mini-white, DMWHITE, EG:BACN33B1.1
ABC transporter of amines that partners with Brown in determination of eye pigmentation - Behavioral abnormalities in , and mutants could arise from reduced amine levels in neurons
Please see the JBrowse view of Dmel\w for information on other features
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Gene model reviewed during 5.45
8.0, 7.9, 2.6 (northern blot)
5.7, 2.6, 1.75 (northern blot)
2.212 (sequence analysis)
There is only one protein coding transcript and one polypeptide associated with this gene
Heterodimer of white with either brown or scarlet.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\w using the Feature Mapper tool.
Microarray data shows w gene expression highest in Malpighian tubules (from FlyAtlas).
Adult males express the 2.6kb wa transcript at about twice the level of females.
w is detected in retina and in the lamina. In the eye, the signal is concentrated in primary pigment cells with some signal in photoreceptors. In the lamina, signal is observed in the epithelial glial cells.
GBrowse - Visual display of RNA-Seq signals
View Dmel\w in GBrowse 21-1.5
1-1.4
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
polyclonal
Source for identity of: w CG2759
Source for merge of: w e(g)
The visual acuity of w mutant males is impaired, but their abnormal courtship behaviour in daylight largely results from an overflow of light.
The absence, or insufficient levels, of extra-retinal w protein increases the sexual arousal of males in general, of which the enhanced male-male courtship, observed in both chaining and single-courtship assays, may be an indirect effect.
w function is required for the courtship disinhibition seen in wild-type males upon repeated exposure to ethanol.
Both enhancer-activated and basal w transcription can be silenced by Pc-G proteins at a large number of chromosomal locations.
w protein is located in the membranes of pigment granules within pigment cells and retinula cells of the eye. No evidence of its presence in the plasma membrane has been seen.
P-element insertions containing the Mcp-element and mediating pairing sensitive silencing of w expression are subject to long distance silencing interactions with other similar inserts. This occurs in cis or in trans. This effect is strongest between nearest neighbours, and weakens as the distance between the partners increase. Addition of more than two elements does not interfere with the silencing effect. The long distance regulatory activity of the Mcp element can be enhanced by placing it in a mini-w transgene which is flanked by scs and scs'.
PEV operating on insertions of the w-containing P{hsp26-pt-T} reflects specialised packaging due to heterochromatin proteins that are associated with sequences that can be, but are not necessarily, repetitive.
The P{FRT(RS3).y}10A insertion, which shows variegation for w expression, reveals imprinted control of gene activity in Drosophila.
Heterochromatic cluster containing Stellate repeats, cause PEV of a reporter mini-w gene.
A transgene array can cause silencing not only of the w reporter genes within the array but also of a vital gene near the array. The size of the array inducing the effect correlates with the frequency of gene silencing. The repeat arrays behave like natural heterochromatin: increased silencing of a transgene array results from rearrangements that place the array more proximal to pericentric heterochromatin, arrays as small as three copies are sensitive to long-range effects of interactions with heterochromatin in both cis and trans, the array is capable of silencing a non-variegating w transgene on a homologue. Essential gene(s) in the 50C region is silenced by the presence of a variegation P{lacW} array.
Study of the wi assay reveals it is not recommended as a general screening test because the background reversion frequencies show high variability among solvents.
The w+mW.hs mutation carried in the P{FRT(whs)} element can be excised from its site of integration by the induction of Scer\FLP1 synthesis. Scer\FLP1 can be used to excise an Scer\FRT-flanked gene after cell division has ceased and the gene, now present on an extrachromosomal circle, is expressed. Most position effects are reverted by the removal of this gene from the chromosome.
Analysis of 6 spontaneous and 73 γ ray-induced w mutations reveals that on the chromosomal and genetic levels all spontaneous mutations show themselves to be point mutations.
Mow changes the expression of w. Alterations in the w structural gene and in a specific cis-regulatory domain are unable to block interaction with Mow mutations but those lacking dosage compensation do block Mow interaction. Mutations of Mow can suppress position effect variegation of w (In(1)wm4h).
One of a class of genes with TATA-less promoters that have a subset of the conserved DPE sequence.
