DROSOPHILA-MELANOGASTER DEFICIENT IN PROTEIN-KINASE A MANIFESTS BEHAVIOR-SPECIFIC ARRHYTHMIA BUT NORMAL CLOCK FUNCTION

Drosophila melanogaster bearing mutations in the DCO gene, which encod es the major catalytic subunit of cAMP-dependent protein kinase (PKA), displays arrhythmic locomotor activity strongly suggesting a role for PKA in the circadian timing system. This arrhythmicity might result f rom a requirement for PKA activity in photic resetting pathways, the t imekeeping mechanism itself, or downstream effector pathways controlli ng overt behavioral rhythms. To address these possibilities, we examin ed the protein and mRNA products from the clock gene period (per) in P KA-deficient flies. The per protein (PER) and mRNA products undergo da ily cycles in the heads and bodies of DCO mutants that are indistingui shable from those observed in control wild-type flies. These results i ndicate that PKA deficiencies affect the proper functioning of element s downstream of the Drosophila timekeeping mechanism. The requirement for PKA in the manifestation of rhythmic activity was preferentially g reater in the absence of environmental cycles. However, PKA does not a ppear to play a universal role in output functions because the clock-c ontrolled eclosion rhythm is normal in DCO mutants. Our results sugges t that PKA plays a critical role in the how of temporal information fr om circadian pacemaker cells to selective behaviors.