INTERACTING EFFECTS OF SODIUM MONOHYDROGENARSENATE AND SELENOCYSTINE ON CROSSING OVER IN DROSOPHILA MELANOGASTER

1969 ◽  
Vol 11 (3) ◽  
pp. 677-688 ◽  
Author(s):  
G. W. R. Walker ◽  
Amelia M. Bradley
Keyword(s):  
Drosophila Melanogaster ◽  
Marked Effect ◽  
Double Exchange ◽  
Crossing Over ◽  
Chromosomal Protein ◽  
General Effect ◽  
Initial Region ◽  
Concentration Region ◽  
Single Exchange ◽  
Concentration Curves

Drosophila melanogaster females of X chromosome genotype y cυ υ f/++++ were reared as larvae on 16-treatment media, representing the various combinations of four concentrations each of sodium monohydrogen arsenate and selenocystine (concentrations were 0, 2, 10 and 50 μM). The fourfold replication of selenocystine curves at four arsenate levels confirmed the existence of a selenocystine effect indicated earlier (Ting and Walker, 1969), as well as the segmental differences in and reversibility of the effect. A marked "sink" in crossing over was found both in total single exchange chromosomes and total double exchange chromosomes at 10 μM selenocystine and peaks in single exchange for segment 1 and for the whole chromosome and for double exchange for segments 1 and 2 at 2 μM were noted. In addition, arsenate was shown to exert a marked effect in the selenocystine-concentration region 0-10 μM; crossover frequencies were quite consistently increased by arsenate treatment at zero selenocystine, and considerable differences were introduced into the initial region (0-2 μM) of selenocystine segmental curves by arsenate treatment, with resultant increases in total single exchange and double exchange curves. In addition, the general effect was noted in arsenate-concentration curves, at 2 and 10 μM As: a drop in double exchange and an increase in single exchanges. Hypotheses are presented relating these effects to possibilities regarding the incorporation of selenocystine and arsenate into chromosomal protein and DNA respectively.

THE EFFECTS OF URETHANE, SODIUM MONOHYDROGEN ARSENATE AND SELENOCYSTINE ON CROSSING-OVER IN DROSOPHILA MELANOGASTER

1975 ◽  
Vol 17 (1) ◽  
pp. 55-66 ◽  
Author(s):  
Zia U. Ahmed ◽  
G. W. R. Walker
Keyword(s):  
Drosophila Melanogaster ◽  
Double Exchange ◽  
Chemical Treatments ◽  
Repair Enzymes ◽  
Recombination Repair ◽  
Single Exchange ◽  
Natural Recombination ◽  
Pupal Mortality ◽  
Male Specific ◽  
Concentration Curves

The effects of 0–25 mM urethane, 0–50 μM selenocystine and 0–100 μM sodium monohydrogen arsenate on marker-exchange frequencies have been studied along a region of the X chromosome of Drosophila melanogaster marked by y, cv, v and f. Clear and consistent effects seen in concentration curves were usually but not always found significant in analyses of variance. Urethane concentration curves rose to a higher level at 0.5 to 3 mM and dropped to control levels between 10 and 25 mM. It is proposed that this reversibility was due to a competition between two categories of lesions mimicking natural recombination sites, those on unpaired regions of the chromosome competing with those on already paired regions for recombination-repair enzymes. Selenocystine affected exchange frequencies mainly toward the ends of the unmarked region, especially y – cv, negatively from 2 to 10 μM and positively above 10 μM. These effects are interpreted as being mediated by selenocystine control over restriction of synaptic pairing to terminal regions, especially y – cv. Interactions between urethane and selenocystine in two-chemical treatments satisfactorily support the above explanations for both the urethane and selenocystine effects. Sodium monohydrogen arsenate effects, tentatively attributed to the arsenate ion, differed markedly from those of the other chemicals: "arsenate" concentration curves for single-exchange classes tended to be broadly convex and those for double-exchange classes concave, while interactions with urethane tended to be synergistic or neutral except in one exchange class (that for single exchange in y – cv). No satisfactory explanation of the arsenate effects has yet been found. At 25 mM only, urethane caused male-specific, 95% pupal mortality.

scholarly journals CENTROMERIC EFFECT ON THE DEGREE OF NONRANDOM DISJUNCTION IN THE FEMALE DROSOPHILA MELANOGASTER

Genetics ◽  
1977 ◽  
Vol 86 (1) ◽  
pp. 121-132
Author(s):  
Hon Fong Louie Mark ◽  
Stanley Zimmering
Keyword(s):  
Drosophila Melanogaster ◽  
X Chromosome ◽  
Negative Correlation ◽  
Sex Chromosome ◽  
Double Exchange ◽  
Distal Region ◽  
Unexpected Result ◽  
Preferential Segregation ◽  
Single Exchange ◽  
Time Required

