Dr Simon Archer

Head of the Department of Biochemistry & Physiology

Qualifications: BSc, PhD

Email:
Phone: Work: 01483 68 6408
Room no: 03 AY 02

Office hours

Please contact Stephanie Aries for an appointment. 

Further information

Biography

Dr Archer received his BSc in Biological Sciences from the University of Sussex and his PhD in Zoology from the University of Bristol, where he studied photoreceptor visual pigment absorbance spectra and colour vision polymorphisms. As a postdoctoral fellow at Bristol, he cloned some of the first vertebrate visual pigment opsin genes, before moving to Sardinia on an EU fellowship to help set up the International Marine Centre at Oristano, where he was Group Leader of Molecular Sensory Ecology. He then joined chronobiology researchers at Surrey, where he is now a Reader in Chronobiology. Dr Archer has published over 60 peer-reviewed papers and invited reviews, and edited two books.

1989-1991 MRC Research Assistant, Biochemistry, University of Bristol

1991 CNR Visiting Scientist, CNR Institute of Biophysics and Cybernetics, Genova, Italy

1991-1999 Senior Researcher and Group Leader, Molecular & Sensory Ecology Group, International Marine Centre, Oristano, Sardinia, Italy

1999-2002 BBSRC Research Associate, Neuroendocrinology Group, School of Biomedical & Life Sciences, University of Surrey

2002-2004 Research Fellow, School of Biomedical & Molecular Sciences, University of Surrey

2004-2007 Lecturer in Molecular Neuroscience, School of Biomedical & Molecular Sciences, University of Surrey

2007-2010 Senior Lecturer in Molecular Neuroscience, Faculty of Health & Medical Sciences, University of Surrey

2010-2014 Reader in Chronobiology, Faculty of Health & Medical Sciences, University of Surrey

2014 - Head of the Department of Biochemistry & Physiology, Faculty of Health & Medical Sciences, University of Surrey

Research Interests

Dr Archer is a member of the Sleep, Chronobiology & Addiction research group

Main research interests include individual differences in sleep and circadian rhythms and the genetics underlying these phenotypic differences. This pioneering research has been at the forefront of the field of the genetics of sleep and circadian rhythms (Archer, Sleep, 2003) and has identified significant associations between genetic variation and the timing of sleep and wake activity (including delayed sleep phase disorder), sleep homeostasis, vulnerability to sleep loss, cognitive performance and brain function (assessed by fMRI), cardiac function, and the phase angle of gene expression in peripheral leukocytes. During this research, techniques have been developed to study whole-genome expression in peripheral blood across a time series and this has led to significant findings in the effects of sleep-wake, sleep deprivation, and mistimed sleep on the regulation of gene expression (Archer et al., Sleep, 2008; Möller-Levet, Archer et al, PNAS, 2013; Archer et al, PNAS, 2014). Transgenic humanised animal models have also been developed to further investigate these mechanisms (Hasan et al., FASEB, 2014).

Research Collaborations

Prof John Groeger, Department of Psychology, University of Hull, UK
Dr Alice Gregory, Psychology Department, Goldsmiths, University of London, UK
Dr Nicola Barclay, Department of Psychology, Northumbria University, UK
Dr Patrick Nolan, MRC Harwell, UK
Dr Luc Schlangen, Philips Lighting, Eindhoven, The Netherlands
Prof Christian Cajochen, Centre for Chronobiology, University of Basel, Switzerland
Prof Pierre Maquet, Cyclotron Research Centre, University of Liege, Belgium

Publications

Highlights

  • Archer SN, Carpen JD, Gibson M, Lim GH, Johnston JD, Skene DJ, von Schantz M. (2010) 'Polymorphism in the PER3 Promoter Associates with Diurnal Preference and Delayed Sleep Phase Disorder'. AMER ACAD SLEEP MEDICINE SLEEP, 33 (5), pp. 695-701.

    Abstract

    Study Objectives: To screen the PER3 promoter for polymorphisms and investigate the phenotypic associations of these polymorphisms with diurnal preference, delayed sleep phase disorder/syndrome (DSPD/DSPS), and their effects on reporter gene expression. Design: Interspecific comparison was used to define the approximate extent of the PER3 promoter as the region between the transcriptional start site and nucleotide position −874. This region was screened in DNA pools using PCR and direct sequencing, which was also used to screen DNA from individual participants. The different promoter alleles were cloned into a luciferase expression vector and a deletion library created. Promoter activation was measured by chemiluminescence. Setting: N/A Patients or Participants: DNA samples were obtained from volunteers with defined diurnal preference (3 x 80, selected from a pool of 1,590), and DSPD patients (n = 23). Interventions: N/A Measurements and Results: We verified three single nucleotide polymorphisms (G −320T, C −319A, G −294A), and found a novel variable number tandem repeat (VNTR) polymorphism (−318 1/2 VNTR). The −320T and −319A alleles occurred more frequently in DSPD compared to morning (P = 0.042 for each) or evening types (P = 0.006 and 0.033). The allele combination TA2G was more prevalent in DSPD compared to morning (P = 0.033) or evening types (P = 0.002). Luciferase expression driven by the TA2G combination was greater than for the more common GC2A (P < 0.05) and the rarer TA1G (P < 0.001) combinations. Deletion reporter constructs identified two enhancer regions (−703 to −605, and −283 to −80). Conclusions: Polymorphisms in the PER3 promoter could affect its expression, leading to potential differences in the observed functions of PER3.

  • Vandewalle G, Archer SN, Wuillaume C, Balteau E, Degueldre C, Luxen A, Maquet P, Dijk D-J. (2009) 'Functional Magnetic Resonance Imaging-Assessed Brain Responses during an Executive Task Depend on Interaction of Sleep Homeostasis, Circadian Phase, and PER3 Genotype'. SOC NEUROSCIENCE JOURNAL OF NEUROSCIENCE, 29 (25), pp. 7948-7956.
  • Groeger JA, Viola AU, Lo JCY, von Schantz M, Archer SN, Dijk D-J. (2008) 'Early morning executive functioning during sleep deprivation is compromised by a PERIOD3 polymorphism'. AMER ACAD SLEEP MEDICINE SLEEP, 31 (8), pp. 1159-1167.
  • Archer SN, Viola AU, Kyriakopoulou V, von Schantz M, Dijk DJ. (2008) 'Inter-individual differences in habitual sleep timing and entrained phase of endogenous circadian rhythms of BMAL1, PER2 and PER3 mRNA in human leukocytes'. AMER ACAD SLEEP MEDICINE SLEEP, 31 (5), pp. 608-617.

    Abstract

    Study Objectives: Individual sleep timing differs and is governed partly by circadian oscillators, which may be assessed by hormonal markers, or by clock gene expression. Clock gene expression oscillates in peripheral tissues, including leukocytes. The study objective was to determine whether the endogenous phase of these rhythms, assessed in the absence of the sleep-wake and light-dark cycle, correlates with habitual sleep-wake timing. Design: Observational, cross-sectional. Setting: Home environment and Clinical Research Center. Participants: 24 healthy subjects aged 25.0 ± 3.5 (SD) years. Measurements: Actigraphy and sleep diaries were used to characterize sleep timing. Circadian rhythm phase and amplitude of plasma melatonin, cortisol, and BMAL1, PER2, and PER3 expression were assessed during a constant routine. Results: Circadian oscillations were more robust for PER3 than for BMAL1 or PER2. Average peak timings were 6:05 for PER3, 8:06 for PER2, 15:06 for BMAL1, 4:20 for melatonin, and 10:49 for cortisol. Individual sleep-wake timing correlated with the phases of melatonin and cortisol. Individual PER3 rhythms correlated significantly with sleep-wake timing and the timing of melatonin and cortisol, but those of PER2 and BMAL1 did not reach significance. The correlation between sleep timing and PER3 expression was stronger in individuals homozygous for the variant of the PER3 polymorphism that is associated with morningness. Conclusions: Individual phase differences in PER3 expression during a constant routine correlate with sleep timing during entrainment. PER3 expression in leukocytes represents a useful molecular marker of the circadian processes governing sleep-wake timing.

  • Viola AU, Archer SN, James LM, Groeger JA, Lo JCY, Skene DJ, von Schantz M, Dijk D-J. (2007) 'PER3 polymorphism predicts sleep structure and waking performance'. CELL PRESS CURRENT BIOLOGY, 17 (7), pp. 613-618.

Journal articles

  • Hasan S, van der Veen DR, Winsky-Sommerer R, Hogben A, Laing EE, Koentgen F, Dijk DJ, Archer SN. (2014) 'A human sleep homeostasis phenotype in mice expressing a primate-specific PER3 variable-number tandem-repeat coding-region polymorphism.'. FASEB J,

    Abstract

    In humans, a primate-specific variable-number tandem-repeat (VNTR) polymorphism (4 or 5 repeats 54 nt in length) in the circadian gene PER3 is associated with differences in sleep timing and homeostatic responses to sleep loss. We investigated the effects of this polymorphism on circadian rhythmicity and sleep homeostasis by introducing the polymorphism into mice and assessing circadian and sleep parameters at baseline and during and after 12 h of sleep deprivation (SD). Microarray analysis was used to measure hypothalamic and cortical gene expression. Circadian behavior and sleep were normal at baseline. The response to SD of 2 electrophysiological markers of sleep homeostasis, electroencephalography (EEG) θ power during wakefulness and δ power during sleep, were greater in the Per3(5/5) mice. During recovery, the Per3(5/5) mice fully compensated for the SD-induced deficit in δ power, but the Per3(4/4) and wild-type mice did not. Sleep homeostasis-related transcripts (e.g., Homer1, Ptgs2, and Kcna2) were differentially expressed between the humanized mice, but circadian clock genes were not. These data are in accordance with the hypothesis derived from human data that the PER3 VNTR polymorphism modifies the sleep homeostatic response without significantly influencing circadian parameters.-Hasan, S., van der Veen, D. R., Winsky-Sommerer, R., Hogben, A., Laing, E. E., Koentgen, F., Dijk, D.-J., Archer, S. N. A human sleep homeostasis phenotype in mice expressing a primate-specific PER3 variable-number tandem-repeat coding-region polymorphism.

