Chromosome damage and early developmental arrest caused by the Rex element of Drosophila melanogaster (original) (raw)
Related papers
Specificity of chromosome damage caused by the Rex element of Drosophila melanogaster
Genetics, 1996
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...
Genetically induced mitotic exchange in the heterochromatin of Drosophila melanogaster
Genetics
Multiple copies of the 18S and 28S ribosomal RNA cistrons are present in both the X and Y chromosomes of Drosophila melanogaster. Data are presented here that identify a locus, Rex, that causes exchange-like events between duplicated ribosomal complexes at the ends of an attached-XY chromosome. Rex: (1) is close to or in the basal heterochromatin of the X chromosome; (2) is semidominant and (its effect) is temperature sensitive; (3) acts maternally; and (4) affects behavior of paternally derived attached-XY chromosomes shortly after fertilization. Though, at this point, the existence of Rex is known only from its effects on behavior of a particular compound chromosome, it presents intriguing possibilities for understanding regulation of chromosome behavior and organization of the ribosomal cistrons.
Genetics, 1991
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 sum, 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.
Genetics, 1988
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.
Proceedings of the National Academy of Sciences, 1981
Drosophila melanogaster females homozygous for the abnormal oocyte mutation produce a large excess of female offspring when crossed with XY/0 males. After several generations in abo homozygous stock, this maternal effect is no longer observed. The disappearance of the abo phenotype is coupled with an increase in the amount of DNA coding for rRNA (rDNA). We have used restriction endonuclease analysis of total DNA extracted from adult females and from single female larval brains to investigate the molecular organization of rDNA before and after the loss of abo phenotype. The rDNA increase is associated with variations of the restriction pattern of the nontranscribed spacer, probably due to a selective increase of rDNA repeats.
1993
We have cloned the three rows (thr) gene, by a combination of chromosome microdissection and P element tagging. We describe phenotypes of embryos homozygous for mutations at the thr locus. Maternal mRNA and protein appear to be sufficient to allow 14 rounds of mitosis in embryos homozygous for thr mutations. However, a small percentage of cells in syncytial blastoderm stage thr embryos sink into the interior of the embryo as if they have failed to divide properly. Following cellularisation all cells complete mitosis 14 normally. All cells become delayed at mitosis 15 with their chromosomes remaining aligned on the spindle in a metaphase-like configuration, even though both cyclins A and B have both been degraded. As cyclin B degradation occurs at the metaphase-anaphase transition, subsequent to the microtubule integrity checkpoint, the delay induced by mutations at the thr locus defines a later point in mitotic progression. Chromosomes in the cells of thr embryos do not undertake anaphase separation, but remain at the metaphase plate. Subsequently they decondense. A subset of nuclei go on to replicate their DNA but there is no further mitotic division.
Genetics, 1986
The abnormal abdomen (aa) syndrome in Drosophila mercatorum is controlled by two major X-linked genetic elements. We have previously shown that the major X-linked element of aa is associated with the presence of large inserts in the 28S gene of the ribosomal RNA (rDNA) genes. We show that, in polytene tissue of wild-type D. mercatorum, the uninterrupted rDNA repeats are overreplicated relative to interrupted repeats. Uninterrupted rDNA repeats are also overreplicated in polytene tissue of hybrid larval offspring from wild-type and aa parents. This overreplication of uninterrupted repeats is not observed in diploid tissues of wild-type hybrids (of wild-type and aa parents) and homozygous aa larvae or in polytene tissue of aa larvae. Furthermore, molecular analysis of an aa line that has reverted to the wild type indicates that the reversion phenomenon is associated with the ability to overreplicate uninterrupted rDNA repeats in polytene tissues. The patterns of differential replication of rDNA genes in wild-type hybrids and aa larvae of D. mercatorum offer a possible mechanism for the tissue-specific control of the aa phenotype and suggest that the molecular basis for the second X-linked genetic element of aa is involved in the control of differential replication in polytene tissues.
Proceedings of the National Academy of Sciences, 1979
Eight X-linked recombination-defective meiotic mutants (representing five loci) and 12 X-linked mutagen-sensitive mutants (representing seven loci) of Drosophila melanogaster have been examined cytologically in neuroblast metaphases for their effects on the frequencies and types of spontaneous chromosome aberrations. Twelve mutants, representing five loci, significantly increase the frequency of chromosomal aberrations. The mutants at these five loci, however, differ markedly both in the types of aberrations produced and the localization of their effects along the chromosome. According to these criteria, the mutants can be assigned to four groups: (i) mutants producing almost exclusively chromatid breaks in both euchromatin and heterochromatin; (ii) mutants producing chromatid and isochromatid breaks in both euchromatin and heterochromatin; (iii) mutants producing chromatid mutants producing chromatid and isochromatid breaks clustered in the heterochromatin.
Genetics, 1991
The euchromatic maternal-effect mutation abnormal oocyte (abo), of Drosophila melanogaster interacts with regions of heterochromatin known as ABO, which reside on the X, Y and second chromosomes. Here, we show that survival of progeny from abo females depends in part upon the maternal dosage of ABO heterochromatin. A comparison was made of the recovery of genotypically identical progeny from abo mothers bearing sex chromosomes of various ABO contents. The results show that the recovery of daughters was decreased if mothers were ABO-/ABO-. However, no decrease was observed if mothers were ABO+/ABO-. In addition, the survival of daughters was greater when they received an ABO-X chromosome from an ABO-/ABO+ mother rather than the father. We suggest that these results reflect a complementation or interaction between the ABO-deficient X and the ABO heterochromatin in the maternal genome. This proposed interaction could occur early in oogenesis in the mother or prior to completion of meio...