Measurements of the frequency of site specific recombination between P-element-borne w alleles on homologous chromosomes shows that structural heterozygosity inhibits the pairing of alleles that lie distal to a rearrangement breakpoint. Variations in cell cycle length can explain different extents of transvection effects in different tissues. Cells with a longer cell cycle have more time to establish the normal pairing relationships that have been restored by rearrangements. Minute mutations, which slow the rate of cell division, partially restore a transvection effect that is disrupted by an inversion breakpoint.
The autosomal "FLP-DFS" technique (using the P{ovoD1-18} P{FRT(whs)} P{hsFLP} chromosomes) has been used to study the zygotic lethal mutation.
In the presence of a P1\cre transgene driven by a dual Hsp70-Dmau\mariner\T promoter, a w reporter gene flanked by P1\loxP sites is excised with virtually 100% efficiency both in somatic and germ cells. A strong maternal effect, resulting from P1\cre recombinase present in the oocyte, is observed as white or mosaic eye colour in F1 progeny. Excision in germ cells of the F1 yields a strong grand-maternal effect, observed as a highly skewed ratio of eye-colour phenotypes in the F2 generation.
Position effect variegation appears to have little effect on overall accessibility to Ecol\dam methylase.
Eye mosaic test is used to evaluate the genotoxicity of polychlorinated biphenyls (PCBs).
The wi somatic assay allows detection of genotoxic agents which induce loss of a tandem duplication.
Full dosage compensation of the w gene requires both the X chromosome environment and multiple dosage compensation elements, some near the promoter and some in the coding region.
Dosage compensation of autosomally integrated mini-w genes flanked by gypsy\su(Hw)BR sequences is greatly improved compared to insertions not flanked by gypsy\su(Hw)BR, such that complete or nearly complete compensation was observed at the majority of X and autosomal insertion sites. The su(Hw) protein is essential for this enhanced dosage compensation. gypsy\su(Hw)BR may protect the mini-w gene from a negative autosomal chromatin environment. su(Hw) mutations do not affect dosage compensation of the endogenous w gene.
Mis-expression of w in mature males causes a marked change in their sexual behaviour inducing male-male courtship. Most males participate forming male-male courtship chains, circles and lariats. When exposed to an active homosexual courtship environment non-transformant males alter their behaviour and actively participate in male-male chaining. These results demonstrate both genetic and environmental factors play a role in male sexual behaviour.
The response of the wi system to ten carcinogens is assayed.
P-element induced chromosome breakage is repaired six times more frequently when a homologous template is located anywhere on the X chromosome than on an autosome. This cis-advantage can operate over more than 15Mb of DNA.
5' splice site mutation of w can be suppressed by compensatory mutations in the 5' end of U1, both molecularly in transformed cells and phenotypically in transformed flies.
w locus confers protective action against X ray damage, resulting in a reduced frequency of dominant lethals. There is at least one genetic factor, located near w, which is responsible for the adaptive response (AR). The AR can be induced by a minimal dose of 0.2mGy, increasing the conditioning dose does not influence the response.
Ligation mediated PCR procedure has been used to quantitate the accessibility of restriction sites in the chromatin fibre in both the active and inactivated forms of w. Inactivation is not accompanied by substantial change in the accessibility of the chromatin fibre.
At the DNA sequence level D.melanogaster populations from Zimbabwe are more than twice as variable as populations from U.S.A. Most variants are not shared between the two geographic regions and areas of low recombination rates have mutations that are nearly fixed.
In vitro splicing in both human and Drosophila cell nuclear extracts has been used to investigate the signals required for the splicing of a small intron.
A test locus for investigating site-specific mutagenesis using the I-element.
P-element mobilization has been to study the repair of double strand breaks in the white locus in premeiotic germ cells: distribution of conversion tracts is unaffected by changes in the length of sequence homology between the broken ends of the template, indicating that only a short match is required, and frequency of repair is highly sensitive to single base mismatches in the homologous region.
Phenotypic variation of the genetic components underlying oviposition behaviour is analysed using the complete diallel mating design.
Several regions of the genome that act as dosage-dependent modifiers of w alleles have been identified.
Alleles of w respond to dosage compensation in metafemales (3X;2A) as a continum of the male and female responses.
