Domain-swapping experiments for shakB and ogre indicate that residues crucial for innexin function are found in the intracellular loop and well as a short stretch N-terminal to the second transmembrane domain.

Electroretinograms for molecular chimeras and rescue constructs for shakB and ogre indicate that innexins are not interchangeable in their roles of promoting normal neural development in flies.

Mutations in shakB eliminate electrical, but not chemical synapses in the giant fiber escape system.

shakB expressed in paired Xenopus oocytes localises to the membrane and its presence induces the formation of intercellular channels.

shakB causes a reduction in number of structural gap junctions relative to wild type, this action is localised to the middle and upper depths of the lamina.

Expression of neuronal shakB protein coincides with, and is essential for, the establishment of functional electrical (gap-junctional) synapses.

shakB is necessary for gap-junctional communication between the neurons of the giant fibre system.

Multiple transcripts are produced from shakB by differential splicing and alternate promoter usage. Essential and neural transcripts of shakB are differentially expressed in the embryonic mesoderm and pupal nervous system. On the basis of its expression pattern and the phenotypes of mutants at shakB and homologous genes, shakB and its homologues may be involved in the organization of cellular membranes.

shakB locus encodes two proteins, one necessary for the giant fibre system and one necessary for viability. Neural only mutations map to neural specific exons, lethal mutations map to viable specific exons and inactivate the other protein, neural lethal mutations map to the common exons and inactivate both proteins.

Dye coupling between the giant fiber and its post-synaptic targets is absent in neural shakB mutants. The shakB protein may act to stabilise the gap junctions.

Driving of tergotrochanteral muscle motorneuron by the giant fiber is defective in mutant genotypes, despite its generally normal pathfinding i.e. growing into the normal synaptic region, suggesting that shakB may disrupt cell recognition, synaptogenesis, or synaptic function in the tergotrochanteral muscle motorneuron or its presynaptic partners.

Gene cloned from a P element induced allele and the sequence suggests a membrane protein gene product.

shakB encodes a putative 120 amino acid protein with 48% identity to that of ogre.

Behavioural data suggests antennal and maxillary basiconic sensilla may be important receptors for short chain alcohols and organic acids but less crucial for acetates, aldehydes and ketones.

shakB locus may contain two functional domains: one required for viability and the other for a normal neuronal phenotype.

Mutations disrupt the synaptic transmission of the giant fibre (GF) - tergotrochanteral muscle (TTM, jumping muscle) pathway and the giant fibre (GF) - dorso-longitudinal muscle (DLM) pathway.

Some of the shakB mutants are viable but defective in their neural phenotypes as homo-, hemi-, or heterozygotes, but other mutants are homozygous lethals that may or may not complement the viable shakB alleles. The viable mutants have difficulty in controlling leg movements and show leg tremors under ether anesthesia (Homyk et al., 1980). They show no escape response; the flies are unable to jump into the air and fly away at a light off stimulus (Thomas, 1980; Thomas and Wyman, 1984). Unlike the mutant Sh, the leg tremors of shakB are weak and end when the legs are severed from the body (indicating a central nervous system defect). In wild-type flies, the thoracic muscles involved in the escape response are driven by the giant fiber (GF) neuron pathway connecting the brain and thoracic ganglia. In the mutant shakB, the synapse between the GF axon and the postsynaptic interneuron (PSI) or between the PSI and the dorsal longitudinal muscle (DLM) seems to be defective; thus the DLM does not respond to visual stimulation by depressing the wings in flight. The synapse between the GF axon and the motor neuron of the tergotrochanter muscle (TTM) also seems to be defective, resulting in a weak response or no response from the TTM, the muscle that extends the leg in jumping. The motor neurons 'pass over' the midline of the thoracic central nervous system and send aberrant branches into each contralateral mesothoracic ganglion. The abnormal neural phenotype is more pronounced if shakB is uncovered by a deficiency (Wyman and Thomas, 1983; Baird and Hillis, 1985; Baird, Schalet and Wyman, 1990). The muscles themselves and their neuro-muscular junctions are not abnormal (Thomas and Wyman, 1984). Viable shakB mutants are also characterized by electroretinogram (ERG) abnormalities; the corneal negative component is reduced and the on- and off- transients are reduced or absent. Neurons in the brain are affected, as indicated by failure of one of the superoesophageal brain commissures to fill with cobalt when the antennal nerve is backfilled (Aceves-Pina). shakB³ (= Pas) is partially dominant to wild type in regard to the mutant's elimination of the jump response, but the other viable alleles are recessive. +/Df(1)16-3-35 and +/Df(1)A118 are behaviorally normal, but Df(1)16-3-35/Df(1)A118 females are shakB in phenotype.

Source for merge of: shakB CG12678

Source for merge of: shakB CG15451

Annotations CG32508 and CG12678 merged as CG34358 in release 5.2 of the genome annotation.

Annotations CG1321 and CG15451 merged as CG32508 in release 3 of the genome annotation.

A number of homozygous lethal alleles have been located in the shakB region. Six of them do not complement the shakB neural phenotype; two of the remainder have been tested and found to complement this neural phenotype, but do not complement the lethality of the other lethal alleles. The six noncomplementing lethals also fail to complement Df(1)16-3-35 (distal deficiency) and Df(1)A118 (proximal deficiency), while the two complementing lethals complement Df(1)A118 but not Df(1)16-3-35.