Eye Color Mutants Research Articles

Polymorphisms of inversions and Adh alleles in eye colour mutant experimental populations of Drosophila melanogaster

Polymorphisms of inversions and Adh alleles in eye colour mutant experimental populations of Drosophila melanogaster

Polymorphisms of inversions and Adh alleles in eye colour mutant experimental populations of Drosophila melanogaster

Polymorphisms of inversions and Adh alleles in eye colour mutant experimental populations of Drosophila melanogaster

Eye-Colour Mutants of the Honeybee

Eye-Colour Mutants of the Honeybee

Changes in Pigmentation in Mosquitoes (Diptera: Culicidae) in Response to Color of Environment

In laboratory experiments, coloration of larvae of two species of anopheline mosquitoes was modified significantly by color of the rearing background. Larvae of Anopheles albimanus Wiedemann, Anopheles quadrimaculatus Say, Culex quinquefasciatus Say, Culex salinarius Coquillett, Aedes aegypti (L.), and Aedes taeniorhynchus Wiedemann were reared in darkness and on either black, white, or green backgrounds, illuminated by either fluorescent lighting or sunlight. Normal strains of Anopheles and Culex larvae reared in black containers developed darker larval pigmentation than larvae reared on the other backgrounds or in darkness. Response of anophelines was more intense than that of culicines. Larval body-color mutants of A. albimanus responded similarly to wild-type on black background, but eye-color mutants of A. albimanus and A. quadrimaculatus did not respond to color of the rearing container. No changes in pigmentation were noted in either Aedes species under any of the test conditions. When normal fourth-instar A. albimanus were introduced into a bicolored (half white, half black) container, a significant majority of larvae selectively moved onto the color, either black or white, of their original rearing container.

Genetic-molecular basis for a simple Drosophila melanogaster somatic system that detects environmental mutagens.

We have developed a simple, objectively scorable test for the mutagenicity of chemical compounds which can be fed Drosophila melanogaster. The test depends upon the somatic reversion of the X chromosome, recessive eye color mutation, white-ivory (wi) to wild type (w+). Reversions are scored as clones of w+ facets in the wi eyes of eclosing adults. To increase the sensitivity, a tandem quadruplication containing four wi mutations was synthesized. Thus, in homozygous females eight wi mutations are potentially revertible. Six mutagenic compounds, all alkylating agents, all gave positive results at several concentrations tested. Molecular analysis demonstrates that the induced reversions, germinal and somatic, are associated with the loss of 2.9-kilobase DNA duplicated in the wi mutation.

Two mutations in Oryzaephilus surinamensis (L.) (Coleoptera: Silvanidae)

Clear eye ( c) and dark body colour ( d) mutations in Oryzaephilus surinamensis (L.) are described. The c mutation is phenotypically identical to “pearl” (Blackman, 1966), lacking pigment in the compound eyes and also in the larval ocelli and Malpighian tubules. These structures are deeply pigmented in the wild type. The d mutation appears as a blackish-brown coloration of the adult, pupa and larva; the wild type body colour is chestnut brown. Crosses made between clear-eyed and dark insects and also crosses of individuals, showing both mutations, with wild type insects showed that the mutations were characterised by recessive autosomal inheritance and were not linked. There was some evidence that the viability of insects homozygous for both mutations was slightly reduced.

Pigment patterns in mutants affecting the biosynthesis of pteridines and xanthommatin in Drosophila melanogaster.

Eye-color mutants of Drosophila melanogaster have been analyzed for their pigment content and related metabolites. Xanthommatin and dihydroxanthommatin (pigments causing brown eye color) were measured after selective extraction in acidified butanol. Pteridines (pigments causing red eye color) were quantitated after separation of 28 spots by thin-layer chromatography, most of which are pteridines and a few of which are fluorescent metabolites from the xanthommatin pathway. Pigment patterns have been studied in 45 loci. The pteridine pathway ramifies into two double branches giving rise to isoxanthopterin, "drosopterins," and biopterin as final products. The regulatory relationship among the branches and the metabolic blockage of the mutants are discussed. The Hn locus is proposed to regulate pteridine synthesis in a step between pyruvoyltetrahydropterin and dihydropterin. The results also indicate that the synthesis and accumulation of xanthommatin in the eyes might be related to the synthesis of pteridines.

