FB2021_06, released December 14, 2021
Gene: Dmel\gl
Gene: Dmel\gl
none
transcription factor - zinc finger - required for normal development of photoreceptor cells in a larval photoreceptor known as Bolwig's organ, in the adult compound eye and in adult simple eyes, known as ocelli
Please see the JBrowse view of Dmel\gl for information on other features
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Stop-codon suppression (UGA) postulated; FBrf0216884.
Gene model reviewed during 5.44
3.0 (northern blot)
None of the polypeptides share 100% sequence identity.
604 (aa)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\gl using the Feature Mapper tool.
Comment: reported as larval eye primordium
In third instar larvae, gl transcripts are detected in the morphogenetic furrow of the eye imaginal disc. The expression is strongest in the furrow and persists at lower levels in more posterior regions of the disc.
gl transcripts are first detected in the early third-larval instar, and remain through to the adult stage, where they are apparently head-specific.
Expression of gl is not found in the DN1a or DN2 neurons.
gl protein isexpressed in third instar eye imaginal discs. It is first expressed incells along the anterior edge of the morphogenetic furrow. Expression isseen in all cells posterior to the furrow including photoreceptor cells,cone cells, and undifferentiated basal cells. gl expression continuesthroughout ommatidial assembly which is completed by 60 hours afterpupariation. At this time gl is detected in all photoreceptor nuclei butnot in cone cells. Expression is also observed in primary pigment cellsand in secondary and tertiary pigment cells. Outside of the retina, glprotein expression is observed in Bolwig\'s organ, in the ocelli, andpossibly in the brain.
gl protein is present in all cells posterior to the morphogenetic furrow in the eye imaginal disc.
GBrowse - Visual display of RNA-Seq signals
View Dmel\gl in GBrowse 2
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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.
monoclonal
polyclonal
Source for identity of: gl CG7672
gl has two distinct roles in the developing eye, being required both for ommatidium patterning and for photoreceptor differentiation.
Mutant embryos lack the corpus cardiacum.
11 "SS3-2" alleles of gl have been isolated in a screen for dominant modifiers of the sinaGMR.PN eye phenotype.
One of a class of genes with TATA-less promoters that have a subset of the conserved DPE sequence.
Deletion analysis using gl-Ecol\lacZ constructs shows that a 5147bp fragment 5' to the coding region in the gl gene is sufficient for near wild-type expression in the eye. Elements within this sequence that are conserved in both D.melanogaster and D.virilis have been analysed for their ability to confer eye-specific regulation on a heterologous (Hsp70) promoter.
Dvir\gl can provide glass activity in D.melanogaster in vivo. Deletion mutants of gl reveal three carboxy terminal fingers that are required for DNA binding, while two amino terminal fingers are dispensible though they do serve to increase affinity. Cotransfection assays of Schneider cells demonstrate gl is a potent transcriptional activator.
The expression of Calphotin protein was examined in the eye disc of a mutant allele of glass: and shown to be wild type, implying that Cpn expression precedes glass expression in the developing eye.
Observations of mutants support the proposal that axon fascicles can make at least some pathfinding decisions independently of their neighbours.
ro and gl gene products are required for B and B-H2 gene expression in R1 and R6.
gl alleles act as enhancers of spl alleles of N.
Mutant analysis demonstrates that gl is not required for viability. Phenotypic analysis concludes that photoreceptor cell precursors are recruited into developing ommatidia and proceed to establish a neural identity but they are unable to progress to photoreceptor cell identity and later die. Within the compound eye only the photoreceptor cells have an absolute and cell-autonomous requirement for gl function.
The gl mutant phenotype is due to a developmental defect: pattern formation defect.
Null mutations of glass remove photoreceptor cells in all of the three organs in which they occur. The mutants have compound eyes that are reduced in size and elliptical or diamond shaped; the texture is glassy from fused facets and irregular surface. Ocelli are flattened and lack pigment; there is no ocellar neuropil (Moses, Ellis and Rubin, 1989). In larvae, the visual Bolwig organs are absent in gl2, but present in gl3. Neither mutant expresses chaoptin (Moses, Ellis and Rubin, 1989). Color of compound eyes and Malpighian-tubules variably reduced depending on allele. In the presence of the dimorphic sex-linked modifier, msd(gl)d, males have more pigment than females, whereas males have the same eye color as females when they carry the monomorphic allele msd(gl)m (Birchler, 1984). dsx homozygotes of either X constitution but especially XX produce more pigment than dsx+ (Smith and Lucchesi, 1969); however msd(gl) was not controlled by Smith and Lucchesi. Pigmentation increases with increased developmental temperature. At high or very low levels of pigment production the sexual dimorphism disappears. Weak alleles have small smooth eyes and normal pigment levels in both sexes. Mild alleles have eyes reduced to two-thirds normal size and approximately 20% normal eye-pigment levels and male levels approximately 2X female levels. Moderate alleles reduce eye size to half normal and pigment to about 5% normal levels with male levels approximately 3X those of females. Strong alleles have eye area less than half normal and eyes are virtually colorless in both sexes (Smith and Lucchesi). The optic lamina is virtually nonexistent and the medulla is very small and disorganized in gl1; the lamina and medulla are both small and disorganized in gl2 and gl3 (Meyerowitz and Kankel, 1978). Mosaic studies using gl3 show that the gl genotype of the eye, rather than that of the optic lobe, determines the axon array of the optic lobe (Meyerowitz and Kankel, 1978). Structures of individual neurons studied by Garen and Kankel (1983). Retinula cells of the mutant are irregular and rhabdomeres are lacking; the electroretinogram shows no response to light (Pak, Grossfield and White, 1969). gl flies are nonphototactic and males exhibit depressed courtship activity (Merrell and Underhill, 1956; Hall, Tomkins, Kyriacou, Siegal et al., 1980). Wing beat frequency increased (Williams and Reed, 1944).
