Differential magnification of rDNA gene types in bobbed mutants of Drosophila melanogaster

Terracol, Régine

doi:10.1007/bf00330438

Cited by 14 publications

(11 citation statements)

References 47 publications

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“…We do not know why ample rDNA would not supply sufficient rRNA, but consider that the cistrons may have been damaged during I-CreI-induced damage, magnification may have occurred using inactive R1-or R2-interrupted cistrons as template, the copies on the chromosome may be epigenetically inactive, or some other explanation may account for this (Terracol and Prud'Homme 1981;Terracol 1987).…”

Section: Ddctmentioning

confidence: 99%

“…Some revertants of chromosome Y10B, rDNA lÀ481 did not show a large magnification. This may be due to this chromosome being on the threshold of lethal to bobbed, so even small magnifications would be uncovered by this assay, or because the Y10B, rDNA lÀ481-revertant chromosomes possess a different active-to-inactive ratio of rDNA cistrons than does the original Y10B, rDNA lÀ481 chromosome (Terracoland Prud'Homme 1981, 1987Terracol 1987;Ashburner et al 2005).…”

Section: Ddctmentioning

confidence: 99%

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Expression of I-CreI Endonuclease Generates Deletions Within the rDNA of Drosophila

Paredes

Maggert

2009

Genetics

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The rDNA arrays in Drosophila contain the cis-acting nucleolus organizer regions responsible for forming the nucleolus and the genes for the 28S, 18S, and 5.8S/2S RNA components of the ribosomes and so serve a central role in protein synthesis. Mutations or alterations that affect the nucleolus organizer region have pleiotropic effects on genome regulation and development and may play a role in genomewide phenomena such as aging and cancer. We demonstrate a method to create an allelic series of graded deletions in the Drosophila Y-linked rDNA of otherwise isogenic chromosomes, quantify the size of the deletions using real-time PCR, and monitor magnification of the rDNA arrays as their functions are restored. We use this series to define the thresholds of Y-linked rDNA required for sufficient protein translation, as well as establish the rate of Y-linked rDNA magnification in Drosophila. Finally, we show that I-CreI expression can revert rDNA deletion phenotypes, suggesting that double-strand breaks are sufficient to induce rDNA magnification.

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Section: Ddctmentioning

confidence: 99%

Section: Ddctmentioning

confidence: 99%

Expression of I-CreI Endonuclease Generates Deletions Within the rDNA of Drosophila

Paredes

Maggert

2009

Genetics

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“…According to the model of clonal over-replication in situ (Terracol 1987), specific rDNA units amplify intra-chromosomally up to 3.5-fold, lengthening the rDNA array. According to the model of extra-chromosomal over-replication (Ritossa et al 1971;Ritossa 1972;Ritossa 1976) (Graziani et al 1977), neither replicative model is compatible with the observed inability of ring chromosomes to undergo magnification (Coen et al1982;Indik and Tartof 1980;Tartof and David 1976;Yagura et al 1979).…”

Section: Additional Explanatory Detailmentioning

confidence: 99%

“…In the 'clonal chromosome replication' model (Terracol 1987) a cluster of adjacent rDNA copies, or a single rDNA unit, amplifies in situ through a single duplication or reiterated replications. The copy-number increase depends on both the number of replications and the number of rDNA repeats in the sequence that is copied.…”

mentioning

confidence: 99%

Ribosomal DNA Organization Before and After Magnification in Drosophila melanogaster

