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The tau mutation in the Syrian hamster differentially reprograms the circadian clock in the SCN and peripheral tissues

The tau mutation in the Syrian hamster differentially reprograms the circadian clock in the SCN and peripheral tissues
The tau mutation in the Syrian hamster differentially reprograms the circadian clock in the SCN and peripheral tissues
The hypothalamic suprachiasmatic nuclei (SCN), the principal circadian oscillator in mammals, are synchronized to the solar day by the light-dark cycle, and in turn, they coordinate circadian oscillations in peripheral tissues. The tau mutation in the Syrian hamster is caused by a point mutation leading to a deficiency in the ability of Casein Kinase 1{epsilon} to phosphorylate its targets, including circadian PER proteins. How this accelerates circadian period in neural tissues is not known, nor is its impact on peripheral circadian oscillators established. We show that this mutation has no effect on per mRNA expression nor the nuclear accumulation of PER proteins in the SCN. It does, however, accelerate the clearance of PER proteins from the nucleus to an extent sufficient to explain the shortened circadian period of behavioral rhythms. The mutation also has novel, unanticipated consequences for circadian timing in the periphery, including tissue-specific phase advances and/or reduced amplitude of circadian gene expression. The results suggest that the tau mutation accelerates a specific phase, during mid-late subjective night of the SCN circadian feedback loop, rather than cause a global compression of the entire cycle. This reprogrammed output from the clock is associated with peripheral desynchrony, which in turn could account for impaired growth and metabolic efficiency of the mutant.
period gene, PER proteins, Casein Kinas, immunocytochemistry, in situ hybridization, circadian period
0748-7304
99-110
Dey, J.
03b6970f-d32c-49f0-a7a5-4eb529d5228f
Carr, A.-J.F.
de7a03db-2ce0-4e13-995c-68af81afd8cd
Cagampang, F.R.A.
7cf57d52-4a65-4554-8306-ed65226bc50e
Semikhodskii, A.S.
5a3d1058-fe2a-49e1-9b6d-b36de0aa29b3
Loudon, A.S.I
2c471180-b1f6-4d70-aa1c-07ef1fb41e48
Hastings, M.H.
3ff0b568-aa1c-44be-8d5e-7234021c5107
Maywood, E.S.
012d0197-d77d-4be6-9cf7-ead88ef68e4a
Dey, J.
03b6970f-d32c-49f0-a7a5-4eb529d5228f
Carr, A.-J.F.
de7a03db-2ce0-4e13-995c-68af81afd8cd
Cagampang, F.R.A.
7cf57d52-4a65-4554-8306-ed65226bc50e
Semikhodskii, A.S.
5a3d1058-fe2a-49e1-9b6d-b36de0aa29b3
Loudon, A.S.I
2c471180-b1f6-4d70-aa1c-07ef1fb41e48
Hastings, M.H.
3ff0b568-aa1c-44be-8d5e-7234021c5107
Maywood, E.S.
012d0197-d77d-4be6-9cf7-ead88ef68e4a

Dey, J., Carr, A.-J.F., Cagampang, F.R.A., Semikhodskii, A.S., Loudon, A.S.I, Hastings, M.H. and Maywood, E.S. (2005) The tau mutation in the Syrian hamster differentially reprograms the circadian clock in the SCN and peripheral tissues. Journal of Biological Rhythms, 20 (2), 99-110. (doi:10.1177/0748730404274264).

Record type: Article

Abstract

The hypothalamic suprachiasmatic nuclei (SCN), the principal circadian oscillator in mammals, are synchronized to the solar day by the light-dark cycle, and in turn, they coordinate circadian oscillations in peripheral tissues. The tau mutation in the Syrian hamster is caused by a point mutation leading to a deficiency in the ability of Casein Kinase 1{epsilon} to phosphorylate its targets, including circadian PER proteins. How this accelerates circadian period in neural tissues is not known, nor is its impact on peripheral circadian oscillators established. We show that this mutation has no effect on per mRNA expression nor the nuclear accumulation of PER proteins in the SCN. It does, however, accelerate the clearance of PER proteins from the nucleus to an extent sufficient to explain the shortened circadian period of behavioral rhythms. The mutation also has novel, unanticipated consequences for circadian timing in the periphery, including tissue-specific phase advances and/or reduced amplitude of circadian gene expression. The results suggest that the tau mutation accelerates a specific phase, during mid-late subjective night of the SCN circadian feedback loop, rather than cause a global compression of the entire cycle. This reprogrammed output from the clock is associated with peripheral desynchrony, which in turn could account for impaired growth and metabolic efficiency of the mutant.

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More information

Published date: 2005
Keywords: period gene, PER proteins, Casein Kinas, immunocytochemistry, in situ hybridization, circadian period

Identifiers

Local EPrints ID: 25415
URI: https://eprints.soton.ac.uk/id/eprint/25415
ISSN: 0748-7304
PURE UUID: 4dbd1769-f95f-4120-a536-251faf4f5e20
ORCID for F.R.A. Cagampang: ORCID iD orcid.org/0000-0003-4404-9853

Catalogue record

Date deposited: 07 Apr 2006
Last modified: 11 Dec 2018 01:34

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