ArticleMolecular and cellular biology1997
Drosophila melanogaster deficient in protein kinase A manifests behavior-specific arrhythmia but normal clock function.
Article in Molecular and cellular biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 77 citations in OpenAlex.
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- Time-course RNASeq of Camponotus floridanus forager and nurse ant brains indicate links between plasticity in the biological clock and behavioral division of labor.BMC genomics · 2022Article
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- Integration of Circadian Clock Information in theJournal of biological rhythms · 2021Review
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- A Symphony of Signals: Intercellular and Intracellular Signaling Mechanisms Underlying Circadian Timekeeping in Mice and Flies.International journal of molecular sciences · 2019Review
- Coordination between Differentially Regulated Circadian Clocks Generates Rhythmic Behavior.Cold Spring Harbor perspectives in biology · 2018Review
- Locomotion Behavior Is Affected by the GαGenetics · 2017Article
- Circadian Rhythm Neuropeptides in Drosophila: Signals for Normal Circadian Function and Circadian Neurodegenerative Disease.International journal of molecular sciences · 2017Review
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- Dual PDF signaling pathways reset clocks via TIMELESS and acutely excite target neurons to control circadian behavior.PLoS biology · 2014Article
- E and M circadian pacemaker neurons use different PDF receptor signalosome components in drosophila.Journal of biological rhythms · 2013Article
- PKA controls calcium influx into motor neurons during a rhythmic behavior.PLoS genetics · 2013Article
- Old flies have a robust central oscillator but weaker behavioral rhythms that can be improved by genetic and environmental manipulations.Aging cell · 2012Article
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- Circadian organization of behavior and physiology in Drosophila.Annual review of physiology · 2010Review
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- Protein kinase A inhibits a consolidated form of memory in Drosophila.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Drosophila melanogaster bearing mutations in the DCO gene, which encodes 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 from a requirement for PKA activity in photic resetting pathways, the timekeeping mechanism itself, or downstream effector pathways controlling overt behavioral rhythms. To address these possibilities, we examined the protein and mRNA products from the clock gene period (per) in PKA-deficient flies. The per protein (PER) and mRNA products undergo daily cycles in the heads and bodies of DCO mutants that are indistinguishable from those observed in control wild-type flies. These results indicate that PKA deficiencies affect the proper functioning of elements downstream of the Drosophila timekeeping mechanism. The requirement for PKA in the manifestation of rhythmic activity was preferentially greater in the absence of environmental cycles. However, PKA does not appear to play a universal role in output functions because the clock-controlled eclosion rhythm is normal in DCO mutants. Our results suggest that PKA plays a critical role in the flow of temporal information from circadian pacemaker cells to selective behaviors.
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