Lethals In Drosophila Research Articles

When a Fly Has to Fly to Reproduce: Selection against Conditional Recessive Lethals in Drosophila

We propose an experimental model suitable for demonstrating allele frequency change in Drosophila melanogaster populations caused by selection against an easily scorable conditional lethal, namely recessive flightless alleles such as apterous and vestigial. Homozygotes for these alleles are excluded from reproduction because the food source used to establish each generation is accessible only by flight. The observed dynamics of flightless-allele frequencies generally follows the theoretically predicted pattern, with slight deviation toward less intense selection. We also suggest observing selection against flight-independent visible marker alleles in the same population as a meaningful comparison. The proposed experiments can easily be scheduled within one semester, and the expected data provide ample opportunities for discussion of quantitative evolutionary patterns.

Cytogenetic toxicity and no-effect limit dose of pesticides

The no-effect limit dose (NELD) of three commonly used pesticides with respect to their cytogenetic toxicity was determined in a number of test systems using a sufficient number of lower doses to characterize the dose-effect relationship. For lindane, malathion and metacid, this dose was 3.2, 7.0 and 3.0 mg/litre, respectively, for mitosis inhibition and 9.0, 55 and 60 mg/litre, respectively, for chromosome clastogeny in onion root-tip cells. For chromosome clastogeny in mice bone marrow cells, the NELDs of the three pesticides were 1.6, 1.5 and 2.0 mg/kg body weight/day, respectively. These values for dominant lethals and X-chromosome-linked recessive lethals in Drosophila were 20 and 5 μg lindane/litre, 2 and 3.5 μg malathion/litre and 4 and 5.5 μg metacid/litre, respectively. Thus, the NELDs are not only pesticide specific but also organism specific, tissue specific and even damage specific. Furthermore, the NELD values determined are so small that the real human exposure to pesticides cannot be reduced below these levels without compromising the effectiveness of pesticides in use.

Studies on the induction of sex-linked recessive lethal mutations in Drosophila melanogaster by nitroheterocyclic compounds

24 nitroheterocyclic compounds were investigated for their capacity to induce sex-linked recessive lethals in Drosophila, by the adult feeding technique, and in some cases injection or larval-feeding methods. Out of 9 5-nitroimidazoles, ZK 26.173 and ZK 25.095 (moxnidazole) were clearly active whereas nimorazole and ronidazole were marginally mutagenic. Out of 10 5-nitrofurans, nitrovin, furazolidone and furaltadone were unambiguously mutagenic, whereas nitrofurantoin was a borderline case. Nitrofurans were active at lower molar concentrations than nitroimidazoles. Out of a group of 5 related nitro compounds (2 nitrothiophenes, picrolonic acid, niridazole and 4-NQO), only 4-NQO was clearly mutagenic, when fed to larvae. Experiments with germ-free flies showed that, for ZK 26.173 and furazolidone, the gut flora of Drosophila do not play a role in the activation of the compounds to mutagenic metabolites. Furazolidone, 4-NQO, ZK 26.173, ZK 25.095 and furaltadone were tested in mal and cin strains, both of which lack xanthine dehydrogenase and aldehyde oxidase. The latter enzyme and xanthine oxidase are known to carry out nitro reduction in mammalian tissues. For ZK 26.173, the mutation frequencies were drastically reduced in the enzyme-deficient strains, indicating the involvement of one of these enzymes in the activation of this substance.

On two models for the frequency distribution of lethals in Drosophila observed in F 3s derived from a single F 1 gonadal mosaic female, and the transmissibility

In order to estimate for Drosophila the frequency distribution of lethals observed in F 3s derived from a single F 1 gonadal mosiac female, two contrasting models are proposed based on knowledge of the gametogenesis process. In the models, it is thought that the two nuclei produced after the first cleavage division are a lethal carrying one and a lethal free one. This line of thought leads to the conclusion that the mean value of the frequency distribution of lethals in the F 3s must be 1 2 . In the gametogenesis process, separation of a sample occurs two times to establish the potential germ line (Sonnenblick, 1950). In the first model, it is assumed that these samples are formed when the two kinds of nuclei are distributed at random in the mosaic embryo. In the second model, it is premised that the first separation occurs when the two kinds of nuclei are intersected by a randomly directed plane; and that some of the adjacent nuclei are separated to form the germ line. The experimental data of Carlson & Southin (1963) suggest that the frequency distribution of lethals in the F 3s may be rather flat, differing from a binomial curve. In this paper, it is shown that their results can be reproduced by the second model. However, upon closer study it is found that an intermediate state of the two models may be more appropriate.

