s):

Drosophila Melanogaster ◽

Ribosomal Dna ◽

Maternal Effect ◽

Phenotypic Expression ◽

Mutant Phenotype ◽

Y Chromosomes ◽

Homozygous Mutant ◽

Successive Generations ◽

Adult Drosophila

ABSTRACT The recessive maternal-effect mutation, abnormal oocyte (abo:2-38), reduces viability in the offspring of homozygous mutant females. Zygotes lacking specific heterochromatic segments of the X or Y chromosomes are most severely affected. We have shown that abo/abo lines can lose the capacity to express the mutant phenotype, and that elevated rDNA redundancies can be observed in such stocks (KRILIER and LEVINE 1975). In this study, we describe a microhybridization procedure that facilitates the measurement of rDNA redundancy, using a small number of adult Drosophila. We show that instability of the rDNA content persists in an abo/abo line after loss of the capacity to express the phenotype, and that changes in rDNA amounts occur between successive generations of the stock. Further, we show that the rDNA content of XO progeny from abo/abo females is elevated. The effect is directly correlated with the expression of the abo phenotype, and it is not observed in the XO progeny of abo heterozygous females or abo homozygotes from lines that do not show abo expression.

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Reciprocal recombination and the evolution of the ribosomal gene family of Drosophila melanogaster.

Genetics ◽

10.1093/genetics/122.3.617 ◽

1989 ◽

Vol 122 (3) ◽

pp. 617-624 ◽

Cited By ~ 1

Author(s):

S M Williams ◽

J A Kennison ◽

L G Robbins ◽

C Strobeck

Keyword(s):

Drosophila Melanogaster ◽

Gene Family ◽

Ribosomal Rna ◽

Natural Populations ◽

Ribosomal Gene ◽

Gene Region ◽

Ribosomal Rna Gene ◽

Reciprocal Recombination ◽

Y Chromosomes ◽

Length Polymorphisms

Abstract The role of reciprocal recombination in the coevolution of the ribosomal RNA gene family on the X and Y chromosomes of Drosophila melanogaster was assessed by determining the frequency and nature of such exchange. In order to detect exchange events within the ribosomal RNA gene family, both flanking markers and restriction fragment length polymorphisms within the tandemly repeated gene family were used. The vast majority of crossovers between flanking markers were within the ribosomal RNA gene region, indicating that this region is a hotspot for heterochromatic recombination. The frequency of crossovers within the ribosomal RNA gene region was approximately 10(-4) in both X/X and X/Y individuals. In conjunction with published X chromosome-specific and Y chromosome-specific sequences and restriction patterns, the data indicate that reciprocal recombination alone cannot be responsible for the observed variation in natural populations.

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Specificity of Chromosome Damage Caused by the Rex Element of Drosophila melanogaster

Genetics ◽

10.1093/genetics/144.1.109 ◽

1996 ◽

Vol 144 (1) ◽

pp. 109-115 ◽

Cited By ~ 1

Author(s):

Leonard G Robbins

Keyword(s):

Drosophila Melanogaster ◽

Early Development ◽

X Chromosome ◽

Ribosomal Rna ◽

Chromosome Damage ◽

Genetic Element ◽

Single Chromosome ◽

Experimental Cross ◽

Rdna Array ◽

Early Embryos

Abstract Rex is a multicopy genetic element that maps within an X-linked ribosomal RNA gene (rDNA) array of D. melanogaster. Acting maternally, Rex causes recombination between rDNA arrays in a few percent of early embryos. With target chromosomes that contain two rDNA arrays, the exchanges either delete all of the material between the two arrays or invert the entire intervening chromosomal segment. About a third of the embryos produced by Rex homozygotes have cytologically visible chromosome damage, nearly always involving a single chromosome. Most of these embryos die during early development, displaying a characteristic apoptosis-like phenotype. An experiment that tests whether the cytologically visible damage is rDNA-specific is reported here. In this experiment, females heterozygous for Rex and an rDNA-deficient X chromosome were crossed to males of two genotypes. Some of the progeny from the experimental cross entirely lacked rDNA, while all of the progeny from the control cross had at least one rDNA array. A significantly lower frequency of early-lethal embryos in the experimental cross, proportionate to the fraction of rDNA-deficient embryos, demonstrates that Rex preferentially damages rDNA.

