THE NONMUTAGENIC ACTION OF p-p′-DDT AND γ-HEXACHLOROCYCLOHEXANE IN DROSOPHILA MELANOGASTER MEIG. (DIPTERA: DROSOPHILIDAE)

1952 ◽  
Vol 30 (6) ◽  
pp. 375-377 ◽  
Author(s):  
D. P. Pielou
Keyword(s):  
Drosophila Melanogaster ◽  
Selective Breeding ◽  
Larval Feeding ◽  
Mutagenic Action ◽  
Wild Type ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
Insecticide Tolerance ◽  
Feeding Medium ◽  
Insect Parasites

As experiments are in progress on selective breeding for insecticide tolerance in insect parasites and as various physiologically potent chemicals have been shown to cause mutation in Drosophila melanogaster Meig., tests were made to determine whether p-p′-DDT and γ-hexachlorocyclohexane had any mutagenic action. Wild type males of D. melanogaster that had been exposed to the former insecticide in their larval feeding medium, or, as adults, to the vapor of the latter insecticide, were tested. The Muller-5 method of detecting recessive lethal mutations in the X chromosome was used. No evidence of mutagenic action was found in either insecticidal isomer.

scholarly journals THE INTERCELLULAR DISTRIBUTION OF MUTATIONS INDUCED IN OOCYTES OF DROSOPHILA MELANOGASTER BY CHEMICAL AND PHYSICAL MUTAGENS

Genetics ◽  
1979 ◽  
Vol 92 (1) ◽  
pp. 151-160
Author(s):  
H Traut
Keyword(s):  
Drosophila Melanogaster ◽  
Mitomycin C ◽  
Mutation Frequency ◽  
Lethal Mutation ◽  
X Rays ◽  
Mutagenic Treatment ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
X Irradiation

ABSTRACT When females of Drosophila melanogaster are treated with chemical or physical mutagens, not only in one but also in both of the two homologous X chromosomes of a given oocyte, a recessive sex-linked lethal mutation may be induced. A method is described that discriminates between such "single" and "double mutations." A theory is developed to show how a comparison between the expected and the observed frequency of double mutations yields an indication of the intercellular distribution (random or nonrandom) of recessive lethal mutations induced by mutagenic agents in oocytes and, consequently, of the distribution (homogeneous or nonhomogeneous) of those agents.—Three agents were tested: FUdR (12.5, 50.0 and 81.0,μg/ml), mitomycin C (130.0 μg/ml) and X rays (2000 R, 150 kV). After FUdR feeding, no increase in the mutation frequency usually observed in D. melanogaster without mutagenic treatment was obtained (u=0.13%, namely three single mutations among 2332 chromosomes tested). After mitomycin C feeding, 104. single and three double mutations were obtained. All of the 50 mutations observed after X irradiation were single mutations. The results obtained in the mitomycin C and radiation experiments favor the assumption of a random intercellular distribution of recessive lethal mutations induced by these two agents in oocytes of D. melanogaster. Reasons are discussed why for other types of mutagenic agents nonrandom distributions may be observed with our technique.

scholarly journals Cytogenetic and complementation analyses of recessive lethal mutations induced in the X chromosome of Drosophila by three alkylating agents

1974 ◽  
Vol 24 (1) ◽  
pp. 1-10 ◽  
Author(s):  
J. K. Lim ◽  
L. A. Snyder
Keyword(s):  
Drosophila Melanogaster ◽  
Salivary Gland ◽  
X Chromosome ◽  
Alkylating Agents ◽  
Complementation Analysis ◽  
Ethyl Methanesulphonate ◽  
Induced Mutations ◽  
Recessive Lethal ◽  
Lethal Mutations