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

SUMMARYSalivary-gland chromosomes of 54 methyl methanesulphonate- and 50 triethylene melamine-inducedX-chromosome recessive lethals inDrosophila melanogasterwere 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 thezeste-whiteregion of theXchromosome. 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 thezeste-whiteregion.

Magnetism and x-ray induced sex-linked recessive lethals in Drosophila.

Journal Article Magnetism and X-ray induced sex-linked recessive lethals in Drosophila Get access SIDNEY MITTLER SIDNEY MITTLER professor of biological sciences, Northern-Illinois UniversityDeKalb, Illinois 60115. Search for other works by this author on: Oxford Academic PubMed Google Scholar Journal of Heredity, Volume 64, Issue 4, July 1973, Page 233, https://doi.org/10.1093/oxfordjournals.jhered.a108397 Published: 01 July 1973

The recovery and preliminary characterization of X chromosome mutants affecting imaginal discs of Drosophila melanogaster

A selection method especially designed for isolation of X-linked lethals in Drosophila having defective imaginal discs has generated 26 mutants with high larval viability, but which terminate development in late larval and prepupal stages. The mutants are tentatively classified into four categories, according to the morphological appearance of their imaginal discs in third-instar larvae, and are further characterized with reference to autonomy/nonautonomy and to capacity for in vitro evagination of discs. The four categories are as follows: 1. discs degenerate = extreme reduction of disc tissue (8 mutants). Of 7 mutants tested, all appear to be autonomous. 2. discs small = reduction in size of disc tissue (7 mutants). Of 6 mutants tested, 5 are nonautonomous. However, discs from 4 of the nonautonomous mutants fail to evaginate in vitro . 3. discs large = hypertrophy of disc tissue (1 mutant). The mutant is phenotypically similar to an allele of lethal giant larvae (l(2)gl 4 ) . 4. discs normal = normal appearance of disc tissue (10 mutants). Of 9 mutants tested, 5 are nonautonomous. Discs from one mutant evaginate abnormally in vitro and in vivo .

Specific genetic deletions by a carcinogenic hydrocarbon in Drosophila.

THE unequivocal establishment of the somatic mutation theory of cancer requires the demonstration that all carcinogenic agents can induce some viable alterations in the genic DNA. Earlier studies of the mutagenicity of chemical carcinogens (reviewed in ref. 1) yielded positive results for alkylating and nitroso compounds, but not for hydrocarbons and aromatic amines. On the whole, however, these studies were restricted to point mutations: either at few loci in microorganisms or as exemplified by recessive lethals in Drosophila. The possibility therefore remained that mutability with some agents might have occurred at uninvestigated loci, or involved mutational mechanisms unrelated to those resulting in point mutations. Another complication was that carcinogenicity with certain compounds seemed to require previous metabolic activation2, which might not occur in some of the genetic test systems used. An extensive investigation was therefore undertaken of the mutational spectra of a wide range of carcinogens—or their active metabolites in Drosophila—and most of the results have recently been published already3. The only genetic aberrations induced by all the compounds tested were the dominant visible mutations resulting in the “Minute” phenotype. These are deletion mutations, hemizygously and homozygously lethal, which have often been located in the heterochromatin4—6. This suggested that the significant genetic change in carcinogenesis might well be the elimination of specific heterochromatic gene loci, and experiments were designed to test this possibility.

A refined test for x-ray induced dominant lethals in Drosophila.

Die nach Rontgenbestrahlung frisch abgelegter besamterDrosophila-Eier registrierbare Letalitat kann nach verschiedenen Letalsyndromen aufgegliedert werden. Zur Auswertung stehen Computerprogramme zur Verfugung. Spezielle Tests zeigten, dass mit der beschriebenen Zuchtanordnung bestrahlte und unbestrahlte Populationen, von denen 25–30 Puppen (bzw. Fliegen) pro Zuchtglas uberleben, ohne Beeinflussung durch ungunstige Zuchtbedingungen auf dominante Letalfaktoren gepruft werden konnen.

