Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Eye Color”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

Aesthetic judgment of shapes: eye color, complexity, and first- and second-order symmetry as predictors.

228 subjects, approximately equally divided according to sex and eye color (brown, blue), rated the pleasantness of 20 visual shapes in either of two sets. Factor analyses of pleasingness ratings yielded five stable factors explaining at least 75% of the variance in all cases. Shapes grouped according to factor and subjected to analyses of variance yeilded sex differences for one set (A) and eye color differences for the other (B). Sets A and B were shown to be incomparible and differences in responding between sets were significantly associated with eye color. For individual shapes in Set B, differences in responding associated with eye color were best predicted by rated complexity and the number of angles per figure and brown-eyed subjects were significantly more responsive to complexity than blue-eyed subjects.

Adult↗

Eye color pigment granules in Drosophila mauritiana: mosaics produced by excision of a transposable element.

Compound eyes of the white-peach (wpch) mutant strain of Drosophila mauritiana have some pigment and receptor cells with wild-type eye color pigmentation. These eyes are mosaic, because excision of a transposable element reverts wpch to wild type during the development of somatic cells. Wild-type patches have three types of pigment granule residing in three respective cell types: primary pigment cells, secondary pigment cells, and retinula (visual receptor) cells. Most aspects of these granules, as well as all other aspects of compound eye ultrastructure, are exactly as in the better studied sibling species D. melanogaster. In the wpch parts of the eye, small and giant unpigmented "pigment granules" reside in secondary pigment cells. These white granules are just like the corresponding granules of w mutant D. melanogaster. Small vs. large patches of pigmented cells likely represent excision events occurring late vs. early respectively during development. Mosaics of eye color markers have been important in developmental analyses; the ease of constructing mosaics of D. mauritiana gives this preparation advantages for mosaic analyses.

Animals↗

Eye color and hypertension.

We searched for predictors of essential hypertension in 1,031 persons aged 30-49 who were observed to progress from normotension to hypertension, as compared to an equal number of matched subjects who remained normotensive. Blood pressure status was well documented in both multiphasic screenings and clinical records. Compared to persons with each lighter eye color, those with brown eyes were more prone to develop hypertension, with relative risk of 1.5 (95% confidence interval 1.18-1.96) compared to all persons with nonbrown eyes. The association persisted after control for race, sex, body mass index, alcohol use, educational level, parental history of hypertension, and among whites, for ethnic origin as crudely estimated by last name. Partial confirmation was obtained in three largely independent study groups: 1) 25 pairs of eye-color-discordant dizygotic twins; 2) 894 pairs of incident hypertensives and controls selected only with multiphasic screening blood pressure measurements; and 3) cross-sectional analysis of 152,018 multiphasic screenees. The weak association of eye color with hypertension clearly requires further confirmation. Although it has little potential for use in screening or clinical care, it may have implications regarding etiology. Areas for further exploration include the close metabolic relation of melanins to catecholamines, both derived from the amino acid tyrosine, and the possibility that dark-eyed persons react more quickly and strongly to stimuli than light-eyed persons.

Adult↗

Eye color and noise-induced hearing loss: a population study.

Subjects (N = 130) employed in similar noise environments were given standard audiometric threshold evaluations. Their melanin content, as inferred from their eye color, was noted. The hearing thresholds of "dark-eyed," "medium-eyed," and "light-eyed" subjects were subjected to statistical analysis. Analysis of variance revealed mean threshold differences at 4 and 6 kHz. However, no significant mean threshold differences between eye color groups were seen when mean thresholds were adjusted for years of exposure in a covariance design. It is concluded that although there is a modest relationship between eye color (melanin content) and susceptibility to noise-induced hearing loss, this relationship is less apparent in populations exposed to noise levels below 110 dB (re HTL).

Adult↗

An eye color gene for the detection of transgenic non-drosophilid insects.

A genetic marker for identifying transgenic Musca domestica by changes in eye color is described. The Drosophila melanogaster tryptophan oxygenase gene, vermilion (v), was tested for its ability to genetically complement the mutant tryptophan oxygenase gene in houseflies homozygous for green (ge). The v cDNA, placed under the control of the hsp82 promoter of D. pseudoobscura was transiently expressed in M. domestica embryos homozygous for the tryptophan oxygenase gene, ge, resulting in the rescue of adult eye color. The use of a gene from D. melanogaster to complement an eye color mutant in Musca provides the opportunity to develop a gene vector system for M. domestica and a select group of other non-drosophilid insects in which homologous mutations exist.