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Identical 3′-terminal octanucleotide sequence in 18S ribosomal ribonucleic acid from different eukaryotes. A proposed role for this sequence in the recognition of terminator codons

Biochemical Journal ◽

10.1042/bj1410609a ◽

1974 ◽

Vol 141 (3) ◽

pp. 609-615 ◽

Cited By ~ 74

Author(s):

John Shine ◽

Lynn Dalgarno

Keyword(s):

Saccharomyces Cerevisiae ◽

Protein Synthesis ◽

Drosophila Melanogaster ◽

Ribosomal Rna ◽

Ribonucleic Acid ◽

18S Rrna ◽

Base Sequence ◽

Terminal Sequence ◽

Ribosomal Ribonucleic Acid ◽

Rrna Species

The 3′-terminal sequence of 18S ribosomal RNA from Drosophila melanogaster and Saccharomyces cerevisiae was determined by stepwise degradation from the 3′-terminus and labelling with [3H]isoniazid. The sequence G-A-U-C-A-U-U-AOH was found at the 3′-terminus of both 18S rRNA species. Less extensive data for 18S RNA from a number of other eukaryotes are consistent with the same 3′-terminal sequence, and an identical sequence has previously been reported for the 3′-end of rabbit reticulocyte 18S rRNA (Hunt, 1970). These results suggest that the base sequence in this region is strongly conserved and may be identical in all eukaryotes. As the 3′-terminal hexanucleotide is complementary to eukaryotic terminator codons we discuss the possibility that the 3′-end of 18S rRNA may have a direct base-pairing role in the termination of protein synthesis.

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Effects of permissible maximum-contamination levels of VOC mixture in water on total DNA, antioxidant gene expression, and sequences of ribosomal DNA of Drosophila melanogaster

Environmental Science and Pollution Research ◽

10.1007/s11356-015-4741-y ◽

2015 ◽

Vol 22 (20) ◽

pp. 15610-15620 ◽

Cited By ~ 5

Author(s):

Oguzhan Doganlar ◽

Zeynep Banu Doganlar ◽

Kiymet Tabakcioglu

Keyword(s):

Gene Expression ◽

Drosophila Melanogaster ◽

Ribosomal Dna ◽

Antioxidant Gene ◽

Total Dna ◽

Antioxidant Gene Expression ◽

Contamination Levels

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Rex-induced recombination implies bipolar organization of the ribosomal RNA genes of Drosophila melanogaster.

Genetics ◽

10.1093/genetics/120.4.1053 ◽

1988 ◽

Vol 120 (4) ◽

pp. 1053-1059

Author(s):

L G Robbins ◽

E E Swanson

Keyword(s):

Drosophila Melanogaster ◽

Ribosomal Rna ◽

Mitotic Recombination ◽

Ribosomal Rna Genes ◽

The Other ◽

Other Orientation ◽

Rna Genes ◽

Nucleolus Organizers

Abstract Rex-induced mitotic recombination was used to determine whether nucleolus organizers can pair in both inverted and noninverted orientations. Two target chromosomes, each duplicated for the rDNA region, were exposed to maternal Rex activity. Recombination in one orientation should yield deletion of the material between the two nucleolus organizers, recombination in the other orientation should yield inversion of the same material. Both products were recovered from both target chromosomes. The generality of using Rex-mediated recombination for analysis of the rDNA is considered.

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Sexual Selection Does Not Increase the Rate of Compensatory Adaptation to a Mutation Influencing a Secondary Sexual Trait in Drosophila melanogaster

G3 Genes|Genome|Genetics ◽

10.1534/g3.119.400934 ◽

2020 ◽

Vol 10 (5) ◽

pp. 1541-1551

Author(s):

Christopher H. Chandler ◽

Anna Mammel ◽

Ian Dworkin

Keyword(s):

Drosophila Melanogaster ◽

Sexual Selection ◽

Natural Selection ◽

Spontaneous Mutation ◽

Phenotypic Expression ◽

Theoretical Work ◽

Phenotypic Suppression ◽

Compensatory Adaptation ◽

Deleterious Alleles ◽

Sex Comb

Theoretical work predicts that sexual selection can enhance natural selection, increasing the rate of adaptation to new environments and helping purge harmful mutations. While some experiments support these predictions, remarkably little work has addressed the role of sexual selection on compensatory adaptation—populations’ ability to compensate for the costs of deleterious alleles that are already present. We tested whether sexual selection, as well as the degree of standing genetic variation, affect the rate of compensatory evolution via phenotypic suppression in experimental populations of Drosophila melanogaster. These populations were fixed for a spontaneous mutation causing mild abnormalities in the male sex comb, a structure important for mating success. We fine-mapped this mutation to an ∼85 kb region on the X chromosome containing three candidate genes, showed that the mutation is deleterious, and that its phenotypic expression and penetrance vary by genetic background. We then performed experimental evolution, including a treatment where opportunity for mate choice was limited by experimentally enforced monogamy. Although evolved populations did show some phenotypic suppression of the morphological abnormalities in the sex comb, the amount of suppression did not depend on the opportunity for sexual selection. Sexual selection, therefore, may not always enhance natural selection; instead, the interaction between these two forces may depend on additional factors.

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