  • Archer SN, Laing EE, Möller-Levet CS, van der Veen DR, Bucca G, Lazar AS, Santhi N, Slak A, Kabiljo R, von Schantz M, Smith CP, Dijk DJ. (2014) 'Mistimed sleep disrupts circadian regulation of the human transcriptome.'. Proc Natl Acad Sci U S A,

    Abstract

    Circadian organization of the mammalian transcriptome is achieved by rhythmic recruitment of key modifiers of chromatin structure and transcriptional and translational processes. These rhythmic processes, together with posttranslational modification, constitute circadian oscillators in the brain and peripheral tissues, which drive rhythms in physiology and behavior, including the sleep-wake cycle. In humans, sleep is normally timed to occur during the biological night, when body temperature is low and melatonin is synthesized. Desynchrony of sleep-wake timing and other circadian rhythms, such as occurs in shift work and jet lag, is associated with disruption of rhythmicity in physiology and endocrinology. However, to what extent mistimed sleep affects the molecular regulators of circadian rhythmicity remains to be established. Here, we show that mistimed sleep leads to a reduction of rhythmic transcripts in the human blood transcriptome from 6.4% at baseline to 1.0% during forced desynchrony of sleep and centrally driven circadian rhythms. Transcripts affected are key regulators of gene expression, including those associated with chromatin modification (methylases and acetylases), transcription (RNA polymerase II), translation (ribosomal proteins, initiation, and elongation factors), temperature-regulated transcription (cold inducible RNA-binding proteins), and core clock genes including CLOCK and ARNTL (BMAL1). We also estimated the separate contribution of sleep and circadian rhythmicity and found that the sleep-wake cycle coordinates the timing of transcription and translation in particular. The data show that mistimed sleep affects molecular processes at the core of circadian rhythm generation and imply that appropriate timing of sleep contributes significantly to the overall temporal organization of the human transcriptome.

  • Pereira DS, Tufik S, Van Der Veen DR, Von Schantz M, Archer SN, Gonçalves BSB, Pedrazzoli M. (2014) 'The effect of different photoperiods in circadian rhythms of Per3 knockout mice'. BioMed Research International, 2014

    Abstract

    The aim of this study was to analyse the circadian behavioural responses of mice carrying a functional knockout of the Per3 gene (P e r 3 - / -) to different light: dark (L: D) cycles. Male adult wild-type (WT) and P e r 3 - / - mice were kept under 12-hour light: 12-hour dark conditions (12L: 12D) and then transferred to either a short or long photoperiod and subsequently released into total darkness. All mice were exposed to both conditions, and behavioural activity data were acquired through running wheel activity and analysed for circadian characteristics during these conditions. We observed that, during the transition from 12L: 12D to 16L: 8D, P e r 3 - / - mice take approximately one additional day to synchronise to the new L: D cycle compared to WT mice. Under these long photoperiod conditions, P e r 3 - / - mice were more active in the light phase. Our results suggest that P e r 3 - / - mice are less sensitive to light. The data presented here provides further evidence that Per3 is involved in the suppression of behavioural activity in direct response to light. © 2014 D. S. Pereira et al.

  • Parsons MJ, Nolan PM, Lester KJ, Eley TC, Barclay NL, Archer SN, Gregory AM. (2014) 'Polymorphisms in the circadian expressed genes PER3 and ARNTL2 are associated with diurnal preference and GNβ3 with sleep measures'. Journal of Sleep Research,

    Abstract

    Sleep and circadian rhythms are intrinsically linked, with several sleep traits, including sleep timing and duration, influenced by both sleep homeostasis and the circadian phase. Genetic variation in several circadian genes has been associated with diurnal preference (preference in timing of sleep), although there has been limited research on whether they are associated with other sleep measurements. We investigated whether these genetic variations were associated with diurnal preference (Morningness-Eveningness Questionnaire) and various sleep measures, including: the global Pittsburgh Sleep Quality index score; sleep duration; and sleep latency and sleep quality. We genotyped 10 polymorphisms in genes with circadian expression in participants from the G1219 sample (n = 966), a British longitudinal population sample of young adults. We conducted linear regressions using dominant, additive and recessive models of inheritance to test for associations between these polymorphisms and the sleep measures. We found a significant association between diurnal preference and a polymorphism in period homologue 3 (PER3) (P < 0.005, recessive model) and a novel nominally significant association between diurnal preference and a polymorphism in aryl hydrocarbon receptor nuclear translocator-like 2 (ARNTL2) (P < 0.05, additive model). We found that a polymorphism in guanine nucleotide binding protein beta 3 (GNβ3) was associated significantly with global sleep quality (P < 0.005, recessive model), and that a rare polymorphism in period homologue 2 (PER2) was associated significantly with both sleep duration and quality (P < 0.0005, recessive model). These findings suggest that genes with circadian expression may play a role in regulating both the circadian clock and sleep homeostasis, and highlight the importance of further studies aimed at dissecting the specific roles that circadian genes play in these two interrelated but unique behaviours. © 2014 The Authors.

  • Lazar AS, Santhi N, Hasan S, Lo JC-Y, Johnston JD, Schantz MV, Archer SN, Dijk D-J. (2013) 'Circadian period and the timing of melatonin onset in men and women: Predictors of sleep during the weekend and in the laboratory'. Journal of Sleep Research, 22 (2), pp. 155-159.

    Abstract

    Sleep complaints and irregular sleep patterns, such as curtailed sleep during workdays and longer and later sleep during weekends, are common. It is often implied that differences in circadian period and in entrained phase contribute to these patterns, but few data are available. We assessed parameters of the circadian rhythm of melatonin at baseline and in a forced desynchrony protocol in 35 participants (18 women) with no sleep disorders. Circadian period varied between 23 h 50 min and 24 h 31 min, and correlated positively (n = 31, rs = 0.43, P = 0.017) with the timing of the melatonin rhythm relative to habitual bedtime. The phase of the melatonin rhythm correlated with the Insomnia Severity Index (n = 35, rs = 0.47, P = 0.004). Self-reported time in bed during free days also correlated with the timing of the melatonin rhythm (n = 35, rs = 0.43, P = 0.01) as well as with the circadian period (n = 31, rs = 0.47, P = 0.007), such that individuals with a more delayed melatonin rhythm or a longer circadian period reported longer sleep during the weekend. The increase in time in bed during the free days correlated positively with circadian period (n = 31, rs = 0.54, P = 0.002). Polysomnographically assessed latency to persistent sleep (n = 34, rs = 0.48, P = 0.004) correlated with the timing of the melatonin rhythm when participants were sleeping at their habitual bedtimes in the laboratory. This correlation was significantly stronger in women than in men (Z = 2.38, P = 0.017). The findings show that individual differences in circadian period and phase of the melatonin rhythm associate with differences in sleep, and suggest that individuals with a long circadian period may be at risk of developing sleep problems.

  • Möller-Levet CS, Archer SN, Bucca G, Laing EE, Slak A, Kabiljo R, Lo JC, Santhi N, von Schantz M, Smith CP, Dijk DJ. (2013) 'Effects of insufficient sleep on circadian rhythmicity and expression amplitude of the human blood transcriptome.'. Proc Natl Acad Sci U S A, United States: 110 (12), pp. E1132-E1141.

    Abstract

    Insufficient sleep and circadian rhythm disruption are associated with negative health outcomes, including obesity, cardiovascular disease, and cognitive impairment, but the mechanisms involved remain largely unexplored. Twenty-six participants were exposed to 1 wk of insufficient sleep (sleep-restriction condition 5.70 h, SEM = 0.03 sleep per 24 h) and 1 wk of sufficient sleep (control condition 8.50 h sleep, SEM = 0.11). Immediately following each condition, 10 whole-blood RNA samples were collected from each participant, while controlling for the effects of light, activity, and food, during a period of total sleep deprivation. Transcriptome analysis revealed that 711 genes were up- or down-regulated by insufficient sleep. Insufficient sleep also reduced the number of genes with a circadian expression profile from 1,855 to 1,481, reduced the circadian amplitude of these genes, and led to an increase in the number of genes that responded to subsequent total sleep deprivation from 122 to 856. Genes affected by insufficient sleep were associated with circadian rhythms (PER1, PER2, PER3, CRY2, CLOCK, NR1D1, NR1D2, RORA, DEC1, CSNK1E), sleep homeostasis (IL6, STAT3, KCNV2, CAMK2D), oxidative stress (PRDX2, PRDX5), and metabolism (SLC2A3, SLC2A5, GHRL, ABCA1). Biological processes affected included chromatin modification, gene-expression regulation, macromolecular metabolism, and inflammatory, immune and stress responses. Thus, insufficient sleep affects the human blood transcriptome, disrupts its circadian regulation, and intensifies the effects of acute total sleep deprivation. The identified biological processes may be involved with the negative effects of sleep loss on health, and highlight the interrelatedness of sleep homeostasis, circadian rhythmicity, and metabolism.

