GABA receptor, GABAAR, GABAA receptor, resistance to dieldrin, LCCH1
GABA-A receptor that negatively modulates olfactory associative learning, possibly by gating the input of olfactory information into the mushroom bodies - regulates the length of time required to fall asleep
Gene model reviewed during 5.40
Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Gene model reviewed during 5.46
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Rdl using the Feature Mapper tool.
Rdl protein is expressed in the neuronal processes that overlap the insulin producing cells (IPC), a subset of the dorsomedial neurosecretory cells of the pars intercerebralis.
Rdl is expressed strongly in the soma of l-LNv neurons and at much lower levels in s-LNv neurons. Rdl puncta are also seen close to LNv terminals of the accessory medulla and in PDF varicosities formed by l-LNv neurites in the optic lobe.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Rdl 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.
4kb transcript identified during molecular analysis of the Rdl genomic region.
The actions of a volatile anaesthetic on a GABA-activated chloride channel (Rdl) and the implications of a channel directed point mutation (conferring insensitivity to PTX) on the modulation of the inhibitory currents by isoflurane are studied.
Polyclonal antibody staining shows Rdl protein to be confined to the CNS in adult flies.
Experiments with picrotoxin and four of its analogues suggest that interactions of convulsants with homo-oligomeric and multimeric GABA receptors are qualitatively similar. The Rdl homo-oligomer exhibits a pharmacological profile resembling that of native GABA receptors.
Subunit composition determines picrotoxin and bicuculline sensitivity of GABA receptors.
The Rdl product GABA receptor exhibits a unique pharmacological profile and functions efficiently as a homo-oligomer.
Rdl encodes a GABA-activated chloride channel with novel pharmacology in comparison to mammalian GABA receptors, and functions efficiently as a homomer.
When Rdl cRNA is expressed in Xenopus oocytes the product forms a functional GABA-receptor homo-oligomer.
Rdl is stably expressed in a culture cell line and pharmacological and electrophysiological aspects of the encoded receptor are characterised.
Rdl mutations manifest cyclodiene resistance through two different mechanisms. The A302S mutation weakens drug binding to the antagonist-favoured (desensitized) conformation by a structural change at the drug binding site. It also destabilizes the antagonist-favoured conformation in an allosteric sense. The global association of resistance with the A302S mutation suggests that insecticides have selected residue 302 for replacement because of its unique ability to influence both of these functions. The location of alanine 302 in the sequence of Rdl supports a mechanism of action in which convulsants such as picrotoxin bind within the channel lumen, and induce a conformational change to the desensitized state.
Cloning and characterisation of the complete coding region of a cDNA corresponding to Rdl.
The functional expression of both cyclodiene susceptible and resistant Rdl homomultimers of two alternative splice forms is studied in a baculovirus insect cell system.
Rdl confers insensitivity to cyclodiene insecticides. Sequence analysis of the insensitive allele has allowed the molecular basis of channel insensitivity to be identified.
The same mutation was found in many resistant populations in D.melanogaster. An identical mutation, or another substitution in the same amino acid position in the D.simulans gene has been identified in resistant populations of D.simulans.
The genomic organisation of the Rdl locus has been determined.
Susceptibility to cyclodiene is related to the ratio of susceptible and resistant alleles, not to the absolute number of either.
The Rdl GABA receptor has been cloned via a chromosomal walk and allowed manipulation of the resistance status of an individual to cyclodiene via germ-line transformation.