The passover locus in Drosophila melanogaster: complex complementation and different effects on the giant fiber neural pathway
1990
Drosophila melanogaster bearing the Passover mutationfail to jump in response to a light-off stimulus. Pas also disrupts some of the synapses between the neurons of thegiant fiber system which mediate this escape behavior. We have mapped Pas to the 19E subdivision ofthe polytene X chromosome. Our genetic analyses reveal that deletions of either of twononoverlapping regions fail to fully complement Pas. Heterozygotes of Pas with chromosomal deletions inthe vicinity of polytene band 19E3 exhibit the full set of neuronal defects shown by Pashomozygotes. Alleles of the R-9-29 complementation group, which maps to band 19E3, exhibit a complexpattern of complementation with Pas. Heterozygotes combining the lethal R-9-29 alleles withPas are all viable, some complement the neuronal defects of Pas, but most exhibit these defects. Theviable shaking-B2 mutation also fails to complement Pas, the R-9-29 alleles or the 19E3 deficiencies. TheR-9-29 locus may contain two functional domains, one required for viability the other for normal neuronal phenotype. trans-Heterozygotes bearing mutant alleles or a deficiency of thefirst region (19E3) together with deficiencies of the second region (19E5-6) also exhibit some of the neuronal defects shown by the Passover mutant. Deficiencies which delete the entire 19E3 to 19E6 interval do not produce this phenotype when heterozygous with a normal X chromosome. Thus normal function requires a cis-interaction between the two regions. These findings raise the possibility thatthe gene mutated by Pas is split or separated from a cis-activator by at least one othergene.
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