The shaking B gene in Drosophila regulates the number of gap junctions between photoreceptor terminals in the lamina.

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. In the shakB2 mutant, one site of action are gap junctions between photoreceptor terminals in the cartridges of the lamina, beneath the compound eye, which we assayed from the number of close-apposition profiles in thin-section EM. The number of profiles in the Canton-S (C-S) wild type is about 0.5 per cartridge per section in distal and mid-lamina depths, and significantly less, about one quarter this value, closer to the brain, in the proximal lamina. In shakB2, there are fewer profiles, approximately one quarter the number of appositions in distal and mid-lamina depths as in C-S, and their number does not differ significantly from those at the proximal depth in either the mutant or wild type. Thus mutant action is associated with a reduced number of appositions at distal and mid-lamina depths. 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. The number of gap junctions is reduced in mutant shakB2, and surviving appositions at distal and middle lamina depths possibly have wider clefts than in C-S. Gap junctions are reduced equally between all R1-R6 terminals, so the two different types of junction proposed, shakB2- and non-shakB2-dependent, can apparently express in a single receptor terminal.