ABSTRACT From crosses of females possessing a heteromorphic X-chromosome bivalent, FR1/+, the shorter crossover products were recovered on the average more frequently than the longer reciprocals as predicted by Novitski's (1951) hypothesis of nonrandom disjunction (NRD). The present study stemmed from an unexpected result of these crosses. Evidence for a centromeric effect on NRD was obtained, suggested by a negative correlation between the degree of NRD, c, and the distance between the region of exchange and the centromere as inferred from SET's (single exchange tetrads). Studies on sex chromosome systems other than FR1 confirmed these results. An analogous centromeric effect on preferential segregation had been clearly demonstrated in maize (Kikudome 1958, 1959; Rhoades and Dempsey 1966). However, prior to the present investigation, no such effect of the centromere on NRD in Drosophila had been described, although reanalysis of part of the data of Novitski (1951) and Novitski and Sandler (1956) suggests some evidence of a seriation of increasing c values extending from the most distal region of the chromosome toward the centromere. A suggestion that the effect in Drosophila may be related in some way to the time required for chiasma terminalization, i.e., those terminalizing earlier (distally located crossovers) permitting more random disjunction of the chromatids from the asymmetric dyad and those terminalizing later, progressively less random, is considered and rejected since in general the expected pattern of c values for the various double exchange tetrads (DET's) is inconsistent with that prediction and provides evidence suggesting the possibility of reversals, in part, of c values obtained for SET's.

scholarly journals EXTRACHROMOSOMAL ELEMENT DELTA IN DROSOPHILA MELANOGASTER. IX. INDUCTION OF DELTA-RETAINING CHROMOSOME LINES BY MUTATION AND GENE MAPPING

Genetics ◽  
1973 ◽  
Vol 74 (3) ◽  
pp. 477-487
Author(s):  
Sumio Minamori ◽  
Kinue Sugimoto
Keyword(s):  
Drosophila Melanogaster ◽  
Crossing Over ◽  
Chromosomal Gene ◽  
Ethyl Methane Sulfonate ◽  
Methane Sulfonate ◽  
Multiple Alleles ◽  
Ethyl Methane ◽  
Extrachromosomal Element ◽  
Polygenic System ◽  
Killing Action

ABSTRACT [Delta b], symbolized as [δb], is retained by Sb chromosome lines and transmitted through the females to their progeny. Transmission through the males is not directly demonstrable (Minamori 1969a). [delta r], symbolized as [δr], is retained by Sr chromosome lines and transmitted biparentally (Minamori 1971). The multiplication of delta is suppressed at low temperature. All descendant lines derived from Sb-carrying or Sr-carrying flies in which the presence of delta cannot be demonstrated gradually accumulate their specific delta factors over many generations (Minamori 1969b, 1972). The delta factors and the sensitive chromosomes are inseparably associated. This observation led to the assumption that delta may be a copy of a chromosomal gene or a certain agent integrated into the chromosome (Minamori 1972). This assumption was examined in the present study by experiments designed to induce delta-retaining sensitive chromosomes, and to map the gene(s) responsible for delta-retention and/or for sensitivity to the killing action of delta factor. One sensitive chromosome which retained [δb] (Sb chromosome) was obtained in the presence of [δb] out of 2492 insensitive chromosomes which retained no delta; in addition one Sb chromosome was obtained in the presence of [δr] out of 2131 insensitives. The latter finding suggests that Sb might be induced by a mutation caused by [δb] or [δr], but not by integration of either delta into the chromosome. Four Sb chromosomes and one sensitive chromosome which retained [δr] (Sr chromosome) were obtained out of 1970 insensitives when males carrying the chromosome were fed an alkylating mutagen, ethyl methane sulfonate (EMS). The location of delta-retaining genes was examined by crossing-over experiments employing eight Sb and five Sr chromosomes. The genes on these chromosomes were found to be located in the same region or near one another. The gene for [δb], symbolized as Dab, and the gene for [δr], symbolized as Dar, are assumed to be multiple alleles of a locus at 2-24.9. The sensitivity of the chromosomes was modified appreciably by recombination; hence, the genes controlling this trait are assumed to be a polygenic system. The findings obtained in this study lead to the hypothesis that delta may be produced by a chromosomal gene (Da) and transmitted extrachromosomally.

scholarly journals ORIENTATION DISRUPTOR (ord): A RECOMBINATION-DEFECTIVE AND DISJUNCTION-DEFECTIVE MEIOTIC MUTANT IN DROSOPHILA MELANOGASTER