Animals↗

A role for the deep orange and carnation eye color genes in lysosomal delivery in Drosophila.

Deep orange and carnation are two of the classic eye color genes in Drosophila. Here, we demonstrate that Deep orange is part of a protein complex that localizes to endosomal compartments. A second component of this complex is Carnation, a homolog of Sec1p-like regulators of membrane fusion. Because complete loss of deep orange function is lethal, the role of this complex in intracellular trafficking was analyzed in deep orange mutant clones. Retinal cells devoid of deep orange function completely lacked pigmentation and exhibited exaggerated multivesicular structures. Furthermore, a defect in endocytic trafficking was visualized in developing photoreceptor cells. These results provide direct evidence that eye color mutations of the granule group also disrupt vesicular trafficking to lysosomes.

Amino Acid Sequence↗

Comparative induction of somatic eye-color mutations and sex-linked recessive lethals in Drosophila melanogaster by tryptophan pyrolysates.

The mutagenicities of the products of pyrolysis of tryptophan, Trp-P-1 and Trp-P-2, on Drosophila melanogaster were examined by measuring the effects of these compounds in inducing recessive lethals and somatic eye-color mutations. Since negative results have already been obtained by the standard procedure in males, Trp-P-1 and Trp-P-2 (0.75 to 6 mg/ml) in sucrose solution were given to females for assay of recessive lethal mutations in X-chromosomes. These compounds caused a marginal increase above the control level in the mutation frequency. For the assay of effects on somatic eye-color mutations, Trp-P-1 (200 and 400 ppm) and Trp-P-2 (400 and 800 ppm) were fed to male larvae of a tester strain carrying a genetically unstable marker set of z and w+ on the X-chromosome. These compounds caused dose-dependent increases above the control level in somatic eye-color mutations in adults. It is concluded that, under the conditions used, the somatic eye-color mutation system was more sensitive than the recessive lethal system to the mutagenic effects of tryptophan pyrolysates.

Animals↗

Transport defects as the physiological basis for eye color mutants of Drosophila melanogaster.

Kynurenine-H3 transport and conversion to 3-hydroxykynurenine were studied in organ culture using the Malpighian tubules and developing eyes from wild type and the eye color mutants w, st, ltd, ca, and cn of Drosophila melanogaster. Malpighian tubules from wild type have the ability to concentrate kynurenine and convert it to 3-hydroxykynurenine. The tubules from w, st, ltd, and ca are deficient in the ability to transport kynurenine, as are the eyes of the mutants w, st, and ltd. This defect in kynurenine transport provides a physiological explanation for the phenotypic properties of the mutants. The relationship of these measurements to previous observations on these eye color mutants is discussed and the transport defect hypothesis is consistently supported. We have concluded that several of the eye color mutants in Drosophila are transport mutants.

Animals↗

Purine transport by malpighian tubules of pteridine-deficient eye color mutants of Drosophila melanogaster.

Uptakes of guanine into Malpighian tubules of wild-type Drosophila and the eye color mutants white (w), brown (bw), and pink-peach (pp) have been compared. Tubules for each of these mutants are unable to concentrate guanine intracellularly. The transport of xanthine and riboflavin is also deficient in w tubules. The transport of guanosine, adenine, hypoxanthine, and guanosine monophosphate is similar in wild-type and white Malpighian tubules. These data and other information about these mutants make it likely that these pteridine-deficient eye color mutants do not produce pigments because of the inability to transport a pteridine precursor. This view supports the hypothesis that mutants which lack both pteridine and ommochromes do so because precursors to both classes of pigments share a common transport system.

Animals↗

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 transpositions 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 wsp 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 wsp. 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 area 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.

Age Factors↗

Correlation of eye color on self-paced and reactive motor performance.

Researchers continue to examine the distinctiveness of motor performance by dark- versus light-eyed individuals. Dark-eyed individuals generally perform better at reactive type tasks (boxing, hitting a ball, defensive positions in football, rotary pursuit), while light-eyed individuals perform better at self-paced tasks (bowling, golf, pitching baseballs). Subjects performed two tasks, rotary pursuit and ball tossing (with light and dark background). Eye color (light or dark) and accuracy of performance were recorded for each subject. No significant difference was found between eye color and performance on the pursuit rotor (reactive activity). A significant difference was found between men's and women's performance in throwing a ball (self-paced activity) at a light-colored background.