Non-random localization of lethals in Drosophila

Inconsistencies in allelism tests were observed by Salceda among the lethals, obtained from Sankaranarayanan's populations with radiation histories. These were interpreted as being due to a series of partially overlapping “deletions” clustered within short segments of the chromosome. Lethal mutants in these segments would have been protected from effective elimination by natural selection if they were completely, or nearly completely recessive. If also inversions with breakage points in these segments persisted longer in populations, the non-random distribution of breakage points of inversions from natural populations could be understood.

Ethyl methanesulfonate-induced lethals in Drosophila--frequency-dose relations and multiple mosaicism.

Ethyl methanesulfonate-induced lethals in Drosophila--frequency-dose relations and multiple mosaicism.

Failure to detect an antimutagenic effect of chloramphenicol in ultraviolet-treated polar cap cells (early germ track) of Drosophila.

The ultraviolet-induced rate of second chromosome lethals in Drosophila was not significantly reduced by posttreatment of ultraviolet-treated polar-cap cells (the earlygerm track) with chloramphenicol, even when the parents of the treated eggs and the developing embryos were in addition reared on chloramphenicol-containing food, as indicated by the following data: ultraviolet- induced rate without chloramphenicol posttreatment, 2.0 450 deg C in a 0.7 percent; with posttreatment, 1.3 450 deg C in a 0.7 percent. The control rate was 0.7 450 deg C in a 0.3 percent. Although the ultraviolet-induced rate was rather low (2.0 450 deg C in a 0.7 percent), the rate ofter chloramphenicol treatment (1.3 450 deg C in a 0.7 percent) was still close enough to the induced rate to indicate that the chloramphenicol was not obliterating the induced rate, contrary to what would have occurred in the case of bacteria. (auth)

The frequency-dose relation of x-ray-induced y-suppressed lethals in Drosophila.

An investigation was made to determine the frequencydose relations of total sex-linked recessive lethals as measured by the S-5 technique ard the two major classes of lethals, orthodox and Y-suppressed, of which they are composed. lt was found that orthodox lethals increase linearly with increasing dose. Y- suppressed lethals, which behave for the most part as V-type position effects and constitute a large fraction (83% at 1082r-17.3% at 4328r) of total lethals at all doses studied, increase more rapidly than expected on the basis of linearity. When orthodox and Y-suppressed lethals were combined, it was shown that the frequency-dose relation of total lethals deviated significantiy from linearity. The significance of these doseresponse relationships to recessive lethal origin has been discussed. (auth)

A COMPARISON OF THE RELATIVE EFFECTIVENESS OF RADIATIONS OF DIFFERENT AVERAGE LINEAR ENERGY TRANSFER ON THE INDUCTION OF DOMINANT AND RECESSIVE LETHALS IN DROSOPHILA

An investigation was made of the effects of monochromatic 14-Mev fast neutrons and Co/sup 60/ gamma rays on the induction of dominant lethals and of 14- Mev neutrons on the production of sex-linked recessive lethals in Drosophila. These results were compared with those of other reports from this laboratory, In which radiations of different average LET were used. It was shown that the RBE of different radiations for the induction of both genetic effects studied is dependent on the LET of the radiation used. 34 references. (auth)

Erratum: Biological Effects of Fast Neutrons from an Internal Target Cyclotron: Physical Methods and Dominant Lethals in Drosophila

Erratum: Biological Effects of Fast Neutrons from an Internal Target Cyclotron: Physical Methods and Dominant Lethals in Drosophila

Biological Effects of Fast Neutrons from an Internal Target Cyclotron: Physical Methods and Dominant Lethals in Drosophila

For radiobiological studies in which equal doses of different radiations are given, a challenging result of basic interest emerges. Radiations of different ion density (linear energy transfer, LET) can, under certain conditions, have different effects (1). A number of investigations have been made of the effects of fast neutrons from the Oak Ridge National Laboratory 86-inch cyclotron. Mammalian pathological effects have been discussed elsewhere, along with a description of the associated dosimetry (2, 3). Preliminary reports of a number of cytogenetic effects have been given (4-8). In this paper, further mutational studies on Drosophila will be presented. Since a description of physical methods used in measuring dose is essential for proper evaluation of biological results, a more comprehensive discussion will be given here, including: (1) an upward revision of neutron doses published in earlier reports; (2) a report on results of independent confirmation of earlier work, when so revised; and (3) a description of typical errors in neutron dosimetry.