  • Santhi N, Groeger JA, Archer SN, Gimenez M, Schlangen LJ, Dijk DJ. (2013) 'Morning sleep inertia in alertness and performance: effect of cognitive domain and white light conditions.'. PLoS One, United States: 8 (11)

    Abstract

    The transition from sleep to wakefulness entails a temporary period of reduced alertness and impaired performance known as sleep inertia. The extent to which its severity varies with task and cognitive processes remains unclear. We examined sleep inertia in alertness, attention, working memory and cognitive throughput with the Karolinska Sleepiness Scale (KSS), the Psychomotor Vigilance Task (PVT), n-back and add tasks, respectively. The tasks were administered 2 hours before bedtime and at regular intervals for four hours, starting immediately after awakening in the morning, in eleven participants, in a four-way cross-over laboratory design. We also investigated whether exposure to Blue-Enhanced or Bright Blue-Enhanced white light would reduce sleep inertia. Alertness and all cognitive processes were impaired immediately upon awakening (p<0.01). However, alertness and sustained attention were more affected than cognitive throughput and working memory. Moreover, speed was more affected than accuracy of responses. The light conditions had no differential effect on performance except in the 3-back task (p<0.01), where response times (RT) at the end of four hours in the two Blue-Enhanced white light conditions were faster (200 ms) than at wake time. We conclude that the effect of sleep inertia varies with cognitive domain and that it's spectral/intensity response to light is different from that of sleepiness. That is, just increasing blue-wavelength in light may not be sufficient to reduce sleep inertia. These findings have implications for critical professions like medicine, law-enforcement etc., in which, personnel routinely wake up from night-time sleep to respond to emergency situations.

  • Lazar AS, Santhi N, Hasan S, Lo JC, Johnston JD, Von Schantz M, Archer SN, Dijk DJ. (2012) 'Circadian period and the timing of melatonin onset in men and women: predictors of sleep during the weekend and in the laboratory.'. J Sleep Res,

    Abstract

    Sleep complaints and irregular sleep patterns, such as curtailed sleep during workdays and longer and later sleep during weekends, are common. It is often implied that differences in circadian period and in entrained phase contribute to these patterns, but few data are available. We assessed parameters of the circadian rhythm of melatonin at baseline and in a forced desynchrony protocol in 35 participants (18 women) with no sleep disorders. Circadian period varied between 23 h 50 min and 24 h 31 min, and correlated positively (n = 31, r(s)  = 0.43, P = 0.017) with the timing of the melatonin rhythm relative to habitual bedtime. The phase of the melatonin rhythm correlated with the Insomnia Severity Index (n = 35, r(s)  = 0.47, P = 0.004). Self-reported time in bed during free days also correlated with the timing of the melatonin rhythm (n = 35, r(s)  = 0.43, P = 0.01) as well as with the circadian period (n = 31, r(s)  = 0.47, P = 0.007), such that individuals with a more delayed melatonin rhythm or a longer circadian period reported longer sleep during the weekend. The increase in time in bed during the free days correlated positively with circadian period (n = 31, r(s)  = 0.54, P = 0.002). Polysomnographically assessed latency to persistent sleep (n = 34, r(s)  = 0.48, P = 0.004) correlated with the timing of the melatonin rhythm when participants were sleeping at their habitual bedtimes in the laboratory. This correlation was significantly stronger in women than in men (Z = 2.38, P = 0.017). The findings show that individual differences in circadian period and phase of the melatonin rhythm associate with differences in sleep, and suggest that individuals with a long circadian period may be at risk of developing sleep problems.

  • Adan A, Archer SN, Hidalgo MP, Di Milia L, Natale V, Randler C. (2012) 'Circadian typology: A comprehensive review'. Chronobiology International, 29 (9), pp. 1153-1175.

    Abstract

    The interest in the systematic study of the circadian typology (CT) is relatively recent and has developed rapidly in the two last decades. All the existing data suggest that this individual difference affects our biological and psychological functioning, not only in health, but also in disease. In the present study, we review the current literature concerning the psychometric properties and validity of CT measures as well as individual, environmental and genetic factors that influence the CT. We present a brief overview of the biological markers that are used to define differences between CT groups (sleepwake cycle, body temperature, cortisol and melatonin), and we assess the implications for CT and adjustment to shiftwork and jet lag. We also review the differences between CT in terms of cognitive abilities, personality traits and the incidence of psychiatric disorders. When necessary, we have emphasized the methodological limitations that exist today and suggested some future avenues of work in order to overcome these. This is a new field of interest to professionals in many different areas (research, labor, academic and clinical), and this review provides a state of the art discussion to allow professionals to integrate chronobiological aspects of human behavior into their daily practice. Copyright © Informa Healthcare USA, Inc.

  • Viola AU, Chellappa SL, Archer SN, Pugin F, Götz T, Dijk DJ, Cajochen C. (2012) 'Interindividual differences in circadian rhythmicity and sleep homeostasis in older people: effect of a PER3 polymorphism.'. Neurobiology of aging, 33 (5)

    Abstract

    Aging is associated with marked changes in the timing, consolidation and structure of sleep. Older people wake up frequently, get up earlier and have less slow wave sleep than young people, although the extent of these age-related changes differs considerably between individuals. Interindividual differences in homeostatic sleep regulation in young volunteers are associated with the variable-number, tandem-repeat (VNTR) polymorphism (rs57875989) in the coding region of the circadian clock gene PERIOD3 (PER3). However, predictors of these interindividual differences have yet to be identified in older people. Sleep electroencephalographic (EEG) characteristics and circadian rhythms were assessed in 26 healthy older volunteers (55-75 years) selected on the basis of homozygosity for either the long or short allele of the PER3 polymorphism. Homozygosity for the longer allele (PER3(5/5)) associated with a phase-advance in the circadian melatonin profile and an earlier occurrence of the melatonin peak within the sleep episode. Furthermore, older PER3(5/5) participants accumulated more nocturnal wakefulness, had increased EEG frontal delta activity (0.75-1.50 Hz), and decreased EEG frontal sigma activity (11-13 Hz) during non-rapid eye movement (REM) sleep compared with PER3(4/4) participants. Our results indicate that the polymorphism in the clock gene PER3 may contribute to interindividual differences in sleep and circadian physiology in older people. Copyright © 2012 Elsevier Inc. All rights reserved.

  • Lázár AS, Slak A, Lo JC, Santhi N, von Schantz M, Archer SN, Groeger JA, Dijk DJ. (2012) 'Sleep, diurnal preference, health, and psychological well-being: a prospective single-allelic-variation study.'. Chronobiol Int, England: 29 (2), pp. 131-146.

    Abstract

    Individual differences in sleep and diurnal preference associate with physical and mental health characteristics, but few genetic determinants of these differences have been identified. A variable number tandem repeat (VNTR) polymorphism in the PERIOD3 (PER3) gene (rs57875989) has been reported to associate with diurnal preference, i.e., preferred timing of waking and sleep. Here, the authors investigate in a prospective single-candidate genetic variant study whether allelic variation for this polymorphism associates also with reported actual sleep timing and sleep duration, as well as psychological and health measures. Six hundred and seventy-five subjects, aged 20 to 35 yrs, completed questionnaires to assess sleep and psychological and health characteristics and were genotyped for the PER3 VNTR. Homozygosity for the longer allele (PER3(5/5)) of the VNTR was associated with increased morning preference, earlier wake time and bedtime, and reduced daytime sleepiness. Separate analyses of work and rest days demonstrated that the increase in time in bed during rest days was greatest in PER3(5/5) homozygotes. PER3 genotype modified the effects of sleep timing and duration on fluid intelligence and body mass index. Genotype was not associated with physical or psychological characteristics as assessed by the SF-36 Health Questionnaire, the General Health Questionnaire, the Big Five Inventory, the Behavioral Inhibition System-Behavioral Activation System scales, and the Positive and Negative Affect Scale, even though these measures varied significantly with diurnal preference as assessed by the Morningness-Eveningness Questionnaire. Whereas diurnal preference also predicts mental health and psychological characteristics, as well as sleep timing, the PER3 VNTR specifically affects measures of sleep timing and may also modify the effects of sleep on health outcome measures.

  • Hasan S, Santhi N, Lazar AS, Slak A, Lo J, von Schantz M, Archer SN, Johnston JD, Dijk DJ. (2012) 'Assessment of circadian rhythms in humans: comparison of real-time fibroblast reporter imaging with plasma melatonin.'. FASEB J,

    Abstract

    We compared the period of the rhythm of plasma melatonin, driven by the hypothalamic circadian pacemaker, to in vitro periodicity in cultured peripheral fibroblasts to assess the effects on these rhythms of a polymorphism of PER3 (rs57875989), which is associated with sleep timing. In vitro circadian period was determined using luminometry of cultured fibroblasts, in which the expression of firefly luciferase was driven by the promoter of the circadian gene Arntl (Bmal1). The period of the melatonin rhythm was assessed in a 9-d forced desynchrony protocol, minimizing confounding effects of sleep-wake and light-dark cycles on circadian rhythmicity. In vitro periods (32 participants, 24.61±0.33 h, mean±sd) were longer than in vivo periods (31 participants, 24.16±0.17 h; P<0.0001) but did not differ between PER3 genotypes (P>0.4). Analyses of replicate in vitro assessments demonstrated that circadian period was reproducible within individuals (intraclass correlation=0.62), but in vivo and in vitro period assessments did not correlate (P>0.9). In accordance with circadian entrainment theory, in vivo period correlated with the timing of melatonin (P<0.05) at baseline and with diurnal preference (P<0.05). Individual circadian rhythms can be reliably assessed in fibroblasts but may not correlate with physiological rhythms driven by the central circadian pacemaker.-Hasan, S., Santhi, N., Lazar, A.S., Slak, A., Lo, J., von Schantz, M., Archer, S. N., Johnston, J. D., Dijk, D.-J. Assessment of circadian rhythms in humans: comparison of real-time fibroblast reporter imaging with plasma melatonin.

