multiple wing hair, BP1018
Gene model reviewed during 5.48
Gene model reviewed during 5.44
Low-frequency RNA-Seq exon junction(s) not annotated.
None of the polypeptides share 100% sequence identity.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\mwh using the Feature Mapper tool.
mwh protein was observed in wing cells after 30 hours APF. It was observed in an uneven zigzag staining pattern at the cell periphery and accumulates near adherens junctions. It accumulates in both growing and emerging wing hairs and accumulates preferentially in the proximal part of the hair and not in the base at that time. Later in hair morphogenesis (after 36 hr APF), it accumulates preferentially in the base of the hairs.
GBrowse - Visual display of RNA-Seq signalsView Dmel\mwh in GBrowse 2
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.
Source for identity of: CG34022 BP1018
Annotations CG13913 and CG34022 merged as CG43772 in release 5.44 of the genome annotation. Merge supported by RNA-Seq junction and coverage data.
mwh appears to function as a repressor of actin filament formation, restricting the production of actin-rich prehairs to distal cell edges in the pupal wing.
mwh has two temporally separate functions in wing development; early proximal mwh protein accumulation restricts hair initiation to the distal side of wing cells, while the later accumulation of mwh protein in the wing hair prevents the formation of ectopic secondary wing hairs.
New annotation (CG34022) in release 4.3 of the genome annotation.
The genotoxicity of six insecticides has been analysed using the wing spot test.
The wing spot test has been used to assay the antigenotoxicity of a number of compounds.
SMART is well suited for the determination of genotoxicity produced by in vivo nitrosation processes and for the study of their modulation by individual compounds or dietary complex mixtures.
The genotoxic effect DEHP is tested using the SMART assay, results reveal DEHP does not have a genotoxic effect.
The genotoxic effect of 4 inhibitors of DNA topoisomerases has been studied using the wing spot assay.
Ethanol reduces the mutagenic effect of γ-irradiation in SMART assay, mainly by decreasing the frequency of mitotic recombination.
The genotoxic effect of integerrimine (ITR) are analysed using the wing spot test: ITR is genotoxic.
Definitive denticle belt phenotypes (abnormal hairs and/or bristles) are foreshadowed by abnormal organisation of the actin cytoskeleton in embryonic epidermal cells.
Vicinal chloroalcohols are investigated for genotoxicity in the wing spot test (SMART): tested compounds are non-genotoxic in this in vivo assay.
Sodium azide is tested for somatic mutation and mitotic recombination induction in wing imaginal disc cells using the wing spot test. Sodium azide induces exclusively mitotic recombination in wing somatic cells after chronic exposure. This activity is reduced in the presence of high bioactivation capacity.
The genotoxic effect PhIP is tested using the SMART assay, results reveal PhIP has a DNA-damaging activity.
The mutagenic and/or carcinogenic activity of electromagnetic fields is estimated using the wing spot test in larvae, exposure causes a statistically significant enhancement of somatic recombination. Supplement of vitamin E suppresses this enhancement.
Wing spots in the SMART reveal enzyme-sulfhydryl blocking agents, such as MMTS and DPDS, are effective antimutagens in vivo.
The effect of chlorophyll on the genotoxic activity of 4-nitroquinoline 1-oxide has been studied using the wing spot test.
The genotoxic effects of N-nitroso-N-methylurea (MNU) and acetone oxime (ACOX) are tested using the SMART test. The effect of Hsap\GST on the genotoxic effect is studied: flies carrying three or more copies of Hsap\GST are significantly more resistant to the genotoxic effect of ACOX.
SMART is used to test the genotoxic effect of fullerene C-60: only at the highest possible fullerene concentration a slight genotoxic effect was observed in wing cells.
Only the maximum possible content of fullerene C60 produces a slight genotoxic effect when using the SMART test.
Assays of a series of compounds in the wing spot test indicates the single mwh spots appear most frequently, followed by less frequent twin spots and then the quite rare flr spots. Some compounds behave in this manner, others do not in that the frequency of single flr spots is equal to or exceeds that of twin spots.
The spectrum of genotoxic events detected by the wing somatic mutation and recombination test (SMART) and the wi eye spot test is different. The wi eye spot test appears not to detect mitotic recombination the way the wing spot test does.
The genetic effects of exposure to a range of concentrations of alpha particles has been studied using the wing-spot test.
Six alkylating agents have been ranked as follows according to their genotoxic potency in the wing spot test: methyl methanesulfonate > mitomycin C > N-dimethylnitrosamine > chlorambucil ~ monocrotaline > N-diethylnitrosamine.
The genotoxicity of 6 phenazine and aminophenazine derivatives is assayed using the wing spot test in larvae, chemicals exhibit significant mutagenicity.
Gamma ray induced somatic clones of wing cells demonstrates the level of induction of mwh-like structures consisting of two trichomes and of true mwh mutations is the same if the former are located on the wing surface. These twi-trichome structures must be taken into account when using the mwh type spots in the method of somatic mosaics of wing cells.
The effects of 10 carcinogens on the wing spot test are evaluated.
Three assays (z-w, wi and wing spot) are used to evaluate the genotoxic response of five chemicals classified as genotoxic non-carcinogens, chemicals significantly increase the frequency of mutant clones.
The wing somatic mutation and recombination test (SMART) of larvae is used to evaluate the genotoxicity of three polycyclic aromatic hydrocarbons (PAHs) and three of their nitro derivatives, genotoxic activity can be detected in somatic cells.
In young larvae only a few but very large spots are induced by application of a mutagen in the wing spot test. In older larvae the frequency is considerably increased but the sizes are smaller. Practically no twin spots (result of mitotic recombination) are found in young or in very old larvae. Results demonstrate the optimal age of the larvae for mutagen treatment is 72 hours.
