Functional consequences of a CKIδ mutation causing familial advanced sleep phase syndrome
Sleep disorders: what larks Until recently, understanding human sleep was hindered by the absence of genetic variants in human sleep patterns. But in 1999 a family was diagnosed with familial advanced sleep phase syndrome (FASPS), and work on sleep genetics was underway. Affected individuals are ‘mo...
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| Published in | Nature (London) Vol. 434; no. 7033; pp. 640 - 644 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
31.03.2005
Nature Publishing Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0028-0836 1476-4687 |
| DOI | 10.1038/nature03453 |
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| Abstract | Sleep disorders: what larks
Until recently, understanding human sleep was hindered by the absence of genetic variants in human sleep patterns. But in 1999 a family was diagnosed with familial advanced sleep phase syndrome (FASPS), and work on sleep genetics was underway. Affected individuals are ‘morning larks’ or ‘early birds’, with a four-hour advance of sleep, temperature and melatonin rhythms. A mutation causing FASPS has now been identified in the casein kinase 1d gene, in a residue conserved from humans to
Drosophila
. In both
Drosophila
and mouse models the mutation causes disruption in circadian rhythms, raising the possibility that they might be useful lab models for the development of drugs to treat sleep disorders.
Familial advanced sleep phase syndrome (FASPS) is a human behavioural phenotype characterized by early sleep times and early-morning awakening
1
. It was the first human, mendelian circadian rhythm variant to be well-characterized, and was shown to result from a mutation in a phosphorylation site within the casein kinase I (CKI)-binding domain of the human
PER2
gene. To gain a deeper understanding of the mechanisms of circadian rhythm regulation in humans, we set out to identify mutations in human subjects leading to FASPS. We report here the identification of a missense mutation (T44A) in the human
CKIδ
gene, which results in FASPS. This mutant kinase has decreased enzymatic activity
in vitro
. Transgenic
Drosophila
carrying the human
CKIδ-T44A
gene showed a phenotype with lengthened circadian period. In contrast, transgenic mice carrying the same mutation have a shorter circadian period, a phenotype mimicking human FASPS. These results show that CKIδ is a central component in the mammalian clock, and suggest that mammalian and fly clocks might have different regulatory mechanisms despite the highly conserved nature of their individual components. |
|---|---|
| AbstractList | Sleep disorders: what larks
Until recently, understanding human sleep was hindered by the absence of genetic variants in human sleep patterns. But in 1999 a family was diagnosed with familial advanced sleep phase syndrome (FASPS), and work on sleep genetics was underway. Affected individuals are ‘morning larks’ or ‘early birds’, with a four-hour advance of sleep, temperature and melatonin rhythms. A mutation causing FASPS has now been identified in the casein kinase 1d gene, in a residue conserved from humans to
Drosophila
. In both
Drosophila
and mouse models the mutation causes disruption in circadian rhythms, raising the possibility that they might be useful lab models for the development of drugs to treat sleep disorders.
Familial advanced sleep phase syndrome (FASPS) is a human behavioural phenotype characterized by early sleep times and early-morning awakening
1
. It was the first human, mendelian circadian rhythm variant to be well-characterized, and was shown to result from a mutation in a phosphorylation site within the casein kinase I (CKI)-binding domain of the human
PER2
gene. To gain a deeper understanding of the mechanisms of circadian rhythm regulation in humans, we set out to identify mutations in human subjects leading to FASPS. We report here the identification of a missense mutation (T44A) in the human
CKIδ
gene, which results in FASPS. This mutant kinase has decreased enzymatic activity
in vitro
. Transgenic
Drosophila
carrying the human
CKIδ-T44A
gene showed a phenotype with lengthened circadian period. In contrast, transgenic mice carrying the same mutation have a shorter circadian period, a phenotype mimicking human FASPS. These results show that CKIδ is a central component in the mammalian clock, and suggest that mammalian and fly clocks might have different regulatory mechanisms despite the highly conserved nature of their individual components. Familial advanced sleep phase syndrome (FASPS) is a human behavioural phenotype characterized by early sleep times and early-morning awakening. It was the first human, Mendelian circadian rhythm variant to be well-characterized, and was shown to result from a mutation in a phosphorylation site within the casein kinase I (CKI)-binding domain of the human PER2 gene. To gain a deeper understanding of the mechanisms of circadian rhythm regulation in humans, we set out to identify mutations in human subjects leading to FASPS. We report here the identification of a missense mutation (T44A) in the human CKI delta gene, which results in FASPS. This mutant kinase has decreased enzymatic activity in vitro. Transgenic Drosophila carrying the human CKI delta -T44A gene showed a phenotype with lengthened circadian period. In contrast, transgenic mice carrying the same mutation have a shorter circadian period, a phenotype mimicking human FASPS. These results show that CKI delta is a central component in the mammalian clock, and suggest that mammalian and fly clocks might have different regulatory mechanisms despite the highly conserved nature of their individual components. |
| Audience | Academic |
| Author | Padiath, Quasar S. Xu, Ying Fu, Ying-Hui Ptáček, Louis J. Jones, Christopher R. Wu, Susan C. Shapiro, Robert E. Saigoh, Kazumasa Saigoh, Noriko |
| Author_xml | – sequence: 1 givenname: Ying surname: Xu fullname: Xu, Ying organization: Department of Neurology, University of California, San Francisco – sequence: 2 givenname: Quasar S. surname: Padiath fullname: Padiath, Quasar S. organization: Department of Neurology, University of California, San Francisco – sequence: 3 givenname: Robert E. surname: Shapiro fullname: Shapiro, Robert E. organization: Department of Neurology, College of Medicine, University of Vermont – sequence: 4 givenname: Christopher R. surname: Jones fullname: Jones, Christopher R. organization: Department of Neurology, University of Utah – sequence: 5 givenname: Susan C. surname: Wu fullname: Wu, Susan C. organization: Department of Neurology, University of California, San Francisco – sequence: 6 givenname: Noriko surname: Saigoh fullname: Saigoh, Noriko organization: Department of Neurology, University of California, San Francisco – sequence: 7 givenname: Kazumasa surname: Saigoh fullname: Saigoh, Kazumasa organization: Department of Neurology, University of California, San Francisco, Department of Neurology, Kinki University School of Medicine – sequence: 8 givenname: Louis J. surname: Ptáček fullname: Ptáček, Louis J. organization: Department of Neurology, University of California, San Francisco, Howard Hughes Medical Institute, UCSF – sequence: 9 givenname: Ying-Hui surname: Fu fullname: Fu, Ying-Hui email: yinghui@itsa.ucsf.edu organization: Department of Neurology, University of California, San Francisco |
| BackLink | http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16648114$$DView record in Pascal Francis |
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| CODEN | NATUAS |
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| Snippet | Sleep disorders: what larks
Until recently, understanding human sleep was hindered by the absence of genetic variants in human sleep patterns. But in 1999 a... Familial advanced sleep phase syndrome (FASPS) is a human behavioural phenotype characterized by early sleep times and early-morning awakening. It was the... |
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| SubjectTerms | Biological and medical sciences Disorders of higher nervous function. Focal brain diseases. Central vestibular syndrome and deafness. Brain stem syndromes Fundamental and applied biological sciences. Psychology Humanities and Social Sciences letter Medical sciences multidisciplinary Nervous system (semeiology, syndromes) Neurology Science Science (multidisciplinary) Sleep. Vigilance Vertebrates: nervous system and sense organs |
| Title | Functional consequences of a CKIδ mutation causing familial advanced sleep phase syndrome |
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