Acquisition of incompatibility by inbred wild-type stocks of Mormoniella

Cross Incompatibility in Mormoniella is characterized by the absence of female progeny when certain stocks are crossed. First described 24 years ago, until recently it has been observed only in about nine stocks marked by R-locus eye color mutations. Recently, It has been found in four of the six wild-type stocks collected from natural populations and inbred in the Mormonlella Stock Center. The incompatibility was reciprocal, nonreclprocal, total, or partial depending on which stocks were crossed. Few mutant stocks maintained in the same laboratory have acquired the incompatibility.

Photoreactivation rescue and hypermutability of ultraviolet-irradiated excisionless Drosophila melanogaster larvae.

There is accumulating evidence suggesting that expression of genes for repair of UV damage to DNA in mammals and fish is regulated developmentally. Therefore, the activity of excision repair and photoreactivation in vivo in young larvae of Drosophila melanogaster was examined in a strain carrying the mutation mus201 that was unable to carry out excision repair. The photoreactivation activity in first-instar larvae was so high that UV-induced lethality in excision-less larvae was almost completely rescued by posttreatment with fluorescent light. Excision repair activity in first-instar repair-proficient larvae was so high that UV irradiation was scarcely able to produce somatic eye-color mutations. In contrast, excisionless larvae showed a high incidence of somatic eye-color mutation after UV-irradiation, and this incidence was reduced to the spontaneous level by posttreatment with fluorescent light. Incorporation of a postreplication repair-defective mutation into the excisionless strain decreased the incidence of UV-induced somatic mutations by a factor of 3. The analogous repair dependence of UV mutagenesis in Drosophila and Escherichia coli is discussed. It is proposed that UV-induced somatic mutations in excisionless Drosophila larvae are caused primarily by pyrimidine dimers and that a constitutive, error-prone pathway for filling daughter-strand gaps opposite dimers is, at least partly, responsible for the fixation of mutations.

Effects of X-rays on the induction of somatic mutations and growth in the retinal pigmented epithelium during development of the mouse eye.

The coat and eye colour mutant beige (bg) leads to the production of distinctive retinal melanocytes with abnormally large pigment granules. Heterozygotes for bg were given 2 Gy acute X-irradiation at various times between day 11.5 of fetal life and 3 days after birth, at which age whole mounts were prepared of the retinal pigmented epithelium (RPE). These were scanned for the presence of mutant retinal melanocytes with large granules, either as single cells or as clones. The earlier the fetal irradiation, the greater was the effect on RPE area at 3 days post-partum (p.p.), which fell to about half normal with the 11.5-day fetal exposures. However, the ultimate size of the retinal melanocytes seemed little affected by the irradiation, although their normal size increased approximately 3-fold between 12.5 days post-coitum (p.c.) and 3 days p.p. Mean numbers of mutant melanocytes per eye were markedly higher than in +/bg controls at all irradiation ages other than 3 days p.p.; when allowance was made for final sizes of irradiated RPE's mutation frequencies fell steadily from 30.0 x 10(-5) at 11.5 days p.c. to 1.0 x 10(-5) at 3 days p.p., with 0.8 x 10(-5) in +/bg and 0.1 x 10(-5) in +/+ controls. The doubling dose of 0.18 Gy at 16.5 days p.c. was similar to that found at 17.5 days p.c. in a previous somatic mutation experiment in which follicular melanocytes were scanned for mutations at different (d and ln) loci.(ABSTRACT TRUNCATED AT 250 WORDS)