  • Lo JC, Groeger JA, Santhi N, Arbon EL, Lazar AS, Hasan S, von Schantz M, Archer SN, Dijk DJ. (2012) 'Effects of partial and acute total sleep deprivation on performance across cognitive domains, individuals and circadian phase.'. PLoS One, United States: 7 (9)

    Abstract

    Cognitive performance deteriorates during extended wakefulness and circadian phase misalignment, and some individuals are more affected than others. Whether performance is affected similarly across cognitive domains, or whether cognitive processes involving Executive Functions are more sensitive to sleep and circadian misalignment than Alertness and Sustained Attention, is a matter of debate.

  • Hasan S, van der Veen DR, Winsky-Sommerer R, Dijk DJ, Archer SN. (2011) 'Altered sleep and behavioral activity phenotypes in PER3-deficient mice.'. Am J Physiol Regul Integr Comp Physiol,

    Abstract

    Sleep homeostasis and circadian rhythmicity interact to determine the timing of behavioral activity. Circadian clock genes contribute to circadian rhythmicity centrally and in the periphery, but some also have roles within sleep regulation. The clock gene Period3 (Per3) has a redundant function within the circadian system and is associated with sleep homeostasis in humans. This study investigated the role of PER3 in sleep/wake activity and sleep homeostasis in mice by recording wheel running activity under baseline conditions in wild-type (WT; n = 54) and in PER3-deficient (Per3(-/-); n = 53) mice, as well as EEG-assessed sleep before and after 6 hours of sleep deprivation in WT (n = 7) and Per3(-/-) (n = 8) mice. Whereas total activity and vigilance states did not differ between the genotypes, the temporal distribution of wheel running activity, vigilance states, and EEG delta activity was affected by genotype. In Per3(-/-) mice, running wheel activity was increased and REM sleep and NREM sleep were reduced in the middle of the dark phase, and delta activity was enhanced at the end of the dark phase. At the beginning of the baseline light period, there was less wakefulness and more REM and NREM in Per3(-/-) mice. Per3(-/-) mice spent less time in wakefulness and more time in NREM sleep in the light period immediately after sleep deprivation and REM sleep accumulated more slowly during the recovery dark phase. These data confirm a role for PER3 in sleep/wake timing and sleep homeostasis.

  • Santhi N, Thorne HC, van der Veen DR, Johnsen S, Mills SL, Hommes V, Schlangen LJ, Archer SN, Dijk DJ. (2011) 'The spectral composition of evening light and individual differences in the suppression of melatonin and delay of sleep in humans.'. J Pineal Res,

    Abstract

    The effect of light on circadian rhythms and sleep is mediated by a multi-component photoreceptive system of rods, cones and melanopsin-expressing intrinsically photosensitive retinal ganglion cells. The intensity and spectral sensitivity characteristics of this system are to be fully determined. Whether the intensity and spectral composition of light exposure at home in the evening is such that it delays circadian rhythms and sleep also remains to be established. We monitored light exposure at home during 6-8 wk and assessed light effects on sleep and circadian rhythms in the laboratory. Twenty-two women and men (23.1 ± 4.7 yr) participated in a six-way, cross-over design using polychromatic light conditions relevant to the light exposure at home, but with reduced, intermediate or enhanced efficacy with respect to the photopic and melanopsin systems. The evening rise of melatonin, sleepiness and EEG-assessed sleep onset varied significantly (P < 0.01) across the light conditions, and these effects appeared to be largely mediated by the melanopsin, rather than the photopic system. Moreover, there were individual differences in the sensitivity to the disruptive effect of light on melatonin, which were robust against experimental manipulations (intra-class correlation = 0.44). The data show that light at home in the evening affects circadian physiology and imply that the spectral composition of artificial light can be modified to minimize this disruptive effect on sleep and circadian rhythms. These findings have implications for our understanding of the contribution of artificial light exposure to sleep and circadian rhythm disorders such as delayed sleep phase disorder.

  • Barclay NL, Eley TC, Mill J, Wong CCY, Zavos HMS, Archer SN, Gregory AM. (2011) 'Sleep Quality and Diurnal Preference in a Sample of Young Adults: Associations With 5HTTLPR, PER3, and CLOCK 3111'. WILEY-BLACKWELL AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS, 156B (6), pp. 681-690.
  • Vandewalle G, Archer SN, Wuillaume C, Balteau E, Degueldre C, Luxen A, Dijk DJ, Maquet P. (2011) 'Effects of light on cognitive brain responses depend on circadian phase and sleep homeostasis.'. Sage J Biol Rhythms, United States: 26 (3), pp. 249-259.

    Abstract

    Light is a powerful modulator of cognition through its long-term effects on circadian rhythmicity and direct effects on brain function as identified by neuroimaging. How the direct impact of light on brain function varies with wavelength of light, circadian phase, and sleep homeostasis, and how this differs between individuals, is a largely unexplored area. Using functional MRI, we compared the effects of 1 minute of low-intensity blue (473 nm) and green light (527 nm) exposures on brain responses to an auditory working memory task while varying circadian phase and status of the sleep homeostat. Data were collected in 27 subjects genotyped for the PER3 VNTR (12 PER3(5/5) and 15 PER3(4/4) ) in whom it was previously shown that the brain responses to this task, when conducted in darkness, depend on circadian phase, sleep homeostasis, and genotype. In the morning after sleep, blue light, relative to green light, increased brain responses primarily in the ventrolateral and dorsolateral prefrontal cortex and in the intraparietal sulcus, but only in PER3(4/4) individuals. By contrast, in the morning after sleep loss, blue light increased brain responses in a left thalamofrontoparietal circuit to a larger extent than green light, and only so in PER3(5/5) individuals. In the evening wake maintenance zone following a normal waking day, no differential effect of 1 minute of blue versus green light was observed in either genotype. Comparison of the current results with the findings observed in darkness indicates that light acts as an activating agent particularly under those circumstances in which and in those individuals in whom brain function is jeopardized by an adverse circadian phase and high homeostatic sleep pressure.

  • Dijk D-J, Archer SN. (2010) 'PERIOD3, circadian phenotypes, and sleep homeostasis'. W B SAUNDERS CO LTD SLEEP MEDICINE REVIEWS, 14 (3), pp. 151-160.
  • Archer SN, Carpen JD, Gibson M, Lim GH, Johnston JD, Skene DJ, von Schantz M. (2010) 'Polymorphism in the PER3 Promoter Associates with Diurnal Preference and Delayed Sleep Phase Disorder'. AMER ACAD SLEEP MEDICINE SLEEP, 33 (5), pp. 695-701.

    Abstract

    Study Objectives: To screen the PER3 promoter for polymorphisms and investigate the phenotypic associations of these polymorphisms with diurnal preference, delayed sleep phase disorder/syndrome (DSPD/DSPS), and their effects on reporter gene expression. Design: Interspecific comparison was used to define the approximate extent of the PER3 promoter as the region between the transcriptional start site and nucleotide position −874. This region was screened in DNA pools using PCR and direct sequencing, which was also used to screen DNA from individual participants. The different promoter alleles were cloned into a luciferase expression vector and a deletion library created. Promoter activation was measured by chemiluminescence. Setting: N/A Patients or Participants: DNA samples were obtained from volunteers with defined diurnal preference (3 x 80, selected from a pool of 1,590), and DSPD patients (n = 23). Interventions: N/A Measurements and Results: We verified three single nucleotide polymorphisms (G −320T, C −319A, G −294A), and found a novel variable number tandem repeat (VNTR) polymorphism (−318 1/2 VNTR). The −320T and −319A alleles occurred more frequently in DSPD compared to morning (P = 0.042 for each) or evening types (P = 0.006 and 0.033). The allele combination TA2G was more prevalent in DSPD compared to morning (P = 0.033) or evening types (P = 0.002). Luciferase expression driven by the TA2G combination was greater than for the more common GC2A (P < 0.05) and the rarer TA1G (P < 0.001) combinations. Deletion reporter constructs identified two enhancer regions (−703 to −605, and −283 to −80). Conclusions: Polymorphisms in the PER3 promoter could affect its expression, leading to potential differences in the observed functions of PER3.