SUMMARYSalivary-gland chromosomes of 54 methyl methanesulphonate- and 50 triethylene melamine-induced X-chromosome recessive lethals in Drosophila melanogaster were analysed. Two of the lethals induced by the mono-functional agent and 11 of those induced by the polyfunctional agent were found to be associated with detectable aberrations. A complementation analysis was also done on 82 ethyl methanesulphonate- and 34 triethylene melamine-induced recessive lethals in the zeste-white region of the X chromosome. The EMS-induced lethals were found to represent lesions affecting only single cistrons. Each of the 14 cistrons in the region known to mutate to a lethal state was represented by mutant alleles, but in widely different frequencies. Seven of the TEM-induced lethals were associated with deletions, only one of which had both breakpoints within the mapped region. Twenty-six of the 27 mutations in which only single cistrons were affected were mapped to 7 of the 14 known loci. One TEM- and two EMS-induced mutations were alleles representing a previously undetected locus in the zeste-white region.

A CYTOGENETIC ANALYSIS OF THE CHROMOSOMAL REGION SURROUNDING THE α-GLYCEROPHOSPHATE DEHYDROGENASE LOCUS OF DROSOPHILA MELANOGASTER

Genetics ◽  
1983 ◽  
Vol 105 (2) ◽  
pp. 371-386
Author(s):  
Michael A Kotarski ◽  
Sally Pickert ◽  
Ross J MacIntyre
Keyword(s):  
Drosophila Melanogaster ◽  
Polytene Chromosome ◽  
Cytogenetic Analysis ◽  
Chromosomal Region ◽  
Chromosome Band ◽  
Recombination Analysis ◽  
Chromosome 2 ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
Glycerophosphate Dehydrogenase

ABSTRACT The chromosomal region surrounding the structural gene for α-glycerophosphate dehydrogenase (αGpdh, 2-20.5) of Drosophila melanogaster has been studied in detail. Forty-three EMS-induced recessive lethal mutations and five previously identified visible mutations have been localized within the 25A-27D region of chromosome 2 by deficiency mapping and in some cases by a recombination analysis. The 43 lethal mutations specify 17 lethal loci. ?Gpdh has been localized to a single polytene chromosome band, 25F5, and there apparently are no lethals that map to the αGpdh locus.

Normale Entwicklung der Fliege Drosophila in Niederfrequenten Magnetfeldern / Normal Development of the Fruitfly Drosophila in VLF Magnetic Fields

1977 ◽  
Vol 32 (1-2) ◽  
pp. 125-132 ◽  
Author(s):  
Karl Georg Götz ◽  
Simon Götz
Keyword(s):  
Drosophila Melanogaster ◽  
Magnetic Fields ◽  
Normal Development ◽  
Control Group ◽  
Wild Type ◽  
Recessive Lethal ◽  
Recessive Lethal Mutation ◽  
Observed Damage ◽  
Mutagenic Effects ◽  
Pulsed Fields

Abstract Attempts to substantiate irreversible actions of a variety of magnetic fields on the fruitfly, Drosophila melanogaster, have been successful and unsuccessful in about equal numbers. The most conspicuous mutagenic effects apparently induced by pulsed H F-fields failed to appear under continuous electromagnetic irradiation. This seems to correlate the observed damage with the VLF-components of the pulsed fields. The present investigation is motivated by the occurrence of these components both in the atmosphere and in the vicinity of electrical appliances. A strain of normally viable wild type males and subnormally viable Attached-X γ ω females was used in which the yield, and the sex ratio, of the progeny indicate, respectively, the extent of developmental damage and of sex-linked recessive lethal mutation induced by the exposure to detrimental conditions. Evaluation of 73,800 flies from subsequent generations of a control group and two test groups raised in steady, or rotating, homogeneous 9.6 kHz magnetic fields of about 2.5 G did not reveal any development of hereditare load in the test groups.

scholarly journals Three neighboring genes interact with the Broad-Complex and the Stubble-stubbloid locus to affect imaginal disc morphogenesis in Drosophila.