Superunstable mutations generated in crosses of π2 strain to a wa strain or its derivatives. Each superunstable mutation gives rise to a large family of new super-unstable mutations with a wide range of phenotypic expression. Mutations with the same phenotype often differ in the specificity of their potential for further mutation. Each superunstable mutation is associated with a specific, "paired", reversible mutation. Active transposase encoded by P elements is necessary to maintain superinstability. X transposable element is also implicated in the mutability system.
Transcriptional analysis of wa demonstrates that the w promoter and the copia promoter are not coordinate in their dosage compensation abilities when assayed in larvae and adults in different genomic locations.
Mutations at white locus have no effect on rate of degeneration of rhabdomeres R1-6 in the time span where ninaE mutations do have an effect.
Chromatographic and autoradiographic analysis of GTP cyclohydrolase uptake of excised pupal eyes demonstrate that the site of action of the w gene in pteridine synthesis is located in an intracellular site, not in the plasma membrane as previously hypothesised.
The unstable z-w assay was used to compare mutation rates in germinal and somatic cells. Formaldehyde and methylmethane sulphonate induce mutations in larval and adult feeding in somatic and germinal cells: methylmethane sulphonate causes an elevated frequency of mutations in somatic and germinal cells and formaldehyde only causes somatic mutations.
The Inr-a regulatory gene interacts with the white locus via regulatory sequences.
Genotoxicity of acrolein is investigated using SMART, SCLT (sex chromosome loss test) and SLRLT (sex linked recessive lethal test). Acrolein is mutagenic in SLRLT when injected but not fed, SCLT does not reveal a clastogenic effect with acrolein and acrolein has a genotoxic effect in SMART.
Recombination of the nucleolus organiser region (NO) by X chromosome inversion onto the In(1)wm51b and In(1)wm4 chromosomes evokes w variegation.
SMART (somatic mutation and recombination test) has been used to assay the effects of tannic acid alone and in combination with chemical genotoxins and γ-radiation on mutation in D.melanogaster.
Lesions in w reduce or eliminate pigmentation in the eyes and ocelli and block pigmentation of the fat body and tubules. w is required for the synthesis of ommochrome in any tissue and is involved in the transport of pigmentation precursors.
The somatic mutation and recombination test (SMART) has been used to assay the genotoxic activity of a number of polycyclic aromatic hydrocarbons.
Removal of UV-induced pyrimidine dimers is measured in genes ade3, N and w in two diploid immortalised cell lines (Kc and SL2) to investigate whether preferential repair forms part of DNA excision repair. Data supports the idea that preferential repair is not restricted to transcriptionally active sequences.
The effects of 4 anti-cancer drugs have been assayed in the wi somatic mutation test.
Some mutations in w are due to insertion of a Stalker element.
Modification of eye colour in z1 genotypes is independent of a specific w allele.
Relative success of mutant w and wild type males is frequency-dependent, if the sex ratio is 1:1 . If the number of females is constant, this success depends on the ratio between mutant and wild type males. The sex ratio changes strongly affect the male mating activity of both genotypes.
Only 2 out of 36 ethyl nitrosourea (ENU) induced alleles at the w locus show an alteration of the normal restriction enzyme pattern, suggesting that most of the ENU-induced mutations are due to very small rearrangements, or, most likely, base-pair changes.
Initiation of transcription at the white promoter is increased by E(wa).
A w cDNA has been cloned and sequenced.
Ultrastructure and Ca-sequestering properties of eye colour pigment granules (PGs) are studied in the eyes of wild type and mutant flies. A new type of ommochrome PG localises in primary pigment cells and basal terminals of the processes of Semper cells. At room temperature these PGs exhibit OsO4-dependent structural ability. X ray microanalysis revealed a less Ca-binding ability of the PGs as compared to those in secondary pigment cells.
Similarity of w and st mutant phenotypes may reflect a common biochemical function for the w and st gene products.
In situ hybridisation of recombinant DNA probes to polytene chromosomes of D.melanogaster and D.virilis is performed to study homologies between the chromosomal Muller elements of the two species.
The w locus is surrounded by a critical domain that influences the zeste-white interaction proximally and distally. The domain has cis and/or trans-acting functions. There is no evidence of a physical boundary site delimiting the breakage sensitive zeste-white interaction.
Mutant alleles are useful as markers in clonal analysis.