  • van der Veen DR, Archer SN. (2010) 'Light-Dependent Behavioral Phenotypes in PER3-Deficient Mice'. SAGE PUBLICATIONS INC JOURNAL OF BIOLOGICAL RHYTHMS, 25 (1), pp. 3-8.
  • Van der Veen DR, Archer SN. (2010) 'Light-dependent behavioral phenotypes in PER3-deficient mice (vol 25, pg 3, 2010)'. SAGE PUBLICATIONS INC JOURNAL OF BIOLOGICAL RHYTHMS, 25 (2), pp. 150-150.
  • Barclay NL, Eley TC, Buysse DJ, Archer SN, Gregory AM. (2010) 'DIURNAL PREFERENCE AND SLEEP QUALITY: SAME GENES? A STUDY OF YOUNG ADULT TWINS'. TAYLOR & FRANCIS INC CHRONOBIOLOGY INTERNATIONAL, 27 (2), pp. 278-296.
  • Staples VSL, Archer SN, Arber S, Skene DJ. (2009) 'Daily light exposure profiles in older non-resident extreme morning and evening types'. WILEY-BLACKWELL PUBLISHING, INC JOURNAL OF SLEEP RESEARCH, 18 (4), pp. 466-471.
  • Vandewalle G, Archer SN, Wuillaume C, Balteau E, Degueldre C, Luxen A, Maquet P, Dijk D-J. (2009) 'Functional Magnetic Resonance Imaging-Assessed Brain Responses during an Executive Task Depend on Interaction of Sleep Homeostasis, Circadian Phase, and PER3 Genotype'. SOC NEUROSCIENCE JOURNAL OF NEUROSCIENCE, 29 (25), pp. 7948-7956.
  • Dijk D-J, Archer SN. (2009) 'Light, Sleep, and Circadian Rhythms: Together Again'. PUBLIC LIBRARY SCIENCE PLOS BIOLOGY, 7 (6) Article number ARTN e1000145
  • Ackermann K, Sletten TL, Revell VL, Archer SN, Skene DJ. (2009) 'Blue-Light Phase Shifts PER3 Gene Expression in Human Leukocytes'. TAYLOR & FRANCIS INC CHRONOBIOLOGY INTERNATIONAL, 26 (4) Article number PII 911212256 , pp. 769-779.
  • Skene DJ, Sletten TL, Ackermann K, Herljevic M, Lederle KA, Middleton B, Archer SN, Revell VL. (2009) 'LIGHT AND THE HUMAN CIRCADIAN TIMING SYSTEM: AGE-RELATED CHANGES'. SPRINGER TOKYO JOURNAL OF PHYSIOLOGICAL SCIENCES, 59, pp. 37-37.
  • Ellis J, von Schantz M, Jones KHS, Archer SN. (2009) 'Association between Specific Diurnal Preference Questionnaire Items and PER3 VNTR Genotype'. TAYLOR & FRANCIS INC CHRONOBIOLOGY INTERNATIONAL, 26 (3) Article number PII 910356950 , pp. 464-473.
  • Pugin F, Viola AU, Chellappa SL, Archer S, Dijk DJ, Cajochen C. (2009) 'Can Per3 Length Polymorphism Predict Sleep Duration in Older Individuals?'. KARGER NEUROPSYCHOBIOLOGY, 59 (4), pp. 255-255.
  • Dijk D-J, Archer SN. (2009) 'Circadian and Homeostatic Regulation of Human Sleep and Cognitive Performance and Its Modulation by PERIOD3'. Sleep Medicine Clinics, 4 (2), pp. 111-125.

    Abstract

    Sleep physiology and waking performance are regulated through the interaction of an endogenous circadian process and a sleep-wake-dependent homeostatic process. The two processes are not independent: the observed circadian amplitude of waking performance depends on homeostatic sleep pressure, so that the negative effects of sleep loss are most pronounced in the early morning if homeostatic sleep pressure is high. These findings underscore the close interrelations between sleep, circadian rhythmicity, and waking performance and suggest that some circadian phenotypes are related to changes in sleep-regulatory processes. Understanding the effects of these alterations in clock genes, such as PER3, at the cellular and biochemical level may provide insights into the nature of the sleep homeostat and its interaction with circadian rhythmicity in the regulation of waking performance. © 2009 Elsevier Inc. All rights reserved.

  • Thorne HC, Jones KH, Peters SP, Archer SN, Dijk D-J. (2009) 'Daily and Seasonal Variation in the Spectral Composition of Light Exposure in Humans'. TAYLOR & FRANCIS INC CHRONOBIOLOGY INTERNATIONAL, 26 (5) Article number PII 913454756 , pp. 854-866.
  • Viola AU, James LM, Archer SN, Dijk D-J. (2008) 'PER3 polymorphism and cardiac autonomic control: effects of sleep debt and circadian phase'. AMER PHYSIOLOGICAL SOC AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 295 (5), pp. H2156-H2163.
  • Sahnd J, Partridge JC, Archer S, Potts GW, Lythgoe JN. (2008) 'Spectral absorbance changes in the violet/blue sensitive cones of the juvenile pollack, Pollachius pollachius'. Springer Journal of Comparative Physiology A: sensory, neural, and behavioral physiology, 163 (5), pp. 699-703.

    Abstract

    Using the technique of microspectrophotometry (MSP) we have found that the short wavelength sensitive cones in the retina of the pollack (Pollachius pollachius) shift in spectral absorption from a maximum (λ max) at about 420 nm in the violet to about 460 nm in the blue. This shift is not due to chromophore replacement, which substitutes rhodopsin for a porphyropsin, but is more likely to be due to a change in the opsin. The shift appears to be progressive rather than abrupt and coincides with a change in lifestyle of the fish.

  • Groeger JA, Viola AU, Lo JCY, von Schantz M, Archer SN, Dijk D-J. (2008) 'Early morning executive functioning during sleep deprivation is compromised by a PERIOD3 polymorphism'. AMER ACAD SLEEP MEDICINE SLEEP, 31 (8), pp. 1159-1167.
  • Archer SN, Viola AU, Kyriakopoulou V, von Schantz M, Dijk DJ. (2008) 'Inter-individual differences in habitual sleep timing and entrained phase of endogenous circadian rhythms of BMAL1, PER2 and PER3 mRNA in human leukocytes'. AMER ACAD SLEEP MEDICINE SLEEP, 31 (5), pp. 608-617.

    Abstract

    Study Objectives: Individual sleep timing differs and is governed partly by circadian oscillators, which may be assessed by hormonal markers, or by clock gene expression. Clock gene expression oscillates in peripheral tissues, including leukocytes. The study objective was to determine whether the endogenous phase of these rhythms, assessed in the absence of the sleep-wake and light-dark cycle, correlates with habitual sleep-wake timing. Design: Observational, cross-sectional. Setting: Home environment and Clinical Research Center. Participants: 24 healthy subjects aged 25.0 ± 3.5 (SD) years. Measurements: Actigraphy and sleep diaries were used to characterize sleep timing. Circadian rhythm phase and amplitude of plasma melatonin, cortisol, and BMAL1, PER2, and PER3 expression were assessed during a constant routine. Results: Circadian oscillations were more robust for PER3 than for BMAL1 or PER2. Average peak timings were 6:05 for PER3, 8:06 for PER2, 15:06 for BMAL1, 4:20 for melatonin, and 10:49 for cortisol. Individual sleep-wake timing correlated with the phases of melatonin and cortisol. Individual PER3 rhythms correlated significantly with sleep-wake timing and the timing of melatonin and cortisol, but those of PER2 and BMAL1 did not reach significance. The correlation between sleep timing and PER3 expression was stronger in individuals homozygous for the variant of the PER3 polymorphism that is associated with morningness. Conclusions: Individual phase differences in PER3 expression during a constant routine correlate with sleep timing during entrainment. PER3 expression in leukocytes represents a useful molecular marker of the circadian processes governing sleep-wake timing.

  • Viola AU, Archer SN, James LM, Groeger JA, Lo JCY, Skene DJ, von Schantz M, Dijk D-J. (2007) 'PER3 polymorphism predicts sleep structure and waking performance'. CELL PRESS CURRENT BIOLOGY, 17 (7), pp. 613-618.
  • Jones KHS, Ellis J, Von Schantz M, Skene DJ, Dijk D-J, Archer SN. (2007) 'Age-related change in the association between a polymorphism in the PER3 gene and preferred timing of sleep and waking activities'. BLACKWELL PUBLISHING JOURNAL OF SLEEP RESEARCH, 16 (1), pp. 12-16.
  • Hogben AL, Archer SN, Von Schantz M, Ellis J. (2007) 'Conscientiousness is a predictor of diurnal preference'. Chronobiology International, 24 (6), pp. 1249-1254.

    Abstract

    The relationship between diurnal preference, as measured by the Horne-Östberg questionnaire, and quantifiable personality traits was investigated in 617 participants. A hierarchical multiple regression analysis demonstrated that out of the personality variables, conscientiousness was the single biggest predictor of diurnal preference (β=0.246), after controlling for depression, sleep disorders, shift work, age, gender, and demographic characteristics. Morningness has previously been associated with physiological parameters of the circadian clock and with polymorphisms in circadian clock genes, suggesting the possibility that conscientiousness, too, may be linked to the same parameters. Copyright © Informa Healthcare.

  • von Schantz M, Jenkins A, Archer SN. (2006) 'Evolutionary history of the vertebrate Period genes'. SPRINGER JOURNAL OF MOLECULAR EVOLUTION, 62 (6), pp. 701-707.
  • Carpen JD, von Schantz M, Smits M, Skene DJ, Archer SN. (2006) 'A silent polymorphism in the PER1 gene associates with extreme diurnal preference in humans'. SPRINGER TOKYO JOURNAL OF HUMAN GENETICS, 51 (12), pp. 1122-1125.
  • Von Schantz M, Jenkins A, Archer SN. (2006) 'Evolutionary history of the vertebrate Period genes'. Journal of Molecular Evolution, 62 (6), pp. 701-707.

