Light Entrainment of the Mammalian Circadian Clock by a PRKCA-Dependent Posttranslational Mechanism

Vladimira Jakubcakova; Henrik Oster; Filippo Tamanini; Cristina Cadenas; Michael Leitges; Gijsbertus T.J. van der Horst; Gregor Eichele

doi:10.1016/j.neuron.2007.04.031

Light Entrainment of the Mammalian Circadian Clock by a PRKCA-Dependent Posttranslational Mechanism

Vladimira Jakubcakova, Henrik Oster, Filippo Tamanini, Cristina Cadenas, Michael Leitges, Gijsbertus T.J. van der Horst, Gregor Eichele^*

^*Korrespondierende/r Autor/-in für diese Arbeit

Institut für Neurobiologie

71 Zitate (Scopus)

Abstract

Light is the most potent stimulus for synchronizing endogenous circadian rhythms with external time. Photic clock resetting in mammals involves cAMP-responsive element binding protein (CREB)-mediated transcriptional activation of Period clock genes in the suprachiasmatic nuclei (SCN). Here we provide evidence for an additional photic input pathway to the mammalian circadian clock based on Protein Kinase C α (PRKCA). We found that Prkca-deficient mice show an impairment of light-mediated clock resetting. In the SCN of wild-type mice, light exposure evokes a transient interaction between PRKCA and PERIOD 2 (PER2) proteins that affects PER2 stability and nucleocytoplasmic distribution. These posttranslational events, together with CREB-mediated transcriptional regulation, are key factors in the molecular mechanism of photic clock resetting.

Originalsprache	Englisch
Zeitschrift	Neuron
Jahrgang	54
Ausgabenummer	5
Seiten (von - bis)	831-843
Seitenumfang	13
ISSN	0896-6273
DOIs	https://doi.org/10.1016/j.neuron.2007.04.031
Publikationsstatus	Veröffentlicht - 07.06.2007

Fördermittel

We thank Drs. Parker and Mischak for providing the kdPRKCA construct and recombinant PRKCA. Thanks to Dr. Kazuhiro Yagita (University of Nagoya) for the PER2 EGFP expression plasmid, Erik Engelen (EUMC Rotterdam) for technical assistance, and Dr. Pablo Szendro for useful discussions. This work was supported by EU grant QLG3-CT-2002-01829. G.T.J.v.d.H. received support from SenterNovem (project BSIK030503). H.O. was supported in part by an Otto Hahn Medal fellowship from the Max Planck Society.

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Forschungsschwerpunkt: Gehirn, Hormone, Verhalten - Center for Brain, Behavior and Metabolism (CBBM)

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10.1016/j.neuron.2007.04.031

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title = "Light Entrainment of the Mammalian Circadian Clock by a PRKCA-Dependent Posttranslational Mechanism",

abstract = "Light is the most potent stimulus for synchronizing endogenous circadian rhythms with external time. Photic clock resetting in mammals involves cAMP-responsive element binding protein (CREB)-mediated transcriptional activation of Period clock genes in the suprachiasmatic nuclei (SCN). Here we provide evidence for an additional photic input pathway to the mammalian circadian clock based on Protein Kinase C α (PRKCA). We found that Prkca-deficient mice show an impairment of light-mediated clock resetting. In the SCN of wild-type mice, light exposure evokes a transient interaction between PRKCA and PERIOD 2 (PER2) proteins that affects PER2 stability and nucleocytoplasmic distribution. These posttranslational events, together with CREB-mediated transcriptional regulation, are key factors in the molecular mechanism of photic clock resetting.",

author = "Vladimira Jakubcakova and Henrik Oster and Filippo Tamanini and Cristina Cadenas and Michael Leitges and \{van der Horst\}, \{Gijsbertus T.J.\} and Gregor Eichele",

year = "2007",

month = jun,

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doi = "10.1016/j.neuron.2007.04.031",

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volume = "54",

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journal = "Neuron",

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AU - Jakubcakova, Vladimira

AU - Oster, Henrik

AU - Tamanini, Filippo

AU - Cadenas, Cristina

AU - Leitges, Michael

AU - van der Horst, Gijsbertus T.J.

AU - Eichele, Gregor

PY - 2007/6/7

Y1 - 2007/6/7

N2 - Light is the most potent stimulus for synchronizing endogenous circadian rhythms with external time. Photic clock resetting in mammals involves cAMP-responsive element binding protein (CREB)-mediated transcriptional activation of Period clock genes in the suprachiasmatic nuclei (SCN). Here we provide evidence for an additional photic input pathway to the mammalian circadian clock based on Protein Kinase C α (PRKCA). We found that Prkca-deficient mice show an impairment of light-mediated clock resetting. In the SCN of wild-type mice, light exposure evokes a transient interaction between PRKCA and PERIOD 2 (PER2) proteins that affects PER2 stability and nucleocytoplasmic distribution. These posttranslational events, together with CREB-mediated transcriptional regulation, are key factors in the molecular mechanism of photic clock resetting.

AB - Light is the most potent stimulus for synchronizing endogenous circadian rhythms with external time. Photic clock resetting in mammals involves cAMP-responsive element binding protein (CREB)-mediated transcriptional activation of Period clock genes in the suprachiasmatic nuclei (SCN). Here we provide evidence for an additional photic input pathway to the mammalian circadian clock based on Protein Kinase C α (PRKCA). We found that Prkca-deficient mice show an impairment of light-mediated clock resetting. In the SCN of wild-type mice, light exposure evokes a transient interaction between PRKCA and PERIOD 2 (PER2) proteins that affects PER2 stability and nucleocytoplasmic distribution. These posttranslational events, together with CREB-mediated transcriptional regulation, are key factors in the molecular mechanism of photic clock resetting.

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DO - 10.1016/j.neuron.2007.04.031

M3 - Journal articles

C2 - 17553429

AN - SCOPUS:34249650212

SN - 0896-6273

VL - 54

SP - 831

EP - 843

JO - Neuron

JF - Neuron

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ER -

Light Entrainment of the Mammalian Circadian Clock by a PRKCA-Dependent Posttranslational Mechanism

Abstract

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