Gene model reviewed during 5.50
Gene model reviewed during 5.45
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Gene model reviewed during 5.52
9.5, 7.9, 7.2, 4.8, 3.9 (northern blot)
1054 (aa); 116 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\rdgB using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\rdgB 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.
Mutation affects olfactory physiology in the maxillary palp in a manner analogous to that for the antenna: delay in the return to the resting potential following odorant stimulation.
The calcium content of light and dark raised flies demonstrates that calcium accumulation is a secondary effect, rather than primary effect, in the degeneration process.
The pattern of expression of rdgB protein in the adult Drosophila head has been studied.
Retarding the light induced photoreceptor degeneration in rdgB mutants by calcium channel blockers suggests that toxic increase in intracellular calcium by means of voltage gated calcium channel leads to photoreceptor degeneration in mutants.
rdgB gene product is required for normal response in the peripheral olfactory system. rdgB is required for both visual and olfactory physiology suggesting that visual and olfactory transduction share at least one common molecular step.
Sequence analysis shows that rdgB encodes a putative integral membrane protein, that has sequences in common with proposed functional domains of Ca2+-ATPase, and may therefore act as a Ca2+ transporter.
rdgB mutations, especially those causing R1-6-specific degeneration (notably rdgB9), frequently used in experiments aimed at assessing behavioral and physiological significance of light input through central photoreceptors only; hence, phototaxis mediated by R7,8 (Willmund and Fischbach, 1977; Broda and Willmund, 1981; Hu and Stark, 1980; Miller, Hansen and Stark, 1981); optomotor responses eliminated by degeneration of R1-6 (Heisenberg and Buchner, 1977); visual learning not impaired; intensity discrimination less acute than in wild type; no positive indication of color discrimination (Bicker and Reichert, 1978). Visual pigment specific to outer photoreceptors (Harris et al., 1976); absence of physiological effects of rdgB on ocelli (Hu et al., 1978); and physiological effects of a trp mutation on the central photoreceptors (Chen and Stark, 1983).
Photoreceptors in each facet of compound eye show light-induced degeneration; morphology is essentially normal on eclosion, but maintenance of mutant adults on diurnal light regime causes severe degeneration within approximately one week (Harris and Stark, 1977); the cell bodies and axons of photoreceptors begin to look ultrastructurally abnormal after three days (Stark and Carlson, 1982); the various rdgB mutations tend to cause the outer photoreceptors (R1-6) in each facet to degenerate more than the inner two cells (R7,8), such that rdgB9 and rdgB1 have R7,8 preserved in nearly all ommatidia, rdgB6 and rdgB8 retain most central cells and rdgB7 plus rdgB5 show progressively worse degeneration of R7,8 with rdgB5 retaining these cells in only 10% of the facets according to Harris and Stark (1977); degeneration of R7,8 not confirmed, however, by Stark et al. (1983). After R1-6 have degenerated and the central cells have or have not, depending on the allele, R7,8 retain at least quasi-normal function as indicated by electroretinograms (Stark, 1977); degeneration is photoreceptor autonomous in mosaics (Hotta and Benzer, 1970; Harris and Stark, 1977); autonomous in mixed ommatidia at the electron-microscope level (Hofbauer and Campos-Ortega, 1976); ultrastructural details of degeneration include electron-dense cytoplasm with liposomes, lysosome-like bodies, myeloid bodies and vacuoles and electron-dense reticulum and degenerate mitochondria, electron opaque photoreceptor axons lacking synaptic vesicles and containing seemingly none of the typical presynaptic structures (Stark and Carlson, 1982). Degenerating photoreceptors are associated with degeneration in the first order optic ganglion (the lamina), though the second order medulla is spared (Stark, Chen, Johnson and Frayer, 1983); high temperature treatments accelerate degeneration, whereas homozygosity for an Acph-1-null mutation delays it slightly (Harris and Stark, 1977). After rearing of rdgB animals in room light, the R1-6 cells are physiologically non-functional at eclosion (revealed by ERGs), in spite of apparently normal cellular structure (Harris and Stark, 1977). Prolonged depolarizing afterpotentials (induced by strong blue light) are abnormally short-lived and cannot be reversed by orange light, unlike the response of wild-type (Harris and Stark, 1977); degeneration of the photoreceptors is dramatically retarded by rearing in the dark followed by maintenance of adults under this condition (Harris and Stark, 1977); the same retardation of the mutations' effects occur when an rdgB mutation is linked to an ERG-minus norpA mutation (Harris and Stark, 1977), although degeneration does eventually occur in the double mutants (Stark et al., 1983); three norpA mutations were induced based on their inhibition of rdgB-induced degeneration (Harris and Stark, 1977), with two of the new mutations leading to very small ERGs but the third, norpA56, allowing for apparently normal retinal physiology (also see Stark, Chen, Johnson and Frayer, 1983); this mutation revealed as a norpA allele, based on uncoverage of its degeneration-suppressing effects by an ERG-minus norpA mutation (Harris and Stark, 1977); norpA56's suppressing effects are allele-specific, to the extent that rdgB9-induced degeneration is retarded (and this was the rdgB allele used to isolate this suppressor), but the effects of another allele, rdgB1, are not (Harris and Stark, 1977); ort1 ninaE1 (formerly "oraJK84"), an opsin-deficient genotype, also blocks light induced degeneration of receptor cells in rdgB9 (Stark and Carlson, 1985). Two rdgB alleles (unspecified) are associated with premature death of adults exposed to 29oC (Homyk, Pye and Pak, 1981); further indications of pleiotropic action of this gene come from isolation of a hypoactive rdgB allele <up>originally hypoF (Homyk et al., 1980)</up>; this mutation (mapping between v and f, as does rdgB) was shown to be an rdgB allele by Homyk and is now called rdgB23; it causes adults to be somewhat inactive in their general movements and their jumping ability to be weak; there are no light-on or light-off transient spikes in the ERG and optomotor responses are eliminated; two polypeptide spots observed in two-dimensional gel analysis of eye-specific proteins are reduced in intensity in an rdgB mutant -- the same spots as affected by rdgA (Hotta, 1979)