et al. 2012

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In all eukaryotes, the ribosomal RNA genes are stably inherited redundant elements. In Drosophila melanogaster, the presence of a Ybb 2 chromosome in males, or the maternal presence of the Ribosomal exchange (Rex) element, induces magnification: a heritable increase of rDNA copy number. To date, several alternative classes of mechanisms have been proposed for magnification: in situ replication or extra-chromosomal replication, either of which might act on short or extended strings of rDNA units, or unequal sister chromatid exchange. To eliminate some of these hypotheses, none of which has been clearly proven, we examined molecularvariant composition and compared genetic maps of the rDNA in the bb 2 mutant and in some magnified bb + alleles. The genetic markers used are molecular-length variants of IGS sequences and of R1 and R2 mobile elements present in many 28S sequences. Direct comparison of PCR products does not reveal any particularly intensified electrophoretic bands in magnified alleles compared to the nonmagnified bb 2 allele. Hence, the increase of rDNA copy number is diluted among multiple variants. We can therefore reject mechanisms of magnification based on multiple rounds of replication of short strings. Moreover, we find no changes of marker order when pre-and postmagnification maps are compared. Thus, we can further restrict the possible mechanisms to two: replication in situ of an extended string of rDNA units or unequal exchange between sister chromatids. IN eukaryotes the 18S, 5.8/2S, and 28S rDNAs are contained in the same transcription unit, and many (hundreds to thousands) of rDNA transcription units are organized in clusters located in one or a few chromosomes. In Drosophila melanogaster each rDNA copy, Figure 1, is about 8 kb long and, in addition to the coding sequences, includes an external transcribed spacer (ETS) upstream of the 18S sequence and two internal transcribed spacers (ITS-1 and ITS-2) located between the 18S and 5.8/2S sequences and the 5.8/ 2S and 28S sequences, respectively (Wellauer and Dawid 1977;Tautz et al. 1988). Contiguous rDNA units are separated by intergenic spacers (IGS). The variable length of the IGS can reach 10-11 kb because it contains diverse numbers of 95-, 330-, and 240-bp-long subrepeats (Pellegrini et al. 1977;Long and Dawid 1980;Simeone et al. 1985;Tautz et al. 1987;Glover 1991).The genome of wild-type D. melanogaster has two similar rDNA clusters. A 2800-kb cluster is in the pericentromeric heterochromatin of the X chromosome long arm. The other, 2200 kb long, is located at the base of the short arm of the Y chromosome (Ritossa 1976;Polanco et al. 1998). Because of their heterochromatic locations, meiotic recombination in the rDNA arrays is rare. Both clusters consist of about 200-250 rDNA units (Tartof 1971;Tautz et al. 1988), in both head-totail (tandem) and head-to-head (reversed) orientations, with a variable number of orientation switches in different stocks (Robbins and Swanson 1988). Cytologically, the rDNA cluster corresponds to the n...

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“…Ribosomal DNA evolution in Drosophila has been essentially studied with 'bobbed' mutants because of the possibility of following variations in the amount of functional rDNA by variation of the intensity of the 'bobbed' phenotype, particularly in the case of the magnification phenomenon (Ritossa, 1972;Locker & Prud 'homme, 1973;Tartof, 1973;Terracol & Prud'homme, 1986;Terracol, 1987). This method needs particular crosses and genotypes with a very low level of active ribosomal units (Tartof, 1974;Hawley & Tartof, 1985;Marcus et al 1986) and cannot be used to follow variations in the rDNA amount in wild-type flies.…”

Section: Introductionmentioning

confidence: 99%

X chromosome variations of Bacillus thuringiensis supernatant resistance and ribosomal DNA content in Drosophila melanogaster wild-type Oregon R lines

Paumard-Rigal

Rosenberg-Bourgin

1993

Heredity

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We have used the supernatant of Bacillus thuringiensis cultures to follow variations of the ribosomal DNA content in a wild-type Oregon R line of Drosophila melanogaster. These variations are revealed by differences in the degree of resistance to the lethal effect of the supernatant added in the culture medium. Different X chromosomes, all originated from the same X chromosome, confer different degrees of resistance. Increases and reductions in the number of the X ribosomal DNA transcriptional units have been found and are correlated with variations in the degree of supernatant resistance. However, no significant variations in X rDNA content were observed between the initial line and this line tested 20 generations later. These results show that the X rDNA is subjected to frequent modifications that must be essentially complementary and thus originate from reciprocal molecular events. Variations of resistance have been observed in the absence of recombination between homologous chromosomes; this is in agreement with the hypothesis that unequal recombinations between sister chromatids are largely involved in the variations of the X ribosomal DNA in Oregon R wild-type strains.

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Differential magnification of rDNA gene types in bobbed mutants of Drosophila melanogaster

Cited by 14 publications

References 47 publications

Expression of I-CreI Endonuclease Generates Deletions Within the rDNA of Drosophila

Expression of I-CreI Endonuclease Generates Deletions Within the rDNA of Drosophila

Ribosomal DNA Organization Before and After Magnification in Drosophila melanogaster

X chromosome variations of Bacillus thuringiensis supernatant resistance and ribosomal DNA content in Drosophila melanogaster wild-type Oregon R lines

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