Genetics ◽  
1991 ◽  
Vol 127 (4) ◽  
pp. 747-759 ◽  
Author(s):  
P J Gotwals ◽  
J W Fristrom
Keyword(s):  
Drosophila Melanogaster ◽  
Transcription Factors ◽  
Genetic Markers ◽  
Imaginal Disc ◽  
Wing Disc ◽  
Unit Interval ◽  
Genetic Interactions ◽  
Wild Type ◽  
Recessive Lethal ◽  
Broad Complex

Abstract The Broad-Complex (BR-C) is a complex regulatory locus at 2B-5 on the X chromosome of Drosophila melanogaster. The wild-type BR-C products are apparent transcription factors necessary for imaginal disc morphogenesis. Alleles of the Stubble-stubbloid (Sb-sbd) locus at 89B9-10 act as dominant enhancers of broad alleles of the BR-C. Sb-sbd wild-type products are necessary for appendage elongation. We report, here, on three new loci implicated in imaginal disc morphogenesis based on their genetic interactions with both BR-C and/or Sb-sbd mutants. Enhancer of broad (E(br)) was identified as a dominant enhancer of the br1 allele of the BR-C and is a recessive lethal. Mapping of E(br) has led to the identification of two loci, blistered and l(2)B485, mutants of which interact with E(br) and the Sb-sbd locus. Blistered, but not l(2)B485, interacts strongly with the BR-C. Alleles of the blistered locus are viable and disrupt proper wing disc morphogenesis independent of genetic interactions. All three loci map within the 0.6-map unit interval between the genetic markers speck and Irregular facets and to the cytological region 60C5-6; 60E9-10 at the tip of chromosome 2R. Genetic evidence is consistent with the view that the BR-C regulates blistered.

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.

scholarly journals The Effect of Temperature on the Mutation Rate in Drosophila Melanogaster

1958 ◽  
Vol 11 (1) ◽  
pp. 85 ◽  
Author(s):  
BL Sheldon
Keyword(s):  
Drosophila Melanogaster ◽  
Mutation Rate ◽  
Shock Treatment ◽  
Effect Of Temperature ◽  
Adult Males ◽  
Heat Shock Treatment ◽  
Recessive Lethal ◽  
Lethal Mutations ◽  
Consistent Treatment ◽  
Large Response

The incidence of sex�linked recessive lethal mutations in Drosophila melano� gaster after heat shock treatment of both larvae and adult males is reported. There was no increase in the mutation rate after treatment of larvae and the results with adult males were not consistent. Treatment of the latter at 38�C caused an increase in mutation rate, due apparently to the large response of a few sensitive males. Treatment at 40�C caused no increase, and if one sensitive male was excluded, the mutation rate was significantly less than control. These results do not entirely support those of previous workers in the literature and possible reasons for this are discussed.

P32-INDUCED LETHAL MUTATIONS IN DROSOPHILA

1951 ◽  
Vol 29 (3) ◽  
pp. 234-239 ◽  
Author(s):  
T. J. Arnason ◽  
R. L. Irwin ◽  
J. W. T. Spinks
Keyword(s):  
X Rays ◽  
Total Radiation ◽  
Wild Type ◽  
Larval Food ◽  
X Chromosomes ◽  
Recessive Lethal ◽  
Initial Concentration ◽  
Lethal Mutations ◽  
Total Radiation Dose ◽  
Food Medium

X-chromosomes of P32-treated wild-type Drosophila melanogaster were tested for the presence of recessive lethal mutations. Treated larvae were reared in food medium containing initially 6.5, 32.5, 65.0, or 162.5 mrd. P32 per ml. Of 838 tested chromosomes 42 had recessive lethals. The frequency of mutation was roughly proportional to P32 content of the food. An initial concentration of 18.8 mrd. P32 in larval food is expected to produce about the same frequency of recessive lethal mutations as is obtained with 1000 r. of X rays applied to mature sperm. A fly reared in medium having an initial concentration of 32.5 mrd. per ml. receives, prior to mating, a calculated total radiation dose of 0.62 gram roentgens. At this dosage 4.2% recessive lethals were recorded. For equivalent amounts of ionization P32 is here apparently 2.3 times as effective as X rays.

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