Mutation in Drosophila

Royzman I, Whittaker AJ, Orr-Weaver TL 1997 Mutations in Drosophila DP and E2F distinguish Gj-S progression from an associated transcriptional program. Genes Dev 11 1999-2011... 

A genetic screen for novel clock mutations in Drosophila sA to the discovery of the first kinase that plays a role in circadian rhythmicity (Price et al 1998). Doubletime dht) is a member of the casein kinase 1 (CKl) family, and is 86% identical to human casein kinase Is (CKls) within the kinase domain (Kloss et al 1998). Originally, two mutations were isolated that produce short (18 h dht ) and long (27 h dbt ) behavioural rhythms. Since then, many period-altering mutations and loss-of-function alleles have been described. The majority of these mutations reside in the kinase domain of dbt, altering its ability to bind and/or phosphorylate its substrate (Fig. 1). All of the DBT point mutations analysed alter the phosphorylation state and accumulation of PER, indicating that DBT affects... 

In a test for sex-linked recessive lethal mutations in Drosophila, Wild et al. 8 found no evidence of mutagenicity of CS. More than 9,000 chromosomes were tested, and the frequencies of mutations in the treated groups did not differ from those in the concurrent negative controls or the historical negative controls. The available information on the toxicity of CS under the treatment conditions is minimal. The actual dosages received by the flies are also uncertain, particularly because CS breaks down rapidly in water. Nevertheless, the available data give no indication of mutagenicity of CS in Drosophila. 

Di(2-ethylhexyl) adipate did not induce gene mutations, sister chromatid exchanges, chromosomal aberrations or micronuclei in rodent cells in vitro. It did not induce sex-linked recessive lethal mutations in Drosophila when administered either by diet or injection. Di(2-ethylhexyl) adipate was not mutagenic to either Photo-... 

Butadiene did not induce somatic cell mutation and recombination or sex-linked recessive lethal mutation in Drosophila melanogaster. 

Chloroprene induced a small increase in sex-linked recessive lethal mutations in Drosophila melanogaster without a dose-response relationship in one study, but had no effect in another study. Chloroprene was not mutagenic to V79 Chinese hamster lung cells in the presence of S15 liver supernatants from phenobarbital-treated mice and rats. 

Acetaldehyde causes gene mutations in bacteria and gene mutations, sister chromatid exchanges, micronuclei and aneuploidy in cultured mammalian cells, without metabolic activation. In vivo, it causes mutations in Drosophila melanogaster but not micronuclei in mouse germ cells. It causes DNA damage in cultured mammalian cells and in mice in vivo. Acetaldehyde-DNA adducts have been found in white blood cells from human alcohol abusers. 

Based on the known chemical reactivity of aziridine and its ability to form adducts with DNA, sex-linked recessive lethal mutations in Drosophila, dominant lethal effects in Drosophila and mice, and gene mutation at the hrpt locus of CHO cells in vitro, it is probable that the biological effects of aziridine would be expressed in any mammalian species. 

Dimethylformamide did not induce sex-linked recessive lethal mutations in Drosophila melanogaster in experiments where it was used as a solvent for other substances to be tested and the responses were, therefore, compared with those of untreated controls. 

In single studies, dimethyl sulfate induced somatic mutations in Drosophila melanogaster and in stamen hairs of Tradescantia clone BNL 4430. 

After in-vivo administration, phenol induced micronuclei in mice and chromosomal aberrations in rats. It also caused oxidative DNA damage in mice, and it bound covalently to rat DNA. In cultured mammalian cells, phenol caused mutations, sister chromatid exchanges and micronuclei. It bound to cellular protein (but not to DNA) and inhibited intercellular communication. It did not induce recessive lethal mutations in Drosophila melanogaster and had only a weak effect in inducing segregation in Aspergillus nidulans. Phenol was not mutagenic in bacteria. 

Unless otherwise indicated, studies were carried out with an 80/20 mixture of 2,4/2,6-toluene diisocyanates. In one of two studies, toluene diisocyanate induced mutations in Salmonella typhimurium strains TAIOO, TAI 538, and TA98 in the presence of an exogenous metabolic activation system only. It induced sex-linked recessive lethal mutations in Drosophila in a single study. 

Trichloroethane did not cause mutation in plants or sex-linked mutation in Drosophila. It did not induce DNA damage, gene conversion, mutation or aneuploidy in yeast or genetic crossing-over or aneuploidy in fungi, but it was mutagenic to some bacterial strains. 

In one study, a mixture of cis- and trans- 1,3-dichloropropene gave positive results for induction of mutations in Drosophila melanogaster. 

P-Propiolactone was mutagenic to bacteria. In yeast, it induced mitotic gene conversion, aneuploidy and mutations. It produced heritable translocations and sex-linked recessive lethal mutations in Drosophila melanogaster. In vitro, it induced cell transformation and gene mutations in human cells, and cell transformation, gene mutations, chromosomal aberrations and sister chromatid exchanges in mammalian cells. 

Mitchell, I.D., Gilbert, P.J., Brice, A.J. White, D.J. (1981) Somatic eye mutation in Drosophila melanogaster as a short-term test for mutagens and carcinogens. Carcinogenesis, 2, 783-786... 

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