scholarly journals Rex and a suppressor of Rex are repeated neomorphic loci in the Drosophila melanogaster ribosomal DNA.

Genetics ◽  
1991 ◽  
Vol 129 (1) ◽  
pp. 119-132 ◽  
Author(s):  
R S Rasooly ◽  
L G Robbins
Keyword(s):  
Drosophila Melanogaster ◽  
Molecular Analysis ◽  
Ribosomal Dna ◽  
High Frequency ◽  
Intergenic Spacer ◽  
Mitotic Division ◽  
Dna Arrays ◽  
Single Chromosome ◽  
Target Chromosome ◽  
Common Laboratory

Abstract The Rex locus of Drosophila melanogaster induces a high frequency of mitotic exchange between two separated ribosomal DNA arrays on a single chromosome. The exchanges take place in the progeny of Rex mothers and occur very early, before the third mitotic division. A number of common laboratory stocks have also been found to carry dominant suppressors of Rex (Su(Rex)). Rex was mapped to the X centric heterochromatin, proximal to su(f), by genetic and molecular analysis of two spontaneous recombinants. Using deficiencies and duplications of the heterochromatin, both Rex and one Su(Rex) were shown to behave as neomorphs. Rex-induced exchange in a target chromosome bearing both Rex and Su(Rex) was then used to map these functions to the bb locus itself. Molecular analysis of the recombinants, using length variants of the ribosomal DNA intergenic spacer as genetic markers, mapped Su(Rex) and Rex within the bb locus and demonstrated that both are repeated elements.

scholarly journals DIFFERENTIATION OF DROSOPHILA CELLS LACKING RIBOSOMAL DNA, IN VITRO

Genetics ◽  
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.

Genetic and molecular analysis in the 70CD region of the third chromosome of Drosophila melanogaster

Gene ◽  
2000 ◽  
Vol 246 (1-2) ◽  
pp. 157-167 ◽  
Author(s):  
Thorsten Burmester ◽  
Mátyás Mink ◽  
Margit Pál ◽  
Zsolt Lászlóffy ◽  
Jean-Antoine Lepesant ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Molecular Analysis ◽  
The Third

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

Genetics ◽  
1996 ◽  
Vol 144 (1) ◽  
pp. 109-115 ◽  
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.

scholarly journals Competition Between Different Variegating Rearrangements for Limited Heterochromatic Factors in Drosophila melanogaster

Genetics ◽  
1997 ◽  
Vol 145 (4) ◽  
pp. 945-959
Author(s):  
Vett K Lloyd ◽  
Donald A Sinclair ◽  
Thomas A Grigliatti
Keyword(s):  
Drosophila Melanogaster ◽  
Chromosome Rearrangement ◽  
Position Effect ◽  
Position Effect Variegation ◽  
Euchromatic Region ◽  
Single Chromosome ◽  
Mosaic Expression ◽  
Effect Variegation ◽  
Protein Components

Position effect variegation (PEV) results from the juxtaposition of a euchromatic gene to heterochromatin. In its new position the gene is inactivated in some cells and not in others. This mosaic expression is consistent with variability in the spread of heterochromatin from cell to cell. As many components of heterochromatin are likely to be produced in limited amounts, the spread of heterochromatin into a normally euchromatic region should be accompanied by a concomitant loss or redistribution of the protein components from other heterochromatic regions. We have shown that this is the case by simultaneously monitoring variegation of a euchromatic and a heterochromatic gene associated with a single chromosome rearrangement. Secondly, if several heterochromatic regions of the genome share limited components of heterochromatin, then some variegating rearrangements should compete for these components. We have examined this hypothesis by testing flies with combinations of two or more different variegating rearrangements. Of the nine combinations of pairs of variegating rearrangements we studied, seven showed nonreciprocal interactions. These results imply that many components of heterochromatin are both shared and present in limited amounts and that they can transfer between chromosomal sites. Consequently, even nonvariegation portions of the genome will be disrupted by re-allocation of heterochromatic proteins associated with PEV. These results have implications for models of PEV.

Multigene Family of Ribosomal DNA in Drosophila melanogaster Reveals Contrasting Patterns of Homogenization for IGS and ITS Spacer Regions: A Possible Mechanism to Resolve This Paradox

Genetics ◽  
1998 ◽  
Vol 149 (1) ◽  
pp. 243-256 ◽  
Author(s):  
Carlos Polanco ◽  
Ana I González ◽  
Álvaro de la Fuente ◽  
Gabriel A Dover
Keyword(s):  
Drosophila Melanogaster ◽  
Concerted Evolution ◽  
Multigene Family ◽  
Natural Populations ◽  
Intergenic Spacer ◽  
Meiotic Pairing ◽  
Y Chromosomes ◽  
Mutation Distribution ◽  
Chromosome Exchanges

Abstract The multigene family of rDNA in Drosophila reveals high levels of within-species homogeneity and between-species diversity. This pattern of mutation distribution is known as concerted evolution and is considered to be due to a variety of genomic mechanisms of turnover (e.g., unequal crossing over and gene conversion) that underpin the process of molecular drive. The dynamics of spread of mutant repeats through a gene family, and ultimately through a sexual population, depends on the differences in rates of turnover within and between chromosomes. Our extensive molecular analysis of the intergenic spacer (IGS) and internal transcribed spacer (ITS) spacer regions within repetitive rDNA units, drawn from the same individuals in 10 natural populations of Drosophila melanogaster collected along a latitudinal cline on the east coast of Australia, indicates a relatively fast rate of X-Y and X-X interchromosomal exchanges of IGS length variants in agreement with a multilineage model of homogenization. In contrast, an X chromosome-restricted 24-bp deletion in the ITS spacers is indicative of the absence of X-Y chromosome exchanges for this region that is part of the same repetitive rDNA units. Hence, a single lineage model of homogenization, coupled to drift and/or selection, seems to be responsible for ITS concerted evolution. A single-stranded exchange mechanism is proposed to resolve this paradox, based on the role of the IGS region in meiotic pairing between X and Y chromosomes in D. melanogaster.

Sign in / Sign up

Export Citation Format

Share Document