    Abstract

    Circadian clock genes are remarkably conserved between eucoelomates. Although Drosophila has one copy of each major component, vertebrates have two or (in the case of the Period genes) three paralogs (Per1-3). We investigated the possibility that the vertebrate Per genes arose through two genome duplications during the emergence of vertebrates. Phylogenetic trees have placed zebrafish and mammalian Per1 and 2 together in a separate branch from Per3. The positions of four coding region splice sites were conserved between Drosophila per and the human paralogs, the fifth one being unique to Drosophila. The human PER genes shared the positions of all coding region splice sites, except the first two in PER1 and PER2 (which PER3 lacks). The phases of all splice sites were conserved between all four genes with two exceptions. Analysis of all genes within 10 Mb of the human PER1-3 genes, which are located 7.8-8.8 Mb from the telomeres on chromosomes 17, 2, and 1, identified several orthologous neighbors shared by at least two PER genes. Two gene families, HES (hairy and Enhancer of Split) and KIF1 (kinesin-like protein 1), were represented in all three of these paralogons. Although no functional fourth human PER paralog exists, five representatives from the same gene families were found close to the telomer of chromosome 3. We conclude that the ancestral chordate Per gene underwent two duplication events, giving rise to Per1-3 and a lost fourth paralog. © Springer Science+Business Media, Inc. 2006.

  • Jenkins A, Archer SN, von Schantz M. (2005) 'Expansion during primate radiation of a variable number tandem repeat in the coding region of the circadian clock gene Period3'. SAGE PUBLICATIONS LTD JOURNAL OF BIOLOGICAL RHYTHMS, 20 (5), pp. 470-472.
  • Carpen JD, Archer SN, Skene DJ, Smits M, von Schantz M. (2005) 'A single-nucleotide polymorphism in the 5 '-untranslated region of the hPER2 gene is associated with diurnal preference'. BLACKWELL PUBLISHING JOURNAL OF SLEEP RESEARCH, 14 (3), pp. 293-297.
  • Carpen JD, Archer SN, Skene DJ, Von Schantz M, Smits M. (2005) 'A single-nucleotide polymorphism in the 5′-untranslated region of the hPER2 gene is associated with diurnal preference'. Journal of Sleep Research, 14 (3), pp. 293-297.

    Abstract

    The PERIOD2 (PER2) gene is a key component of the molecular mechanism that generates circadian rhythms in mammals. A missense mutation in the human PER2 gene has previously been linked to advanced sleep phase syndrome (ASPS). We have investigated three other single-nucleotide polymorphisms in the hPER2 gene, one downstream of the transcription start site (C-1228T), one in exon 2 in the 5′-untranslated region (5′-UTR) (C111G), and one missense mutation (G3853A) causing a glycine to glutamine substitution in the predicted protein. Subjects selected from a group of 484 volunteers for extreme morning or evening preference, or intermediate diurnal preference were genotyped with regard to the three polymorphisms (n = 35 for each group). Whereas allele frequencies for the other two polymorphisms did not differ significantly between any of the groups, the 111G allele frequency was significantly higher in subjects with extreme morning preference (0.14) than in subjects with extreme evening preference (0.03) (Fisher's exact test, two-sided P value = 0.031, odds ratio = 5.67). No significant difference in 111G allele frequency was observed between either of these groups and subjects with intermediate diurnal preference. Computer prediction indicated that the C111G polymorphism, which occurs 12 bases upstream from the translation start codon, might alter the secondary structure of the transcript. The PER2 111G allele associates with morning preference and is a potential candidate allele for ASPS. © 2005 European Sleep Research Society.

  • Van Der Heijden KB, Blok MJ, Spee K, Curfs LM, Archer SN, Smits MG, Gunning WB. (2005) 'No evidence to support an association of PER3 clock gene polymorphism with ADHD-related idiopathic chronic sleep onset insomnia'. Biological Rhythm Research, 36 (5), pp. 381-388.

    Abstract

    Idiopathic chronic sleep onset insomnia (SOI) in children with Attention-Dencit/Hyperactivity Disorder (ADHD) shows typical characteristics of the delayed sleep phase syndrome and could, therefore, be considered a circadian rhythm sleep disorder. A variable number tandem repeat (VNTR) polymorphism of the clock gene PER3 is associated with the delayed sleep phase syndrome and, hence, may associate with ADHD-related chronic SOI as well. Here, we investigated an association between ADHD-related chronic SOI and the VNTR polymorphism of PER3 in 10 medication naïve children with rigorously diagnosed ADHD and SOI (ADHD-SOI), and in 10 normal controls. Actigraphic sleep onset and sleep duration and salivary dim light melatonin onset (DLMO) were evaluated in ADHD-SOI. The 4-repeat allele frequency was lower in ADHD-SOI (0.65) than in normal controls (0.75) (p = 0.73) with an odds ratio of 0.62 (CI 0.16-2.4). In ADHD-SOI, mean (± SD) DLMO (21:38 ± 0:50 h), sleep onset (22:17 ± 0:46 h), and sleep duration (9:26 ± 0:41 h) were not significantly related to the 4-repeat allele frequency. The present findings suggest no association between ADHD-related idiopathic chronic sleep onset insomnia and the PER3 VNTR polymorphism. © 2005 Taylor & Francis.

  • Jenkins A, Archer SN, Von Schantz M. (2005) 'Expansion during primate radiation of a variable number tandem repeat in the coding region of the circadian clock gene Period3'. Journal of Biological Rhythms, 20 (5), pp. 470-472.
  • Archer SN, Ahuja P, Caffe R, Mikol C, Foster RG, van Veen T, von Schantz M. (2004) 'Absence of phosphoglucose isomerase-1 in retinal photoreceptor, pigment epithelium and Muller cells'. BLACKWELL PUBLISHING LTD EUROPEAN JOURNAL OF NEUROSCIENCE, 19 (11), pp. 2923-2930.
  • von Schantz M, Archer SN. (2003) 'Clocks, genes and sleep'. ROYAL SOC MEDICINE PRESS LTD JOURNAL OF THE ROYAL SOCIETY OF MEDICINE, 96 (10), pp. 486-489.
  • Von Schantz M, Archer SN. (2003) 'Clocks, genes and sleep'. Journal of the Royal Society of Medicine, 96 (10), pp. 486-489.
  • Archer SN, Robilliard DL, Skene DJ, Arendt J, Von Schantz M, Smits M, Williams A. (2003) 'A length polymorphism in the circadian clock gene Per3 is linked to delayed sleep phase syndrome and extreme diurnal preference'. Sleep, 26 (4), pp. 413-415.

    Abstract

    Study Objectives: To investigate the link between extreme diurnal preference, delayed sleep phase syndrome, and a length polymorphism in Per3. Design: Subjects were genotyped using polymerase chain reaction. Patients or Participants: Subjects with defined diurnal preference as determined by the Horne-Östberg questionnaire and patients with delayed sleep phase syndrome. Measurements and Results: The Per3 polymorphism correlated significantly with extreme diurnal preference, the longer allele associating with morningness and the shorter allele with eveningness. The shorter allele was strongly associated with the delayed sleep phase syndrome patients, 75% of whom were homozygous. Conclusion: The length of the Per3 repeat region identifies a potential genetic marker for extreme diurnal preference.

  • Robilliard DL, Archer SN, Arendt J, Lockley SW, Hack LM, English J, Skene DJ, Von Schantz M, Leger D, Smits MG, Williams A. (2002) 'The 3111 Clock gene polymorphism is not associated with sleep and circadian rhythmicity in phenotypically characterized human subjects'. Journal of Sleep Research, 11 (4), pp. 305-312.

    Abstract

    Mutations in clock genes are associated with abnormal circadian parameters, including sleep. An association has been reported previously between a polymorphism (3111C), situated in the 3′-untranslated region (3′-UTR) of the circadian gene Clock and evening preference. In the present study, this polymorphism was assessed in: (1) 105 control subjects with defined diurnal preference, (2) 26 blind subjects with free-running circadian rhythms and characterized with regard to circadian period (τ) and (3) 16 delayed sleep phase syndrome patients. The control group was chosen from a larger population (n = 484) by Horne-Östberg questionnaire analysis, from which three subgroups were selected (evening, intermediate and morning preference). Data from sleep diaries completed by 90% of these subjects showed a strong correlation between preferred and estimated timings of sleep and wake. The mean timings of activities for the evening group were at least 2 h later than the morning group. Genetic analysis showed that, in contrast with the previously published finding, there was no association between 3111C and eveningness. Neither was there an association between 3111C and τ, nor a significant difference in 3111C frequency between the normal and delayed sleep phase syndrome groups. To assess the effect of this polymorphism on messenger RNA (mRNA) translatability, luciferase reporter gene constructs containing the two Clock polymorphic variants in their 3′-UTR were transfected into COS-1 cells and luciferase activity measured. No significant difference was observed between the two variants. These results do not support Clock 3111C as a marker for diurnal preference, τ, or delayed sleep phase syndrome in humans.