The spotted region of the w locus is 590-1270bp 5' to the transcription start site. Mutational analysis demonstrates that the region has two distinct cis-acting regulatory elements and a third element mapping 3' at -670bp.
Different parts of the 1.8kb region preceding the transcription start of w are required for the expression of the gene in different tissues and at different developmental stages. Sequences required for dosage compensation are contained between -216 and the transcription start site. Another sequence >1080bp upstream of the transcription start is required for the z interaction.
Temperature sensitive period of w expression is 3-4 days before eclosion, heat induction at this period causes a large number of dark red spots in an orange red background.
Novel class of w mutations have been selected and analyzed.
Regulation of the w gene locus has been studied using P element mediated transformation and in vitro mutagenesis. A 3.4kb segment of the w locus gives no detectable phenotypic expression.
The white locus is involved in the production and distribution of ommochrome (brown) and pteridine (red) pigments found in the compound eyes and ocelli of adult flies as well as the pigments in adult testis sheaths and larval Malpighian tubules; the specific function of the protein it encodes is still unknown, but it is believed to be a membrane-associated ATP-binding transport protein for pigment precursors in both the ommochrome and pteridine pathways (Sullivan and Sullivan, 1975; Mount, 1987; Dreesen, Johnson and Henikoff, 1988; Tearle, Belote, McKeown, Baker and Howells, 1989). w1 was the first BLUFF mutant found in D.melanogaster (Morgan, 1910; Morgan and Bridges, 1916). Mutant alleles do not appreciably affect the viability and fertility of the flies. Extreme white alleles as well as white deficiencies remove both brown and red pigments, the w1 allele having very little, if any, pteridine (Hadorn and Mitchell, 1951); isoxanthopterin is present in considerable quantity during pupation but is eliminated during the first three days of adult life (Hadorn, 1954). Hypomorphic alleles are visibly lighter in combination with w1 than when present as homozygotes. Intermediate white alleles result in partial loss of ommochromes and pteridines; some alleles also affect the distribution of these pigments in the compound eyes (Lewis, 1956; Green, 1959a; Green, 1959c). Although the mutants are positively phototactic, they show no optomotor responses (Kalmus, 1943). Wild-type alleles are incompletely dominant over mutant alleles, w/w+ heterozygotes, though visibly indistinguishable from w+/w+, have less red pigment (Muller, 1935; Ziegler-Gunder and Hadorn, 1958; Green, 1959b). Mutant larval discs transplanted into wild-type host develop autonomously (Beadle and Ephrussi, 1936). Early genetic studies identified mutations separable by intralocus recombination into at least seven groups spanning 0.03 cm (Lewis, 1952; MacKendrick and Pontecorvo, 1952; Green, 1959a; Judd, 1959). Mutants occupying the centromere-proximal sites apparently play a regulatory role (Judd, 1976). Subsequent molecular analysis has localized the proximal mutations to the 5' end of the transcription unit (we) and the upstream flanking sequences (wsp1) (Judd, 1987). Mutations at the distal sites have been mapped to the protein coding exons and the introns between them. The proximally-located regulatory mutants (we, for example) do not show dosage compensation; they suppress the zeste gene and some of them (the wsp1 alleles) affect the distribution of the red and brown screening pigments of the eyes. Most of the distally-located structural mutants show dosage compensation, wa/Y males having the same eye color as wa/wa females and do not suppress (but may interact with) zeste. Green (1959a) found that wi fails to show dosage compensation and does not suppress zeste; but wh exhibits both zeste suppression and dosage compensation. In spite of their heterogeneity, the alleles at the white locus fail to complement each other except for wsp1 which partially complements all other w alleles except in the presence of za (Babu and Bhat, 1980). Some white alleles (wc for example) are extremely unstable (Green, 1976); w1 is slightly unstable, giving rise to we and wh, mutants with darker eyes than w1. The locus is characterized by asymmetrical recombination involving transposons; the mutants wr,def and wr,dup are the result of such exchange (Davis, Shen and Judd, 1987). Some P-element white transformations show reproducible patterns of pigmentation which can be altered by the trans-acting gene zeste (Rubin, Hazelrigg, Karess, Laski, Laverty, Levis, Rio, Spencer and Zuker, 1985).