Genetical and Cytological Studies of Lethals induced by Chemical Treatment inDrosophila melanogaster.

Thepresent paper forms a continuation of studies of recessive sex-linked lethals inDrosophila melanogasterpublished previously (1938, 1941). In these, lethals occurring spontaneously, induced by X-ray treatment and by ultra-violet light were examined cytologically in the salivary gland chromosomes.The genetic factors which stop or change the development of an individual in such a way that its death ensues under normal conditions are termed lethals. A lethal effect may be connected with a mutation of a gene or with its absence from the chromosome: those which cannot be proved to be associated with the absence of a cytologically detectable part of the chromosome are considered as due to “point” mutations.The absence of a microscopically identifiable section of a chromosome with all its genetical and structural elements is called a deficiency. With few exceptions (Muller, 1935; Demerec and Hoover, 1936) the deficiencies in the X-chromosome, whatever their size and whatever loci they involve, are lethal for males. In females heterozygous for them deficiencies of small or even moderate size usually do not produce any visible phenotypical effect, although some cases are known (Mohr, 1923; Slizynska, 1938) in which a heterozygous deficiency for a particular band is always associated with a definite phenotype. Thus a lethal effect may or may not be the result of a deficiency, while a deficiency in the X-chromosome almost always has a lethal effect in the males.In 1941 Auerbach (1943, 1946 in press) succeeded in producing “visible” and lethal mutations and chromosomal rearrangements by chemical treatment in which adult males were exposed to vapours of (C1CH2CH2)2S in a specially designed apparatus. The object of this paper is to show what proportion of sex-linked recessive lethals produced inDrosophila melanogasterby these new agents is connected with detectable deficiencies. Besides finding out whether chemically produced lethals are associated with detectable deficiencies, the problem of the relation between lethals and “visible” mutations is discussed on the basis of their respective distributions along the chromosome. It should be stated that the lethals connected with gross structural changes represent probably only a small fraction of such lethals actually produced since many of them were eliminated by zygotic lethality.

Ö.winge's paper on “the interaction between two closely linked lethals in drosophila as the cause of the apparent constancy of the mutant “Spread””

Ö.winge's paper on “the interaction between two closely linked lethals in drosophila as the cause of the apparent constancy of the mutant “Spread””

DOUBLE SEX-LINKED LETHALS IN DROSOPHILA MELANOGASTER

Acta ZoologicaVolume 3, Issue 1 p. 135-152 DOUBLE SEX-LINKED LETHALS IN DROSOPHILA MELANOGASTER Gert Bonnier, Gert Bonnier Zootomical Institute; University of Stockholm.Search for more papers by this author Gert Bonnier, Gert Bonnier Zootomical Institute; University of Stockholm.Search for more papers by this author First published: June 1922 https://doi.org/10.1111/j.1463-6395.1922.tb01019.xCitations: 2AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume3, Issue1June 1922Pages 135-152 RelatedInformation

The interaction between two closely linked lethals in drosophila as the cause of the apparent constancy of the mutant „spread”

1. By examination of the mutant „Spread” (wings) ofDrosophila melanogaster it appeared thatSpread, located in the IIIrd chromosome at 61, is not — asstated in the literature—recessive but dominant (to normal wings). 2. Spread acts lethally in double dose. 3. The wild type possesses a dominant indispensable factorVital (Vit) that is closely linked tospread. Its allelomorph,vit, also has a lethal effect in double dose. 4. The formula of the Spread mutant isSpr Vit/spr vit; thus it is double heterozygotic. It is only the strong linkage betweenSpr andVit that causes that the Spread type seems to be constant. 5. The distance betweenSpread andVital is scarcely 1.0. 6. The Spread mutant is an instance of a double heterozygote, which on account of the interaction of two lethal factors (Spr andvit) reminds of and has been construed as a constant homozygotic type.