FB2021_05, released October 15, 2021
Gene: Dmel\bw
FB2021_05, released October 15, 2021
Gene: Dmel\bw
Gene: Dmel\bw
Gene: Dmel\bw
Plum
Please see the JBrowse view of Dmel\bw for information on other features
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Gene model reviewed during 5.52
Gene model reviewed during 5.44
Gene model reviewed during 5.57
Mutation in sequenced strain: complex; multiple in-frame stops; see allele report bw[1]..
3.0, 2.8 (northern blot)
675 (aa)
Heterodimer of brown with white.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\bw using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signals
View Dmel\bw in GBrowse 2
2-103
2-108.4
2-105
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.
Alleles designated bwR: brown-Rearranged were X-ray-induced derivatives of bw or bw+ by Slatis, 48k16. (Slatis, 1955). They exhibit variegated phenotype in combination with +. Mostly homozygous lethal; survivors have brown eyes. More complete descriptions in Lindsley and Grell, 1968. All associated with chromosome rearrangements with one breakpoint in 59DE and one in proximal heterochromatin.
bw can be simultaneously acted upon by pericentric and distal blocks of heterochromatin.
An element, P{Prat:bw} encoding a very low pigment level has been used to generate tandem arrays of up to 19 transposon copies at cytological location 65A10. The tandem arrays have altered polytene chromosome morphology.
One of a class of genes with TATA-less promoters that have a subset of the conserved DPE sequence.
Fluorescent in situ hybridisation (FISH) to interphase diploid nuclei demonstrates that the insertion of heterochromatin into bw causes the aberrant association of bw and its homologous copy with heterochromatin. The cytological association of the heterochromatic region is affected by chromosomal distance from heterochromatin and by genic modifiers of PEV.
Studies of PEV using a transposon-borne bw allele support a model in which local alterations affect the affinity of a gene region for nearby heterochromatin via homology-based pairing, rather than heterochromatin being propagated along the chromosome.
Dp(?;2)bwD position effect variegation (PEV) is observed as the very strong dominant variegating effect on the bw+ copy present on the homologous chromosome. Dp(?;2)bwD fails to coalesce with the chromocenter when its position along the chromosome places it beyond a threshold distance from heterochromatin. This threshold depends upon configuration of Dp(?;2)bwD chromosome and its paired homolog. The basis of silencing is paractivation across paired copies of the duplication as opposed to cis-spreading along the chromosome.
The D.virilis and D.melanogaster bw genes show functional conservation: Dvir\bw+ rescues the D.melanogaster mutant bw phenotype. Sequences required for transactivation are also conserved as Dvir\bw in D.melanogaster shows dominant PEV.
Dvir\bw transformed into D.melanogaster can be expressed. Induction of a PEV mutation in the Dvir\bw transgene reveals that Dvir\bw is capable of being trans-inactivated in D.melanogaster. These results support the conclusion that sequences responsible for trans-inactivation are conserved to regulate bw expression.
The sequence-specific component of the bw locus that is responsible for trans-inactivation may be the site at which a bw-specific transcription factor binds. Deletion analysis of the 8.4kb EcoRI fragment carrying the wild type bw+t8.4 from the P{bw+L}92C construct demonstrates that a 3.8kb fragment containing the bw coding region and 850bp of upstream sequences includes the genetic element responsible for trans-inactivation.
Chromatographic pattern of pteridine eye pigments neodrosopterin, sepiapterin, pterin, aurodrosopterin, acetyldihidrohomopterin, isoxanthopterin, biopterin and drosopterin measured in bw alleles.
Analysis of variance of developmental time and viability of pteridine pathway mutants in sf, se, Hn, dke and bw, indicated that viability of induced and natural population alleles is the same whereas developmental time tends to be longer for induced mutations as compared to natural population alleles.
Trans inactivation at bw requires some feature or component of heterochromatin, somatic pairing between variegating and wild-type alleles and a sequence in or near the bw gene in trans to the source of the heterochromatin. 35 lines carrying ectopic copies of bw were examined in the presence of dominant "bwV" alleles: no mutant spots or clones characteristic of trans-inactivation were seen. One transformant, "R26", has the P element construct colocalized with the resident bw+ and was trans-inactivated, suggesting that trans-inactivation is a chromosome-local phenomenon. Induction of position effect variegation on an ectopic copy of bw by chromosome rearrangement causes trans-inactivation of its paired homolog. Excisions and deletions of the copy of bw in cis to the rearrangement partially suppress transinactivation in a size-dependent manner, as if local somatic pairing (disrupted by the deletions) is necessary for trans-inactivation to occur.
bw has no substantial affect on ommochrome pigmentation in the fat body, ocelli or tubules.
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.
Transinactivation at the bw gene is antimorphic, occurs at the level of mRNA accumulation and is sensitive to certain structural configurations of the bw chromosomal region.
A bw cDNA has been cloned and sequenced.
Mutant alleles are useful as markers in clonal analysis.
Uptake studies indicate that bw, like w, blocks the transport of guanine and xanthine, likely pteridine precursors (Sullivan and Sullivan, 1975). Sequence comparisons between the predicted bw- and w-encoded proteins show that they are similar to one another and to subunits of active transport family members (Mount, 1987; Dreesen, Johnson and Henikoff, 1988).
Waaler, 15th Oct. 1919.