  • Bozzano A, Murgia R, Vallerga S, Hirano J, Archer S. (2001) 'The photoreceptor system in the retinae of two dogfishes, Scyliorhinus canicula and Galeus melastomus: possible relationship with depth distribution and predatory lifestyle'. ACADEMIC PRESS LTD JOURNAL OF FISH BIOLOGY, 59 (5), pp. 1258-1278.
  • Diss JKJ, Archer SN, Hirano J, Fraser SP, Djamgoz MBA. (2001) 'Expression profiles of voltage-gated Na+ channel alpha-subunit genes in rat and human prostate cancer cell lines'. WILEY-LISS PROSTATE, 48 (3), pp. 165-178.
  • Archer SN, Thompson S, Lucas RJ, Foster RG, von Schantz M. (2000) 'Analysis of differentially expressed genes in the wildtype and rd mouse retina by macroarray screening.'. ASSOC RESEARCH VISION OPHTHALMOLOGY INC INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 41 (4), pp. S27-S27.
  • Lintas C, Hirano J, Archer S. (1998) 'Genetic variation of the European eel (Anguilla anguilla)'. SPRINGER VERLAG MOLECULAR MARINE BIOLOGY AND BIOTECHNOLOGY, 7 (4), pp. 263-269.
  • Archer S, Hirano J, Diss JKJ, Fraser SP, Djamgoz MBA. (1998) 'Expression and localization in the fish retina of a homologue of the Alzheimer's related PS1 gene'. LIPPINCOTT WILLIAMS & WILKINS NEUROREPORT, 9 (13), pp. 3115-3122.
  • Archer S, Hirano J, Diss JKJ, Fraser SP, Djamgoz MBA. (1998) 'Expression and localization in the fish retina of a homologue of the Alzheimer's related PS1 gene'. LIPPINCOTT WILLIAMS & WILKINS NEUROREPORT, 9 (9), pp. 2049-2056.
  • Archer S. (1998) 'Eels see in multicolour'. EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER BIOFUTUR, (179), pp. 30-32.
  • Diss JKJ, Stewart D, Fraser SP, Black JA, Dib-Hajj S, Waxman SG, Archer SN, Djamgoz MBA. (1998) 'Expression of skeletal muscle-type voltage-gated Na+ channel in rat and human prostate cancer cell lines'. ELSEVIER SCIENCE BV FEBS LETTERS, 427 (1), pp. 5-10.
  • Archer SN, Hirano J. (1998) 'Rod opsin sequence in the John Dory: further evidence for the spectral tuning of rhodopsin'. ACADEMIC PRESS LTD JOURNAL OF FISH BIOLOGY, 52 (1), pp. 209-212.
  • Hirano J, Archer SN, Djamgoz MBA. (1998) 'Dopamine receptor subtypes expressed in vertebrate (carp and eel) retinae: Cloning, sequencing and comparison of five D-1-like and three D-2-like receptors'. HARWOOD ACAD PUBL GMBH RECEPTORS & CHANNELS, 5 (6), pp. 387-404.
  • Djamgoz MBA, Hankins MW, Hirano J, Archer SN. (1997) 'Neurobiology of retinal dopamine in relation to degenerative states of the tissue'. PERGAMON-ELSEVIER SCIENCE LTD VISION RESEARCH, 37 (24), pp. 3509-3529.
  • Archer SN, Hirano J. (1997) 'Opsin sequences of the rod visual pigments in two species of Poeciliid fish'. ACADEMIC PRESS LTD JOURNAL OF FISH BIOLOGY, 51 (1), pp. 215-219.
  • Archer S, Hirano J. (1996) 'Absorbance spectra and molecular structure of the blue-sensitive rod visual pigment in the conger eel (Conger conger)'. ROYAL SOC PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, 263 (1371), pp. 761-767.
  • Archer S, Hope A, Partridge JC. (1995) 'The molecular basis for the green-blue sensitivity shift in the rod visual pigments of the European eel'. ROYAL SOC PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, 262 (1365), pp. 289-295.
  • ARCHER SN, LYTHGOE JN, HALL L. (1992) 'ROD OPSIN CDNA SEQUENCE FROM THE SAND GOBY (POMATOSCHISTUS-MINUTUS) COMPARED WITH THOSE OF OTHER VERTEBRATES'. ROYAL SOC PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, 248 (1321), pp. 19-25.
  • PARTRIDGE JC, ARCHER SN, VANOOSTRUM J. (1992) 'SINGLE AND MULTIPLE VISUAL PIGMENTS IN DEEP-SEA FISHES'. CAMBRIDGE UNIV PRESS JOURNAL OF THE MARINE BIOLOGICAL ASSOCIATION OF THE UNITED KINGDOM, 72 (1), pp. 113-130.
  • ARCHER SN, LYTHGOE JN. (1990) 'THE VISUAL PIGMENT BASIS FOR CONE POLYMORPHISM IN THE GUPPY, POECILIA-RETICULATA'. PERGAMON-ELSEVIER SCIENCE LTD VISION RESEARCH, 30 (2), pp. 225-233.
  • Partridge JC, Shand J, Archer SN, Lythgoe JN, van Groningen-Luyben WAHM. (1989) 'Interspecific variation in the visual pigments of deep-sea fishes'. Journal of Comparative Physiology A, 164 (4), pp. 513-529.

    Abstract

    Visual pigments in the rods of 38 species of deep-sea fish were examined by microspectrophotometry. 33 species were found to have a single rhodopsin with a wavelength of maximum absorbance (λ) in the range 470-495 nm. Such visual pigments have absorbance maxima close to the wavelengths of maximum spectral transmission of oceanic water. 5 species, however, did not conform to this pattern and visual pigments were found with λ values ranging from 451 nm to 539 nm. In 4 of these species two visual pigments were found located in two types of rod. Some 2-pigment species which have unusual red sensitivity, also have red-emitting photophores. These species have both rhodopsin and porphyropsin pigments in their retinae, which was confirmed by HPLC, and the two pigments are apparently located in separate rods in the same retinal area. In deep-sea fishes the occurrence of 'unusual' visual pigments seems to be correlated with aspects of the species' depth ranges. In addition to ecological influences we present evidence, in the form of λ spectral clustering, that indicates the degree of molecular constraint imposed on the evolution of visual pigments in the deep-sea. © 1989 Springer-Verlag.

  • PARTRIDGE JC, ARCHER SN, LYTHGOE JN. (1988) 'VISUAL PIGMENTS IN THE INDIVIDUAL RODS OF DEEP-SEA FISHES'. SPRINGER VERLAG JOURNAL OF COMPARATIVE PHYSIOLOGY A-SENSORY NEURAL AND BEHAVIORAL PHYSIOLOGY, 162 (4), pp. 543-550.
  • ARCHER SN, ENDLER JA, LYTHGOE JN, PARTRIDGE JC. (1987) 'VISUAL PIGMENT POLYMORPHISM IN THE GUPPY POECILIA-RETICULATA'. PERGAMON-ELSEVIER SCIENCE LTD VISION RESEARCH, 27 (8), pp. 1243-1252.

