High impact information on shakB

• In the adult central nervous system, and in the pupa during GF synapse formation, Pas is consistently expressed in the GF and in a large thoracic cell in the location of its postsynaptic targets [1].
• Drosophila Shaking-B protein forms gap junctions in paired Xenopus oocytes [2].
• The Drosophila melanogaster genes Passover and l(1)ogre and the Caenorhabditis elegans gene unc-7 define a gene family whose function is not known [3].
• Whereas all heterozygotes between these lethal alleles and Pas are viable, only some alleles complement the neural defect of Pas [4].
• Alleles of a lethal complementation group exhibit a complex pattern of complementation with Pas alleles [4].

Biological context of shakB

• On the basis of the expression patterns of shaking-B transcripts and the phenotypes conferred by mutations of shaking-B and homologous genes, we suggest that Shaking-B proteins and their homologues may be involved in the organisation of cellular membranes [5].
• We have mapped Pas to the 19E subdivision of the polytene X chromosome [6].
• Heterozygotes of Pas with chromosomal deletions in the vicinity of polytene band 19E3 exhibit the full set of neuronal defects shown by Pas homozygotes [6].
• The molecular structure of insect gap junctions differs from that in vertebrates, and in Drosophila is possibly encoded by the shaking B (= Passover) locus. shaking B2 is a null allele that acts in the nervous system [7].
• Mutations in the Drosophila shaking-B gene perturb synaptic transmission and dye coupling in the giant fiber escape system [8].

Anatomical context of shakB

• We propose that R1-R6 gap junctions are partitioned into at least two strata, proximal and distal, and that two populations of gap junctions exist, one extending throughout the lamina that does not require shakB, and a second at distal and mid-depth levels, which does [7].
• To test directly whether Shaking-B is a channel protein, we expressed it in paired Xenopus oocytes [2].
• Essential and neural transcripts from the Drosophila shaking-B locus are differentially expressed in the embryonic mesoderm and pupal nervous system [5].
• The Passover locus in Drosophila melanogaster: complex complementation and different effects on the giant fiber neural pathway [6].
• The shaking B gene in Drosophila regulates the number of gap junctions between photoreceptor terminals in the lamina [7].

Physical interactions of shakB

• We have examined the effects of mutations in two loci--the Shaker complex and shaking-B-on the taste pathway of Drosophila melanogaster Meigen at the behavioural and electrophysiological levels [9].

Other interactions of shakB

• Each chimera rescued either shakB or ogre but never both [10].
• Our previous work has described the development of the Giant Fibre in early metamorphosis and the involvement of the shaking-B locus in the formation of its electrical synapses [11].
• Localization of the genes shaking-B, small optic lobes, sluggish-A, stoned and stress-sensitive-C to a well-defined region on the X-chromosome of Drosophila melanogaster [12].

Analytical, diagnostic and therapeutic context of shakB

• Immunocytochemistry with shaking-B peptide antisera demonstrates that the expression of shaking-B protein in the region of GFS synapses coincides temporally with the onset of synaptogenesis; expression persists thereafter [13].
• Flies bearing the X-chromosome mutation Passover (Pas) fail to jump in response to a light-off stimulus, and electrical stimulation of the GF in the brain no longer elicits the normal response in the TTM [14].

References