Disease relevance of ine

• We show that ine mutants lacking both isoforms are hypersensitive to osmotic stress, which we assayed by maintaining flies on media containing NaCl, KCl, or sorbitol, and that this hypersensitivity is completely rescued by high-level ectopic expression of the ine-RB isoform [1].
• Genomic fragments from this region, isolated from bacteriophage P1 clones, included those that detect transcriptional defects in rosA mutants in RNA blot experiments [2].

High impact information on ine

• The ine cDNA contains an open reading frame of 658 amino acids with a high degree of sequence similarity to members of the Na+/Cl(-)-dependent neurotransmitter transporter family [3].
• We conclude that ine mutations cause increased excitability of the Drosophila motor neuron by causing the defective reuptake of the substrate neurotransmitter of the ine transporter and thus overstimulation of the motor neuron by this neurotransmitter [3].
• Mutations in ine were localized on cloned DNA by restriction mapping and restriction fragment length polymorphism (RFLP) mapping of ine mutants [3].
• In situ hybridization of ine transcripts to developing embryos revealed expression of this gene in several cell types, including the posterior hindgut, Malpighian tubules, anal plate, garland cells, and a subset of cells in the central nervous system [3].
• We provide evidence that this hypersensitivity represents a role for ine that is distinct from the increased neuronal excitability phenotype of ine mutants [1].

Biological context of ine

• We utilized the potassium channel blocking drugs quinidine and dideoxy forskolin (DDF) to test the effects of ine on synaptic transmission [4].
• Finally, we show that each ine genotype exhibits a "threshold" [NaCl]: long-term maintenance on NaCl-containing media above, but not below, the threshold causes lethality [1].
• Inebriated is expressed in tissues and cells actively involved in K(+) transport, which suggests that it may have a role in ion transport, particularly of K(+) [5].
• The Drosophila receptor oscillation A (rosA) mutations, which cause electroretinogram (ERG) defects, including oscillations, were localized to the 24F4-25A2 region of chromosome 2L [2].

Anatomical context of ine

• We cloned the inebriated homologue MasIne from Manduca sexta and expressed it in Xenopus laevis oocytes [5].
• Drosophila rosA gene, which when mutant causes aberrant photoreceptor oscillation, encodes a novel neurotransmitter transporter homologue [2].
• Tissue in situ experiments identified the rosA transcript to be localized to many tissues, with higher levels of hybridization in the nervous system and digestive tract [2].

Associations of ine with chemical compounds

• Application of DDF to ine mutants had no effects either in the presence or absence of quinidine [4].

Other interactions of ine

• However, in a Sh mutant background, ine mutations cause downturned wings and an indented thorax [4].

Analytical, diagnostic and therapeutic context of ine

• In this paper, we describe the cloning and sequence analysis of ine [3].

References