scholarly journals POLYTENIZATION OF THE RIBOSOMAL GENES ON THE X AND Y CHROMOSOMES OF DROSOPHILA MELANOGASTER

Genetics ◽  
1982 ◽  
Vol 100 (3) ◽  
pp. 375-385 ◽  
Author(s):  
Sharyn A Endow

ABSTRACT It has previously been shown (Endow and Glover 1979), that polytenization of the ribosomal genes in D. melanogaster Ore-R X/Y cells and in hybrid X/X cells (Endow 1980) involves replication of genes predominantly from one of the cell's two nucleolus organizers. This analysis takes advantage of strain-specific differences in X and Y chromosome rDNA hybridization patterns detected using the Southern blotting technique. In this report, I extend the previous observations by examining polytene rDNA patterns in wild-type and hybrid X/Y cells. A dominance hierarchy for the X and Y chromosomes from three strains of D. melanogaster is presented and possible mechanisms of replicative dominance are discussed.

1986 ◽  
Vol 6 (4) ◽  
pp. 1023-1031
Author(s):  
R Terracol ◽  
N Prud'homme

In Drosophila melanogaster, the multiply repeated genes encoding 18S and 28S rRNA are located on the X and Y chromosomes. A large percentage of these repeats are interrupted in the 28S region by insertions of two types. We compared the restriction patterns from a subcloned wild-type Oregon R strain to those of spontaneous and ethyl methanesulfonate-induced bobbed mutants. Bobbed mutations were found to be deficiencies that modified the organization of the rDNA locus. Genes without insertions were deleted about twice as often as genes with type I insertions. Type II insertion genes were not decreased in number, except in the mutant having the most bobbed phenotype. Reversion to wild type was associated with an increase in gene copy number, affecting exclusively genes without insertions. One hypothesis which explains these results is the partial clustering of genes by type. The initial deletion could then be due either to an unequal crossover or to loss of material without exchange. Some of our findings indicated that deletion may be associated with an amplification phenomenon, the magnitude of which would be dependent on the amount of clustering of specific gene types at the locus.


1986 ◽  
Vol 6 (4) ◽  
pp. 1023-1031 ◽  
Author(s):  
R Terracol ◽  
N Prud'homme

In Drosophila melanogaster, the multiply repeated genes encoding 18S and 28S rRNA are located on the X and Y chromosomes. A large percentage of these repeats are interrupted in the 28S region by insertions of two types. We compared the restriction patterns from a subcloned wild-type Oregon R strain to those of spontaneous and ethyl methanesulfonate-induced bobbed mutants. Bobbed mutations were found to be deficiencies that modified the organization of the rDNA locus. Genes without insertions were deleted about twice as often as genes with type I insertions. Type II insertion genes were not decreased in number, except in the mutant having the most bobbed phenotype. Reversion to wild type was associated with an increase in gene copy number, affecting exclusively genes without insertions. One hypothesis which explains these results is the partial clustering of genes by type. The initial deletion could then be due either to an unequal crossover or to loss of material without exchange. Some of our findings indicated that deletion may be associated with an amplification phenomenon, the magnitude of which would be dependent on the amount of clustering of specific gene types at the locus.


1989 ◽  
Vol 54 (2) ◽  
pp. 127-135 ◽  
Author(s):  
Mohamed Makni ◽  
Mohamed Marrakchi ◽  
Nicole Prud'Homme

SummaryIn Drosophila melanogaster up to two thirds of the rDNA genes contain insertion sequences of two types in the 28S coding region. Comparison of the ribosomal insertion transcripts in the wild type and in two bobbed mutants reared at two temperatures showed that the level of type I transcripts is dependent on both the number of genes with type I insertions in the bobbed loci and the intensity of bobbed phenotype. Importantly, a long transcript of 8·7 kb hybridized to the ribosomal probe, the INS I probe and also to the restriction fragment of the rDNA downstream of the point of insertion was found in one bobbed mutant. This result and also those from sandwich hybridization indicate that some interrupted ribosomal genes are functional.