TISSUE-SPECIFIC AND COMPLEX COMPLEMENTATION PATTERNS IN THE PUNCH LOCUS OF DROSOPHILA MELANOGASTER

Mutations in the Punch locus result in loss of GTP cyclohydrolase activity, but all mutations do not affect the enzyme in the same way. There are at least three classes of Punch mutations. One class results in a dominant eye color, recessive lethal phenotype. A second class of mutations also causes a recessive lethal phenotype, but heterozygous mutants have normal eye color. They show loss of GTP cyclohydrolase function in all tissues where activity can be measured. Alleles comprising a third class are recessive eye color mutations that are homozygous viable. Individuals with this third type of mutation show loss of enzyme activity in the eye, but show normal or near-normal activity elsewhere. In order to examine the organization and function of this locus further, we have performed interallelic complementation tests on 25 Punch mutations, monitoring viability and enzyme activity in prepupae and adults. Most allele combinations are lethal. Those that complement do so in ways that are tissue-or stage-specific and unpredictable. Tests of mutants with tissue-specific phenotypes and of individuals mutant for complementing Punch lethal alleles lead us to conclude that Punch is a complex locus, both with respect to its organization and to its products.

Orange-eye: A sex-linked recessive mutation in Ephestia cautella (Walker) (Lepidoptera: Pyralidae)

A new eye color mutant, orange eye ( O), is described for Ephestia cautella. Preliminary data revealed that this mutation was inherited as a sex-linked recessive. The character is generally recognizable in only the late pupae and adult stages. The viability and reproductive potential of this strain are not significantly different from the wild type.

Xanthurenic acid 8-O-beta-D-glucoside, a novel tryptophan metabolite in eye-color mutants of Drosophila melanogaster.

An unknown fluorescent metabolite has been isolated from heads of eye-color mutants of Drosophila melanogaster. Only a few mutations cause it to accumulate, viz. cardinal (cd), dark red brown (drb), Henna-recessive (Hnr), purple (pr), Punch2 (Pu2), Punch-Grape (PuGr), and scarlet (st). After purification by ion-exchange chromatography, the spectroscopic, chemical, and enzymatic analyses revealed that it is a novel quinoline derivative: xanthurenic acid 8-O-beta-D-glucoside. Feeding experiments suggest that this glucoside is synthesized from 3-hydroxykynurenine and that free xanthurenic acid is not a precursor. The results from the analysis for its occurrence in double mutants, together with the fact that xanthurenic acid 8-glucoside share the same precursor as xanthurenic acid and xanthommatin, suggest that xanthurenic acid 8-glucoside formation is closely related to the regulation of the last step in the biosynthesis of xanthommatin.

Studies of the X chromosome of Anopheles albimanus

Snow (sn) is a recessive, eye color mutant that is phenotypically indistinguishable from the previously described mutant, white eye (we). The loci for these mutants are over 30 map units apart on the X chromosome. Analysis of salivary gland chromosomes of radiation-induced X-autosome translocations were used to define the positions of sn and we on the distal euchromatic portion of the long arm of the X chromosome. A recessive lethal trait (bubble head) was also mapped relative to we and sn, and the gene order on the long arm of the X chromosome is as follows: centromere – ? – snow – bubble head – white eye. Translocation breakpoints in the euchromatic portion of the X chromosome caused sterility or lethality in males hemizygous for the translocations, but breaks in the heterochromatin had no effect. Crossing-over was greatly reduced when translocation breakpoints were located in the euchromatic part of the X chromosome. The translocations were used to determine that the nucleolar organizer region is probably on the short arm of the X chromosome.Key words: Anopheles albimanus, eye colour mutant, X chromosome.

Genetic analysis of three new eye colour mutations in the mosquito, Anopheles stephensi.

Three new eye colour mutants, scarlet eye (wsca), red-spotted eye (prs) and pigmentless eye (p) were isolated in the malaria vector, Anopheles stephensi. Genetic analysis revealed that all three mutants are sex-linked and recessive to the wild type. Scarlet eye is allelic to white eye but is not to either red-spotted eye or pigmentless eye, which are allelic to each other; 5.7% recombination was observed between the white eye and pigmentless eye loci.

