Meiotic pairing sites and genes involved in segregation of the X and Y chromosomes of Drosophila melanogaster

2000 ◽  
pp. 139-152 ◽  
Author(s):  
Bruce D. McKee ◽  
Chia-sin Hong ◽  
Siuk Yoo
Keyword(s):  
Drosophila Melanogaster ◽  
Meiotic Pairing ◽  
Y Chromosomes

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.

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

Genetics ◽  
1989 ◽  
Vol 122 (3) ◽  
pp. 617-624 ◽  
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.

Differential elimination of rDNA genes in bobbed mutants of Drosophila melanogaster

1986 ◽  
Vol 6 (4) ◽  
pp. 1023-1031
Author(s):  
R Terracol ◽  
N Prud'homme
Keyword(s):  
Drosophila Melanogaster ◽  
Gene Copy Number ◽  
Rdna Locus ◽  
Gene Copy ◽  
Specific Gene ◽  
Type I ◽  
28S Rrna ◽  
Wild Type ◽  
Y Chromosomes ◽  
Genes Encoding

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.

scholarly journals Differential elimination of rDNA genes in bobbed mutants of Drosophila melanogaster.

1986 ◽  
Vol 6 (4) ◽  
pp. 1023-1031 ◽  
Author(s):  
R Terracol ◽  
N Prud'homme
Keyword(s):  
Drosophila Melanogaster ◽  
Gene Copy Number ◽  
Rdna Locus ◽  
Gene Copy ◽  
Specific Gene ◽  
Type I ◽  
28S Rrna ◽  
Wild Type ◽  
Y Chromosomes ◽  
Genes Encoding

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.

scholarly journals The cytogenetic boundaries of the rDNA region within heterochromatin of the X chromosome of Drosophila melanogaster and their relation to male meiotic pairing sites

1982 ◽  
Vol 39 (2) ◽  
pp. 149-156 ◽  
Author(s):  
R. Appels ◽  
A. J. Hilliker
Keyword(s):  
Drosophila Melanogaster ◽  
Rrna Genes ◽  
Type I ◽  
28S Rrna ◽  
Meiotic Pairing ◽  
Coding Region ◽  
Intervening Sequences ◽  
Single Region ◽  
Rrna Sequences

SummaryThe proximal breakpoints of the inversion chromosomes In(1)ωm4 and In(1)m51b were shown, by in situ hybridization, to define the boundaries of the ribosomal DNA region located within the X chromosome heterochromatin (Xh). We estimate that at least 95% of the rDNA is located between the In(1)ωm4 and In(1)ωm51b proximal breakpoints. In contrast only 60–70% of the Type I intervening sequences located in Xh are located between these breakpoints. The Type I intervening sequences in the rDNA region occur as inserts in the 28S rRNA sequences while the remainder of the sequences are distal to the In(1)ωm4 breakpoint and not associated with rRNA genes.The regions of Xh which contain rDNA and Type I intervening sequences were related to regions shown by Cooper (1964) to contribute to meiotic pairing between the X and Y chromosomes in male Drosophila. We demonstrate that the rRNA coding region contributes to X / Y pairing. However, no single region of Xh is required for fidelity of male meiotic pairing of the sex chromosomes.

scholarly journals MALE-STERILIZING INTERACTIONS BETWEEN DUPLICATIONS AND DEFICIENCIES FOR PROXIMAL X-CHROMOSOME MATERIAL IN DROSOPHILA MELANOGASTER

Genetics ◽  
1981 ◽  
Vol 99 (1) ◽  
pp. 49-64
Author(s):  
Rezaur Rahman ◽  
Dan L Lindsley
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Male Fertility ◽  
Primary Spermatocyte ◽  
Single Factor ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
Y Chromosomes ◽  
Chromosome Material

ABSTRACT The genetic limits of sixty-four deficiencies in the vicinity of the euchromatic-heterochromatic junction of the X chromosome were mapped with respect to a number of proximal recessive lethal mutations. They were also tested for male fertility in combination with three Y chromosomes carrying different amounts of proximal X-chromosome-derived material (BSYy+, y+Ymal126 and y  +  Ymal  +). All deficiencies that did not include the locus of bb and a few that did were male-fertile in all male-viable Df(1)/Dp(1;Y) combinations. Nineteen bb deficiencies fell into six different classes by virtue of their male-fertility phenotypes when combined with the duplicated Y chromosomes. The six categories of deficiencies are consistent with a formalism that invokes three factors or regions at the base of the X, one distal and two proximal to bb, which bind a substance critical for precocious inactivation of the X chromosome in the primary spermatocyte. Free duplications carrying these regions or factors compete for the substance in such a way that, in the presence of such duplications, proximally deficient X chromosomes are unable to command sufficient substance for proper control of X-chromosome gene activity preparatory to spermatogenesis. We conclude that there is no single factor at the base of the X that is required for the fertility of males whose genotype is otherwise normal.

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