2001 ◽  
Vol 78 (2) ◽  
pp. 121-136 ◽  
Author(s):  
XULIO MASIDE ◽  
CAROLINA BARTOLOMÉ ◽  
STAVROULA ASSIMACOPOULOS ◽  
BRIAN CHARLESWORTH

Genomic copy numbers and the rates of movement of nine families of transposable elements (TEs) of Drosophila melanogaster were estimated in two sets of mutation accumulation lines: Beltsville and Madrid. Southern blotting was used to screen a large number of samples from both genetic backgrounds for TEs. The Madrid lines were also screened by in situ hybridization of TEs to polytene chromosomes, in order to obtain more detailed information about the behaviour of TEs in the euchromatin. Southern blotting data provided evidence of insertions and excision events in both genetic backgrounds, occurring at rates of approximately 10−5 and 10−6 per element copy per generation, respectively. In contrast, in situ data from the Madrid background presented a completely different picture, with no evidence for excisions, and a significantly higher rate of transposition (1·01×10−4). Direct comparison of the two data sets suggests that the Southern blotting technique had serious deficiencies: (i) it underestimated element abundance; (ii) it revealed less than 30% of the new insertions detected by in situ hybridization; and (iii) changes in the size of restriction fragments from any source were spuriously identified as simultaneous insertion–excision events. Our in situ data are consistent with previous studies, and suggest that selection is the main force controlling element spread by transposition.


1984 ◽  
Vol 43 (1) ◽  
pp. 93-98 ◽  
Author(s):  
Gioacchino Palumbo ◽  
Sharyn A. Endow ◽  
R. Scott Hawley

SUMMARYThe Ybb− chromosome has been previously shown to induce reduction of X chromosome ribosomal genes in Xbb / Ybb− or Xbb+ / Ybb− flies. These reduction events are presumed to arise as one of the two products of unequal sister chromatid exchanges, which result in both magnified and reduced products. Bobbed reduced chromosomes may also arise as products of other recombinative events such as intrachromatid deletions. In this report we use the Ybb− chromosome to reduce the number of ribosomal genes present on X chromosomes from two wild-type stocks under ‘non-magnifying’ conditions. We then show that the bobbed reduced X chromosomes show no detectable difference in their Southern blot rDNA patterns when compared with the parental wild-type X chromosome. This indicates that reduction events do not preferentially delete certain repeat classes, and supports previous observations that the repeat types present in the D. melanogaster X chromosome nucleolus organizer are not significantly clustered.


Genetics ◽  
1987 ◽  
Vol 116 (2) ◽  
pp. 241-251
Author(s):  
M R Gillings ◽  
R Frankham ◽  
J Speirs ◽  
M Whalley

ABSTRACT The nucleolus organizers on the X and Y chromosomes of Drosophila melanogaster are the sites of 200-250 tandemly repeated genes for ribosomal RNA. As there is no meiotic crossing over in male Drosophila, the X and Y chromosomal rDNA arrays should be evolutionarily independent, and therefore divergent. The rRNAs produced by X and Y are, however, very similar, if not identical. Molecular, genetic and cytological analyses of a series of X chromosome rDNA deletions (bb alleles) showed that they arose by unequal exchange through the nucleolus organizers of the X and Y chromosomes. Three separate exchange events generated compound X·YL chromosomes carrying mainly Y-specific rDNA. This led to the hypothesis that X-Y exchange is responsible for the coevolution of X and Y chromosomal rDNA. We have tested and confirmed several of the predictions of this hypothesis: First, X·YL chromosomes must be found in wild populations. We have found such a chromosome. Second, the X·YL chromosome must lose the YL arm, and/or be at a selective disadvantage to normal X+ chromosomes, to retain the normal morphology of the X chromosome. Six of seventeen sublines founded from homozygous X·YLbb stocks have become fixed for chromosomes with spontaneous loss of part or all of the appended YL. Third, rDNA variants on the X chromosome are expected to be clustered within the X+ nucleolus organizer, recently donated ("Y") forms being proximal, and X-specific forms distal. We present evidence for clustering of rRNA genes containing Type 1 insertions. Consequently, X-Y exchange is probably responsible for the coevolution of X and Y rDNA arrays.


Genetics ◽  
1986 ◽  
Vol 114 (3) ◽  
pp. 859-874
Author(s):  
Donald J Komma ◽  
Sharyn A Endow

ABSTRACT The genetically induced increase in the number of 18S + 28S ribosomal genes known as magnification has been reported to occur in male Drososphila but has not previously been observed in females. We now report that bobbed magnified (bbm) is recovered in progeny of female Drosophila carrying three different X bobbed (Xbb) chromosomes and the helper (see PDF) chromosome, which is a derivative of the Ybb- chromosome. Using different combinations of bb or bb+ X and Y chromosomes, we show that magnification in females requires both a deficiency in ribosomal genes and the presence of a Y chromosome: X/X females that are rDNA-deficient but do not carry a Y chromosome do not produce bbm; similarly, X/X/Y females that carry a Y chromosome but are not rDNA-deficient do not produce bbm. Bobbed magnified is only recovered from rDNA-deficient (see PDF), X/X/Y or (see PDF) females. We have also found that females carrying a ring Xbb chromosome together with the (see PDF) chromosome do not produce bbm, indicating that ring X chromosomes are inhibited to magnify in females as in males. We postulate that the requirement for a Y chromosome is due to sequences on the Y chromosome that regulate or encode factor(s) required for magnification, or, alternatively, affect pairing of the ribosomal genes.—These studies demonstrate that magnification is not limited to males but also occurs in females. Magnification in females is induced by rDNA-deficient conditions and the presence of a Y chromosome, and probably occurs by a mechanism similar to that in males.