Effect of alcohol and competition levels on viability of eye colour mutants of Drosophila melanogaster

Effect of alcohol and competition levels on viability of eye colour mutants of Drosophila melanogaster

Effect of alcohol and competition levels on viability of eye colour mutants of Drosophila melanogaster

Effect of alcohol and competition levels on viability of eye colour mutants of Drosophila melanogaster

Comparative studies of the induction of somatic eye-color mutations in an unstable strain of Drosophila melanogaster by MMS and X-rays at different developmental stages

An unstable white locus in Drosophila melanogaster originally described by Rasmuson and Green (1974) and further by Rasmuson et al. (1978, 1980) contains an IS element. This constellation interacts with the zeste mutation and forms a mutationally unstable system that is sensitive to a variety of mutagens. Mutational shifts between zeste and wild-type eye color as well as deletions and transposition of the white locus are frequently occurring in the unstable X-chromosome in germ line and in somatic tissue. Germinal mutations from zeste to wild-type eye color are associated with an insertion of a piece of DNA, proximal to the w sp site, and the shifts from red to zeste are caused by an excision of the same piece (Rasmuson, in preparation). Mutations to pigmentless phenotype are interpreted as deletions of the white locus, while they always are irreversible and show non-complementation with w sp. The somatic system can be used as a screening test for potential mutagens, described by Rasmuson et al. (1984). This survey is an attempt to correlate the size of the mutated are of the eyes with the age of the larvae at mutagen treatment. X-Rays and MMS were used to give an indication of the mechanism of the instability, according to the different kinds of DNA damage induced. The results show that the mean size of red spots decreased with increasing age of larvae at treatment, while the mutation frequencies were increased because of the multiplication of the cells in the eye anlage susceptible to the mutagens. This is contradictory to the hypothesis maintained by Fahmy and Fahmy (1980) that the somatic shifts are not mutagenic but epigenetic events, due to altered regulation of the gene expression. Red spots induced with MMS are smaller in size than X-ray-induced red spots, indicating a delay in the establishment of mutations from chemically-induced lesions compared to irradiation damage. White spots on the other hand were equally large in size, irrespective of inducing agent and about twice the size of the chemically-induced red spots, implying a faster and more direct action for fixation of deletions than for the production of MMS induced shifts in eye color from zeste to red.

Purification and properties of the enzymes from Drosophila melanogaster that catalyze the conversion of dihydroneopterin triphosphate to the pyrimidodiazepine precursor of the drosopterins.

The enzyme system responsible for the conversion of 2-amino-4-oxo-6-(D-erythro-1',2',3'-trihydroxypropyl)-7,8-dihyd roptridine triphosphate (dihydroneopterin triphosphate or H2-NTP) to 2-amino-4-oxo-6-acetyl-7,8-dihydro-3H,9H-pyrimido[4,5-b]-[1,4]diazepine (pyrimidodiazepine or PDA), a precursor to the red eye pigments, he drosopterins, has been purified from the heads of Drosophila melanogaster. The PDA-synthesizing system consists of two components, a heat-stable enzyme and a heat-labile enzyme. The heat-stable enzyme can be replaced by sepiapterin synthase A, a previously purified enzyme required for the Mg2+-dependent conversion of H2-NTP to an unstable compound that appears to be 6-pyruvoyltetrahydropterin (pyruvoyl-H4-pterin). The heat-labile enzyme, purified to near-homogeneity and termed PDA synthase (Mr = 48,000), catalyzes the conversion of pyruvoyl-H4-pterin to PDA in a reaction requiring the presence of reduced glutathione. Because PDA is two electrons more reduced than pyruvoyl-H4-pterin, the reducing power required for this transformation is probably supplied by glutathione. The PDA-synthesizing system requires the presence of another thiol-containing compound such as 2-mercaptoethanol when incubation conditions 2-mercaptoethanol is no longer required. Evidence is presented to indicate that the Drosophila eye color mutant, sepia, is missing PDA synthase.

3-OH-Kynurenine content and ommochrome formation in the developing compound eye ofEphestia kühniella

The eye color ofEphestia kuhniella is primarily determined by the ommochromes xanthommatin and ommin. The pigmentation, an important part of eye differentiation, occurs mainly during the pupal stage. Comparative studies on eye colour mutants indicate that a first step in ommochrome synthesis is the binding of the precursor 3-OH-kynurenine to developing pigment granules. Both xanthommatin and ommin are present from the early beginning of eye differentiation, and exhibit different developmental profiles.