rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
4
|
pubmed:dateCreated |
2002-6-27
|
pubmed:abstractText |
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.
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Drosophila Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Insect Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ork1 protein, Drosophila,
http://linkedlifedata.com/resource/pubmed/chemical/PER protein, Drosophila,
http://linkedlifedata.com/resource/pubmed/chemical/Period Circadian Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels, Inwardly...,
http://linkedlifedata.com/resource/pubmed/chemical/timeless protein, Drosophila
|
pubmed:status |
MEDLINE
|
pubmed:month |
May
|
pubmed:issn |
0092-8674
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
17
|
pubmed:volume |
109
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
485-95
|
pubmed:dateRevised |
2009-11-19
|
pubmed:meshHeading |
pubmed-meshheading:12086605-Action Potentials,
pubmed-meshheading:12086605-Animals,
pubmed-meshheading:12086605-Biological Clocks,
pubmed-meshheading:12086605-Cell Size,
pubmed-meshheading:12086605-Circadian Rhythm,
pubmed-meshheading:12086605-Dark Adaptation,
pubmed-meshheading:12086605-Drosophila Proteins,
pubmed-meshheading:12086605-Drosophila melanogaster,
pubmed-meshheading:12086605-Gene Expression Regulation, Developmental,
pubmed-meshheading:12086605-Genes, Lethal,
pubmed-meshheading:12086605-Insect Proteins,
pubmed-meshheading:12086605-Motor Activity,
pubmed-meshheading:12086605-Mutation,
pubmed-meshheading:12086605-Nervous System,
pubmed-meshheading:12086605-Neurons,
pubmed-meshheading:12086605-Nuclear Proteins,
pubmed-meshheading:12086605-Period Circadian Proteins,
pubmed-meshheading:12086605-Photic Stimulation,
pubmed-meshheading:12086605-Potassium Channels,
pubmed-meshheading:12086605-Potassium Channels, Inwardly Rectifying,
pubmed-meshheading:12086605-Synapses,
pubmed-meshheading:12086605-Synaptic Transmission
|
pubmed:year |
2002
|
pubmed:articleTitle |
Electrical silencing of Drosophila pacemaker neurons stops the free-running circadian clock.
|
pubmed:affiliation |
Department of Biology, New York University, New York 10003, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|