Conference papers

  • Groeger JA, Lo JC, Santhi N, Arbon EL, Lazar A, Hasan S, Von Schantz M, Archer SN, Dijk DJ. (2012) ''Trait-like' susceptibility to sleep loss varies with circadian phase and the task used to index vulnerable-resilient sleep-deprived performance'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 36-37.
  • Lo JC, Groeger JA, Santhi N, Arbon EL, Lazar AS, Hasan S, Von Schantz M, Archer SN, Dijk DJ. (2012) 'Effects of circadian phase and prior partial sleep deprivation on executive functions during total sleep deprivation are modulated by PER3 polymorphism'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 41-41.
  • Arbon EL, Lazar AS, Lo JC, Slak A, Mccabe PJ, Boyle J, Archer SN, Dijk D-J. (2012) 'Individual differences in sleep revisited: stability across sleep restriction, extension and total sleep loss'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 207-208.
  • Muto V, Meyer C, Jaspar M, Shaffii-Le Bourdiec A, Kusse C, Foret A, Vandewalle G, Collette F, Archer S, Dijk D-J, Maquet P. (2012) 'Influence of sleep homeostasis and circadian rhythm on waking EEG oscillations during a constant routine'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 327-328.
  • Lazar A, Santhi N, Lo J, Slak A, Hasan S, Von Schantz M, Archer S, Dijk D-J. (2012) 'The circadian and homeostatic regulation of sleep spindle activity: effect of the PER3 VNTR polymorphism'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 82-82.
  • Hasan S, Winsky-Sommerer R, Dijk D-J, Archer SN. (2012) 'Sleep in transgenic mouse models for a polymorphism in the human PER3 gene'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 79-79.
  • Jaspar M, Meyer C, Muto V, Shaffii-Le Bourdiec A, Kusse C, Vandewalle G, Collette F, Archer S, Dijk D-J, Maquet P. (2012) 'Influence of sleep homeostasis and circadian rhythm on executive discriminative ability during a constant routine'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 328-328.
  • Shaffii-Le Bourdiec A, Muto V, Jaspar M, Kusse C, Foret A, Archer SN, Le Bourdiec F, Vandewalle G, Collette F, Dijk DJ, Maquet P. (2012) 'Difference in neural correlates of discrimination during sleep deprivation in PER3 homozygous'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 82-82.
  • Groeger JA, Finnan CA, Zoeller S, Mcgregor KM, Archer SN. (2012) 'Effects of genotype and chronotype on time use on work and rest days'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 333-334.
  • Van der Veen DR, Dijk D-J, Archer SN. (2012) 'A role for PERIOD3 in sleep/wake rhythms: photic responses in humanised knock-in mice and gene expression correlates of PER3 expression'. WILEY-BLACKWELL JOURNAL OF SLEEP RESEARCH, Paris, FRANCE: 21st Congress of the European-Sleep-Research-Society 21, pp. 333-333.
  • Schwarz JF, Ingre M, Anund A, Fors C, Karlsson JG, Kecklund G, Van der Veen DR, Archer SN, Dijk D, Akerstedt T. (2012) 'PERIOD3 VNTR POLYMORPHISM MODIFIES SLEEPINESS DURING REAL ROAD DRIVING'. AMER ACAD SLEEP MEDICINE SLEEP, Boston, MA: 26th Annual Meeting of the Association-of-Professional-Sleep-Societies (APSS) 35, pp. A109-A109.
  • Vandewalle G, Archer SN, Wuillaume C, Balteau E, Degueldre C, Luxen A, Dijk D, Maquet P. (2009) 'MODULATION OF FMRI ASSESSED BRAIN RESPONSES TO BLUE AND GREEN LIGHT BY SLEEP HOMFOSTASIS, CIRCADIAN PHASE AND PER3 POLYMORPHISM'. AMER ACAD SLEEP MEDICINE SLEEP, Seattle, WA: 23rd Annual Meeting of the Associated-Professional-Sleep-Societies 32, pp. A1-A1.
  • James LM, Viola AU, Archer SN, Dijk D. (2008) 'Topography of the effects of a PER3 polymorphism on alpha activity in REM sleep under baseline and recovery conditions'. WILEY-BLACKWELL PUBLISHING, INC JOURNAL OF SLEEP RESEARCH, Glasgow, SCOTLAND: 19th Congress of the European-Sleep-Research-Society 17, pp. 1-1.
  • Von Schantz W, Carpen JD, Gibson M, Lim G, Johnston J, Skene DJ, Archer SN. (2008) 'Analysis of the PER3 promoter and haplotypes that associate with diurnal preference and delayed sleep phase disorder'. WILEY-BLACKWELL PUBLISHING, INC JOURNAL OF SLEEP RESEARCH, Glasgow, SCOTLAND: 19th Congress of the European-Sleep-Research-Society 17, pp. 80-80.
  • Groeger JA, Lo JC, Viola AU, Schantz MV, Archer SN, Dijk D. (2008) 'Period3 and the effects of sleep deprivation on executive function: the importance of circadian phase'. WILEY-BLACKWELL PUBLISHING, INC JOURNAL OF SLEEP RESEARCH, Glasgow, SCOTLAND: 19th Congress of the European-Sleep-Research-Society 17, pp. 38-38.
  • Vaughan V, Archer S, Skene DJ, Arber S. (2008) 'Daily light exposure profiles in older extreme morning and evening types'. WILEY-BLACKWELL PUBLISHING, INC JOURNAL OF SLEEP RESEARCH, Glasgow, SCOTLAND: 19th Congress of the European-Sleep-Research-Society 17, pp. 73-73.
  • Vandewalle G, Archer S, Wuillaume C, Balteau E, Degueldre C, Luxen A, Maquet P, Dijk D. (2008) 'Polymorphism in period3 predicts fMRI-assessed inter-individual differences in the effects of sleep deprivation'. WILEY-BLACKWELL PUBLISHING, INC JOURNAL OF SLEEP RESEARCH, Glasgow, SCOTLAND: 19th Congress of the European-Sleep-Research-Society 17, pp. 38-38.
  • Viola AU, James LM, Archer SN, Duk D. (2008) 'PER3 polymorphism affects cardiac autonomic control in healthy people'. WILEY-BLACKWELL PUBLISHING, INC JOURNAL OF SLEEP RESEARCH, Glasgow, SCOTLAND: 19th Congress of the European-Sleep-Research-Society 17, pp. 82-82.
  • Vandewalle G, Archer SN, Wuillaume C, Balteau E, Degueldre C, Luxen A, Maquet P, Dijk D. (2008) 'A period 3 polymorphism predicts FMRI assessed brain responses following sleep loss'. AMER ACAD SLEEP MEDICINE SLEEP, Baltimore, MD: 22nd Annual Meeting of the Associated-Professional-Sleep-Societies 31, pp. A111-A111.
  • James LM, Viola AU, Archer SN, Dijk D. (2008) 'Topography of the effects of a PER3 polymorphism on alpha activity in REM sleep under baseline and recovery conditions'. AMER ACAD SLEEP MEDICINE SLEEP, Baltimore, MD: 22nd Annual Meeting of the Associated-Professional-Sleep-Societies 31, pp. A107-A107.
  • Archer S, Viola A, Von Schantz M, Dijk D. (2007) 'Endogenous circadian rhythm of PER3 RNA in human leucocytes: Association with sleep timing, melatonin rhythm, and PER3 genotype'. AMER ACADEMY SLEEP MEDICINE SLEEP, Minneapolis, MN: 21st Annual Meeting of the Association-Professional-Sleep-Societies 30, pp. A54-A55.
  • Groeger J, Lo J, Viola A, Von Schantz M, Archer S, Dijk D. (2007) 'PER3 polymorphism predictssusceptibility to sleep deprivation-induced impairment of early morning executive performance'. AMER ACADEMY SLEEP MEDICINE SLEEP, Minneapolis, MN: 21st Annual Meeting of the Association-Professional-Sleep-Societies 30, pp. A54-A54.
  • Vaughan V, Meadows R, Archer SN, Skene DJ, Arber S. (2006) 'Diurnal preference in couples: negotiating sleep timing'. BLACKWELL PUBLISHING JOURNAL OF SLEEP RESEARCH, Innsbruck, AUSTRIA: 18th Congress of the European-Sleep-Research-Society 15, pp. 95-95.
  • Von Schantz M, Archer SN. (2006) 'Genetic aspects of delayed sleep phase syndrome (DSPS)'. BLACKWELL PUBLISHING JOURNAL OF SLEEP RESEARCH, Innsbruck, AUSTRIA: 18th Congress of the European-Sleep-Research-Society 15, pp. 5-5.
  • Viola AU, Archer SN, Groeger JA, Skene DJ, Von Schantz M, Dijk DJ. (2006) 'Polymorphism in the clock gene PER3 predicts sleep structure and EEG power spectra'. BLACKWELL PUBLISHING JOURNAL OF SLEEP RESEARCH, Innsbruck, AUSTRIA: 18th Congress of the European-Sleep-Research-Society 15, pp. 53-53.
  • Jones KH, Ellis J, Von Schantz M, Skene DJ, Dijk D, Archer SN. (2006) 'Age-related change in the association between a variable number tandem repeat polymorphism in the (PER3) gene and preferred timing of sleep and waking activities'. BLACKWELL PUBLISHING JOURNAL OF SLEEP RESEARCH, Innsbruck, AUSTRIA: 18th Congress of the European-Sleep-Research-Society 15, pp. 97-98.
  • Archer SN, Robillard DL, Skene DJ, Smits M, Williams A, Arendt J, von Schantz M. (2003) 'A length polymorphism in the circadian clock gene Per3 is linked to delayed sleep phase syndrome and extreme diurnal preference'. AMER ACADEMY SLEEP MEDICINE SLEEP, CHICAGO, ILLINOIS: 17th Annual Meeting of the Associated-Professional-Sleep-Societies 26, pp. A109-A109.
  • Ahuja P, Archer SN, van Veen T, von Schantz M. (2003) 'Neuroleukin/AMF is present around cones and in various spatially restricted cell types of the mouse retina'. ASSOC RESEARCH VISION OPHTHALMOLOGY INC INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, FT LAUDERDALE, FLORIDA: Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology 44, pp. U459-U459.
  • Archer SN, Lucas RJ, Thompson S, Foster RG, von Schantz M. (2002) 'Identification of a novel retinal kinase with promoter elements affected by circadian clock proteins'. ASSOC RESEARCH VISION OPHTHALMOLOGY INC INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, FT LAUDERDALE, FLORIDA: Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology 43, pp. U308-U308.
  • von Schantz M, Archer SN, Ahuja P, van Veen T. (2002) 'Identification of transcripts enriched in the inner retina by differential macroarray hybridization'. ASSOC RESEARCH VISION OPHTHALMOLOGY INC INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, FT LAUDERDALE, FLORIDA: Annual Meeting of the Association-for-Research-in-Vision-and-Ophthalmology 43, pp. U321-U321.

Teaching

BMS1025 Cell Biology
BMS2043 Analytical Biochemistry
BMS2048 Neuroscience, from Neurones to Behaviour
BMS2062 Animal Biology
BMS3066 Biological Rhythms

Departmental Duties

Head of the Department of Biochemistry and Physiology
Biochemistry Admissions Tutor

Affiliations

European Biological Rhythms Society
Society for Research on Biological Rhythms (member of Trainee Awards Committee 2011-present)
European Sleep Research Society (member of Scientific Committee 2010-2014, Chair Scientific Committee 2012-2014, member of Research Network Committee 2010-2014)

Selected Conference/Seminar Invitations

2009 ‘Genetics of sleep, EEG, and vulnerability to sleep loss’, Sanofi-Aventis 7th International Sleep Disorders Forum, Art of Good Sleep Congress, Cannes, France

2010 ‘PER3 and the genetics of sleep and circadian phenotypes in mice and men’, 20th Annual Congress, European Sleep Research Society, Lisbon, Portugal

2011 ‘Genetics of sleep and circadian rhythms in mice’, 6th Quadrennial Worldsleep Congress, Kyoto, Japan

2012 ‘Circadian rhythm disorders’, Royal Society of Medicine conference on ‘Genetics of sleep & sleep disorders’, London, UK

2012 ‘Interaction between sleep & circadian rhythms’, joint ESRS-EBRS symposium, 21st Congress of the European Sleep Research Society, Paris, France

2012 ‘Sleep, body clocks, and health’, University of Surrey Council & Executive meeting, UK

2013 ‘The human clock’, Marie Curie Research Training Network, CNRS, Paris

2014 ‘The contribution of sleep and circadian systems to the regulation of peripheral gene expression – relevance to jet lag, shift work, and circadian disorders’, Royal Society of Medicine conference on ‘Hot topics for healthcare scientists in sleep medicine’, London, UK

2014 ‘Chronotype, sleep, and the human transcriptome’, German Institute of Human Nutrition, Berlin

2014 ‘Mistimed sleep disrupts the circadian regulation of the human transcriptome’, 22nd Congress of the European Sleep Research Society, Tallinn, Estonia

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Assembly date: Thu Jul 31 21:41:37 BST 2014
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