Wing spot test is used to evaluate the genotoxic effect of griseofulvin in somatic larval cells, griseofulvin is genotoxic in somatic cells.
Genotoxic activity in vivo of the naturally occurring glucoside, cycasin, is assayed in the wing spot test.
Ascorbic acid (vitamin C), when used as a pretreatment, protects against mutation/recombination induced by γ rays and chromium (VI) oxide in larvae in the wing spot test.
Wing spot test reveals two triazine herbicides, terbutryn and terbuthylazin, are genotoxic in the wing primordia.
Wing spot test reveals the triazine herbicide, simazine, is genotoxic in the wing primordia.
The attached X and mwh/flr spot test system were used to demonstrate that ginseng and Salvia miltiorrhiza have inhibitory effects on the in vivo mutagenicity induced by N-methyl-N-nitro-N-nitrosoguanidine (MNNG) during spermatogenesis.
The wing spot test has been used to demonstrate that the somatic mutation and recombination test can be used for the genotoxic activity of alcoholic and non-alcoholic beverages.
The adenine derivatives, (R,S)-9-(2,3-dihydroxypropyl)adenine, D-eritadenine and 9-(2-phosphonylmethoxyethyl)adenine, are potent inducers of both single spots and twin spots in a wing-spot assay.
Wing spot tests rank the genotoxic effectiveness of a number of metal salts in the following order: CoCl2 > ZnCl2 > MoCl3 > (MnCl2, NiCl2).
Somatic mutation and recombination test (SMART) is used to determine the relevance of the in vitro effects induced by benzophenone-3: benzophenone-3 is not genotoxic.
Wing-spot assay is used to evaluate the quantitative relationship between BaP-DNA adduct formation, determined by 32P-postlabelling, and the induction of phenotypically mutant cells.
Chloral hydrate is recombinogenic in the wing spot test.
Arsenic acid has an inhibitory effect on the induction of wing spots by gamma irradiation or alkylating agents in a wing-spot assay.
High temperatures cause a small number of mwh spots in the wing-spot assay and cold temperatures yield much greater number of single spots.
The wing spot test is used to evaluate the genotoxicity of the antitumour indenoisoquinoline analogues of nitidine chloride and fagaronine chloride in larvae transheterozygous for mwh and flr, the analogues have a very weak genotoxic effect.
The somatic mutation and recombination test (SMART) in wing cells of three day old larvae transheterozygous for mwh and flr is used to study the mutagenic potential of three benzocphenanthridine alkaloids with antileukemic properties as compared with that of two structurally related aromatic polycyclic hydrocarbons.
The wing spot test has been used to demonstrate that atrazine is genitoxic to the wing disc cells and male germline cells.
Wing spot tests indicate that 2,4-dichlorophenoxyacetic acid is genotoxic in the primordial wing cells of Drosophila.
Four antidepressants and one neuroleptic drug are tested for genotoxicity using the somatic mutation and recombination test (SMART) in wing cells of three day old larvae transheterozygous for mwh and flr, the compounds are genotoxic.
The wing spot test has been used to demonstrate that chloral hydrate is genitoxic to the wing disc cells and male germline cells.
Wild type allele of mwh is present on Dp(3;f)Th and displays mosaic expression on the wings.
The mutagenicity of tepezcohuite has been assayed using the wing spot test.
The wing spot test has been used to assay the mutagenic activity of a number of polycyclic aromatic hydrocarbons.
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.
The mutagenic and recombinogenic activity of 3-beta-hydroxy-13-alpha-amino-13,17-seco-5-alpha-androstan-17-oic-13,17-lactam-p-bis-(2-chloroethyl) aminophenoxyacetate (NSC 294859) has been assayed using a wing somatic mutation and recombination test (SMART).
Wing spot test (SMART) and sex-linked recessive lethal test (SLRLT) are used to test the mutagenicity of sumithion, a broad spectrum insecticide - compound is mutagenic in wing primordial cells and induces recombination at high doses.
Acrylamide is both mutagenic and recombinogenic in wing disc cells and induces sex-linked recessive lethals.
Genotoxicity of a chelating agent, nitrilotriacetic acid (NTA), is investigated using SMART. NTA is active in inducing mitotic recombination and possible aneuploidy in somatic cells.
SMART in wing cells is used to test genotoxicity of 5 tricyclic antidepressants, results implicate the nitrogen atom at position 5 in the 7-membered ring of the tricyclic molecule as being responsible for the genotoxic property of the compounds.
The effects of chemicals classified as non-carcinogens or unclassified, but known to have given one or more positive results, are tested using SMART. Also the sensitivity of SMART compared to SLRLT is tested.
Genotoxicity of ethyl carbamate is tested using SMART: ethyl carbamate induces, in a dose-dependent manner, single as well as twin spots, indicating a recombinogenic activity.
The effects of repair deficiency are studied by comparing the frequency of somatic mutation and mitotic recombination in repair proficient female progeny with that in excision repair defective male progeny. Nine chemical mutagens with various modes of action are tested in this way.
The genetic toxicity of six carcinogens and six non-carcinogens are tested using SMART: carcinogens are highly toxic and the non-carcinogens are non-genotoxic.
The genotoxic activity of a photochemical reaction mixture of 1,3-butadiene and nitrogen dioxide has been assayed using the wing spot test.
SMART is used to assay the effects of NTA and EDTA in germ and somatic cell lines.
Mutant alleles are useful as markers in clonal analysis.
di Pasquale, Dec. 1950.