Passover: A gene required for synaptic connectivity in the giant fiber system of Drosophila

Abstract

Passover (Pas) flies fail to jump in response to a light-off stimulus. The mutation disrupts specific synapses of the giant fibers (GFs), command neurons for this response. Pas was cloned from a P element-induced allele. The cDNA encodes a putative membrane protein of 361 amino acids. Null, hypomorphic, and dominant alleles were sequenced. 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. Pas establishes a new gene family. The Drosophila ogre protein, required for postembryonic neuroblast development, is 47% identical; the C. elegans Unc-7 protein, which when mutated alters the connectivity of a few neurons, is 33% identical.

Genetic basis of tolerance to O 2 deprivation in Drosophila melanogaster

“…Furthermore, we believe that the defects in the mutants are not general ones that affect all synapses. The reason for this is that our studies on shaking B mutants (13,14), which have specific defective connectivity distally to the GF, do not have an abnormal recovery from anoxia (data not shown).…”

“…Because the giant fiber (GF) system has been well studied (13,14), we made use of it to examine mutant and wild-type flies. Unanesthetized flies were placed on a microscope stage in the prone position with the help of soft wax.…”

Deficient assembly and function of gap junctions in Trf1, a trafficking mutant of the human liver-derived cell line HuH-7

“…That gap junctions in insect and other invertebrate cells are likely to be formed by a family of proteins unrelated to connexins [38][39][40] suggests that the enzymatic machinery to perform this modification is not restricted to derivatization of connexins. Should this type of modification be present in membrane proteins other than connexins, the discrepancy between the predicted and measured pIs is so striking that one questions why it had not been discovered earlier.…”

Regulation of Intermuscular Electrical Coupling by theCaenorhabditis elegansInnexininx-6

“…The shaking-B (lethal) mutation causes animals to die early, possibly due to feeding defects (Crompton et al, 1995), whereas the shaking-B (neural) mutation disrupts the gap junctions between giant fibers and its postsynaptic motorneuron partners (Thomas and Wyman, 1984;Krishnan et al, 1993;Phelan et al, 1996;Sun and Wyman, 1996). Ogre mutations lead to defects in optic lobe development and abnormal electrical activity in the eye (Lipshitz and Kankel, 1985;Watanabe and Kankel, 1990).…”