Adult↗

Mutagenic effects of some water-soluble metal compounds in a somatic eye-color test system in Drosophila melanogaster.

Nickel, cadmium, lead, arsenic, manganese and chromium salts as well as MeHgOH were screened for mutagenicity, using a sensitive somatic eye-color test system in Drosophila melanogaster. The test is based on the insertion of a mobile element which causes instability in the white locus that is somatically enhanced by mutagens. This white locus expression is combined with a mutation, zeste, in another gene, to produce a light yellow eye color. Larval feeding with mutagens causes somatic mutations in the eye imaginal disc cells that develop into easily detectable red spots in the yellow eyes of adult males. Survival tests showed large differences in the toxicity of different metals, but only hexavalent chromium increased the frequency of somatic mutations above the control level. When combined treatments were carried out with MMS and various metals, sodium arsenite caused a reduction of the MMS-induced mutation frequency while methylmercury increased the frequency of somatic spots.

Animals↗

Germline transformation using a prune cDNA rescues prune/killer of prune lethality and the prune eye color phenotype in Drosophila.

Null mutations in the prune gene of Drosophila melanogaster result in prune eye color due to reductions in red pigment accumulation. When one copy of the awd(Killer of prune) mutant gene is present in a prune background, the animals die. The cause of prune/Killer of prune lethality remains unknown. The genomic region characterized for the prune locus is transcriptionally active and complex, with multiple and overlapping transcripts. Despite the transcriptional complexity of the genomic region of prune, accumulated evidence suggests that the prune locus is small and consists of a single transcription unit, since every prune allele to date exhibits both prune eye color and prune/Killer of prune lethality. A functional prune product from a single, full-length cDNA was identified in this study that can rescue both the eye phenotype and prune/Killer of prune lethality. The DNA sequences of several mutant prune alleles along with Western blot analysis of mutant proteins provide convincing evidence that prune mutations are nulls, and that the cDNA identified in this study encodes the only product of the prune locus.

Amino Acid Sequence↗

The incidence and time-course of latanoprost-induced iridial pigmentation as a function of eye color.

Latanoprost, a phenyl-substituted analogue of prostaglandin F2 alpha administered as eye drops, induces increased melanogenesis in the iridial melanocytes of monkeys. Similar effects were seen in 12, 23 and 11% of patients in the USA, United Kingdom (UK) and Scandinavia, respectively, during one year of treatment. The highest incidence of induced pigmentation was seen in green-brown, yellow-brown and blue/grey-brown eyes, in that order. The relatively high proportion of patients with green-brown eyes in the UK explains the larger number of affected patients in this country. Typically, a concentric increase of the iris pigmentation appeared after six months (range: 3-17) and was judged to be noticeable by the patient in about 2/3 of the cases. After cessation of latanoprost, no change of the induced pigmentation has been seen in patients followed for two years, and there have been no signs of dispersion of pigment into the anterior chamber. Irides, homogeneously blue, grey, green or brown, were seldom affected. Naevi or freckles on iris, conjunctiva, or eye lids were not affected. It is intriguing that many patients with mixed eye color, particularly the blue-brown eyes, have not developed increased pigmentation even during two years of treatment. This could be due to a relatively slow melanogenesis or to refractory melanocytes in these individuals.

Adrenergic beta-Antagonists↗

Weakener of white (Wow), a gene that modifies the expression of the white eye color locus and that suppresses position effect variegation in Drosophila melanogaster.

A locus is described in Drosophila melanogaster that modifies the expression of the white eye color gene. This trans-acting modifier reduces the expression of the white gene in the eye, but elevates the expression in other adult tissues. Because of the eye phenotype in which the expression of white is lessened but not eliminated, the newly described locus is called the Weakener of white (Wow). Northern analysis reveals that Wow can exert an inverse or direct modifying effect depending upon the developmental stage. Two related genes, brown and scarlet, that are coordinately expressed with white, are also affected by Wow. In addition, Wow modulates the steady state RNA level of the retrotransposon, copia. When tested with a white promoter-Alcohol dehydrogenase reporter. Wow confers the modifying effect to the reporter, suggesting a requirement of the white regulatory sequences for mediating the response. In addition to being a dosage sensitive regulator of white, brown, scarlet and copia, Wow acts as a suppressor of position effect variegation. There are many dosage sensitive suppressors of position effect variegation and many dosage-sensitive modifiers of gene expression. The Wow mutations provide evidence for an overlap between the two types of modifiers.

ATP-Binding Cassette Transporters↗