Genetics ◽  
1984 ◽  
Vol 107 (4) ◽  
pp. 611-634 ◽  
Author(s):  
Kenneth J Livak

ABSTRACT The D. melanogaster DNA segment in the recombinant phage λDm2L1 contains at least eight copies of a tandemly repeated 1250-base pair (bp) sequence (henceforth called the 2L1 sequence). Testes from XO D. melanogaster males contain an abundant 800-base RNA species that is homologous to a 520-bp region of the 2L1 sequence. Blotting experiments show that the 2L1 sequence is repeated in the D. melanogaster genome and is present on both the X and Y chromosomes. With the use of X-Y translocations, the 2L1 sequence has been mapped to a region between kl-1 and kl-2 on the long arm of the Y chromosome. In Oregon-R wild type there are an estimated 200 copies of the 2L1 sequence on the X chromosome and probably at least 80 copies on the Y chromosome. In some other strains the repetition frequency on the Y chromosome is about the same, but the copy number on the X chromosome is much reduced. On the basis of the five strains investigated, there is a correlation between copy number of the 2L1 sequence on the X chromosome and the presence of a particular allele of the Stellate locus (Ste; 1-45.7). It seems that low copy number corresponds to Ste  + and high copy number corresponds to Ste. The Ste locus determines whether single or star-shaped crystals are observed in the spermatocytes of XO males. Studies using D. simulans and D. mauritiana DNA show that the 2L1 sequence is homologous to restriction fragments in male DNA but not female DNA, indicating that this sequence is present only on the Y chromosome in these two species. In DNA derived from D. erecta, D. teissieri and D. yakuba, there is very little, if any, hybridization with the 2L1 sequence probe.


Author(s):  
Karen S. Howard ◽  
H. D. Braymer ◽  
M. D. Socolofsky ◽  
S. A. Milligan

The recently isolated cell wall mutant slime X of Neurospora crassa was prepared for ultrastructural and morphological comparison with the cell wall mutant slime. The purpose of this article is to discuss the methods of preparation for TEM and SEM observations, as well as to make a preliminary comparison of the two mutants.TEM: Cells of the slime mutant were prepared for thin sectioning by the method of Bigger, et al. Slime X cells were prepared in the same manner with the following two exceptions: the cells were embedded in 3% agar prior to fixation and the buffered solutions contained 5% sucrose throughout the procedure.SEM: Two methods were used to prepare mutant and wild type Neurospora for the SEM. First, single colonies of mutant cells and small areas of wild type hyphae were cut from solid media and fixed with OSO4 vapors similar to the procedure used by Harris, et al. with one alteration. The cell-containing agar blocks were dehydrated by immersion in 2,2-dimethoxypropane (DMP).


Genetics ◽  
1980 ◽  
Vol 95 (3) ◽  
pp. 727-742 ◽  
Author(s):  
R Frankham ◽  
D A Briscoe ◽  
R K Nurthen

ABSTRACT Abdominal bristle selection lines (three high and three low) and controls were founded from a marked homozygous line to measure the contribution of sex-linked "mutations" to selection response. Two of the low lines exhibited a period of rapid response to selection in females, but not in males. There were corresponding changes in female variance, in heritabilities in females, in the sex ratio (a deficiency of females) and in fitness, as well as the appearance of a mutant phenotype in females of one line. All of these changes were due to bb alleles (partial deficiencies for the rRNA tandon) in the X chromosomes of these lines, while the Y chromosomes remained wild-type bb+. We argue that the bb alleles arose by unequal crossing over in the rRNA tandon.—A prediction of this hypothesis is that further changes can occur in the rRNA tandon as selection is continued. This has now been shown to occur.—Our minimum estimate of the rate of occurrence of changes at the rRNA tandon is 3 × 10-4. As this is substantially higher than conventional mutation rates, the questions of the mechanisms and rates of origin of new quantitative genetic variation require careful re-examination.


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