Genetics ◽  
1976 ◽  
Vol 84 (3) ◽  
pp. 545-572
Author(s):  
James M Mason
Keyword(s):  
Drosophila Melanogaster ◽  
Genetic Map ◽  
Crossing Over ◽  
Prophase I ◽  
Sister Chromatids

ABSTRACT The effects of a semidominant autosomal meiotic mutant, orientation disruptor (symbol: ord), located at 2-103.5 on the genetic map and in region 59B-D of the salivary map, have been examined genetically and cytologically. The results are as follows. (1) Crossing over in homozygous females is reduced to about seven percent of controls on all chromosomes, with the reduction greatest in distal regions. (2) Crossing over on different chromosomes is independent. (3) Reductional nondisjunction of any given chromosome is increased to about thirty percent of gametes from homozygous females. The probability of such nondisjunction is the same among exchange and nonexchange tetrads with the exception that a very proximal exchange tends to regularize segregation. (4) Equational nondisjunction of each chromosome is increased to about ten percent of gametes in homozygous females; this nondisjunction is independent of exchange. (5) The distributive pairing system is operative in homozygous females. (6) In homozygous males, reductional nondisjunction of each chromosome is increased to about ten percent, and equational nondisjunction to about twenty percent, of all gametes. (7) Cytologically, two distinct meiotic divisions occur in spermatocytes of homozygous males. The first division looks normal although occasional univalents are present at prophase I and a few lagging chromosomes are seen at anaphase I. However, sister chromatids of most chromosomes have precociously separated by metaphase II. Possible functions of the ord+ gene are considered.

Facultative heterochromatization in parahaploid male mealybugs: involvement of a heterochromatin-associated protein

Development ◽  
2001 ◽  
Vol 128 (19) ◽  
pp. 3809-3817 ◽  
Author(s):  
Silvia Bongiorni ◽  
Milena Mazzuoli ◽  
Stefania Masci ◽  
Giorgio Prantera
Keyword(s):  
Monoclonal Antibody ◽  
Drosophila Melanogaster ◽  
Constitutive Heterochromatin ◽  
Planococcus Citri ◽  
Chromosomal Protein ◽  
Paternal Chromosome ◽  
Localization Pattern ◽  
Males And Females ◽  
Male Specific ◽  
Nonhistone Chromosomal Protein

The behavior of chromosomes during development of the mealybug Planococcus citri provides one of the most dramatic examples of facultative heterochromatization. In male embryos, the entire haploid paternal chromosome set becomes heterochromatic at mid-cleavage. Male mealybugs are thus functionally haploid, owing to heterochromatization (parahaploidy). To understand the mechanisms underlying facultative heterochromatization in male mealybugs, we have investigated the possible involvement of an HP-1-like protein in this process. HP-1 is a conserved, nonhistone chromosomal protein with a proposed role in heterochromatinization in other species. It was first identified in Drosophila melanogaster as a protein enriched in the constitutive heterochromatin of polytene chromosome. Using a monoclonal antibody raised against the Drosophila HP-1 in immunoblot and immunocytological experiments, we provide evidence for the presence of an HP-1-like in Planococcus citri males and females. In males, the HP-1-like protein is preferentially associated with the male-specific heterochromatin. In the developing male embryos, its appearance precedes the onset of heterochromatization. In females, the HP-1-like protein displays a scattered but reproducible localization pattern along chromosomes. The results indicate a role for an HP-1-like protein in the facultative heterochromatization process.

scholarly journals A heat-shock-activated cDNA encoding GAGA factor rescues some lethal mutations in the Drosophila melanogaster Trithorax-like gene

2001 ◽  
Vol 78 (1) ◽  
pp. 13-21 ◽  
Author(s):  
H. GRANOK ◽  
B. A. LEIBOVITCH ◽  
S. C. R. ELGIN
Keyword(s):  
Drosophila Melanogaster ◽  
Heat Shock ◽  
Position Effect ◽  
Efficient Production ◽  
Position Effect Variegation ◽  
Chromosomal Protein ◽  
Gaga Factor ◽  
Genetic Rescue ◽  
Regulation Of Synthesis

GAGA factor is an important chromosomal protein involved in establishing specific nucleosome arrays and in regulating gene transcription in Drosophila melanogaster. We developed a transgenic system for controlled heat-shock-dependent overexpression of the GAGA factor 519 amino acid isoform (GAGA-519) in vivo. Efficient production of stable protein from these transgenes provided genetic rescue of a hypomorphic Trithorax-like (Trl) lethal allele to adulthood. Nevertheless, supplemental GAGA-519 did not suppress position effect variegation (PEV), a phenomenon commonly used to measure dosage effects of chromosomal proteins, nor did it rescue other lethal alleles of Trl. The results suggest requirements for the additional isoforms of GAGA factor, or for more precise regulation of synthesis, to carry out the diverse functions of this protein.

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