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Electrical silencing of Drosophila pacemaker neurons stops the free-running circadian clock.
- Source :
-
Cell [Cell] 2002 May 17; Vol. 109 (4), pp. 485-95. - Publication Year :
- 2002
-
Abstract
- Electrical silencing of Drosophila circadian pacemaker neurons through targeted expression of K+ channels causes severe deficits in free-running circadian locomotor rhythmicity in complete darkness. Pacemaker electrical silencing also stops the free-running oscillation of PERIOD (PER) and TIMELESS (TIM) proteins that constitutes the core of the cell-autonomous molecular clock. In contrast, electrical silencing fails to abolish PER and TIM oscillation in light-dark cycles, although it does impair rhythmic behavior. On the basis of these findings, we propose that electrical activity is an essential element of the free-running molecular clock of pacemaker neurons along with the transcription factors and regulatory enzymes that have been previously identified as required for clock function.
- Subjects :
- Animals
Cell Size genetics
Dark Adaptation genetics
Drosophila melanogaster cytology
Drosophila melanogaster genetics
Gene Expression Regulation, Developmental genetics
Genes, Lethal genetics
Insect Proteins genetics
Insect Proteins metabolism
Motor Activity genetics
Mutation genetics
Nervous System cytology
Nervous System embryology
Neurons cytology
Nuclear Proteins genetics
Nuclear Proteins metabolism
Period Circadian Proteins
Photic Stimulation
Potassium Channels genetics
Potassium Channels, Inwardly Rectifying genetics
Potassium Channels, Inwardly Rectifying metabolism
Synapses genetics
Synapses metabolism
Action Potentials genetics
Biological Clocks genetics
Circadian Rhythm genetics
Drosophila Proteins
Drosophila melanogaster metabolism
Nervous System metabolism
Neurons metabolism
Potassium Channels deficiency
Synaptic Transmission genetics
Subjects
Details
- Language :
- English
- ISSN :
- 0092-8674
- Volume :
- 109
- Issue :
- 4
- Database :
- MEDLINE
- Journal :
- Cell
- Publication Type :
- Academic Journal
- Accession number :
- 12086605
- Full Text :
- https://doi.org/10.1016/s0092-8674(02)00737-7