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SUMMARY:Towards Human Systems Biology of Sleep/Wake Cycles: Phosphorylatio
 n Hypothesis of Sleep - Dr Hiroki Ueda\, University of Tokyo\, RIKEN BDR
DTSTART:20240215T160000Z
DTEND:20240215T170000Z
UID:TALK211696@talks.cam.ac.uk
CONTACT:120880
DESCRIPTION:The field of human biology faces three major technological cha
 llenges. Firstly\, the causation problem is difficult to address in humans
  compared to model animals. Secondly\, the complexity problem arises due t
 o the lack of a comprehensive cell atlas for the human body\, despite its 
 cellular composition. Lastly\, the heterogeneity problem arises from signi
 ficant variations in both genetic and environmental factors among individu
 als. To tackle these challenges\, we have developed innovative approaches.
  These include 1) mammalian next-generation genetics\, such as Triple CRIS
 PR for knockout (KO) mice and ES mice for knock-in (KI) mice\, which enabl
 es causation studies without traditional breeding methods\; 2) whole-body/
 brain cell profiling techniques\, such as CUBIC\, to unravel the complexit
 y of cellular composition\; and 3) accurate and user-friendly technologies
  for measuring sleep and awake states\, exemplified by ACCEL\, to facilita
 te the monitoring of fundamental brain states in real-world settings and t
 hus address heterogeneity in human.\n\nBy integrating these three technolo
 gies\, we have made significant progress in addressing two major scientifi
 c challenges in sleep research: 1) understanding sleep regulation (sleep m
 echanisms) and 2) determining the role of sleep (sleep functions). With re
 gard to sleep mechanisms\, we have recently proposed the phosphorylation h
 ypothesis of sleep\, which emphasizes the role of the sleep-promoting kina
 se CaMKIIα/CaMKIIβ (Tatsuki et al.\, 2016\; Tone et al.\, 2022\; Ode et 
 al.\, 2020) and the involvement of calcium signaling pathways (Tatsuki et 
 al.\, 2016). According to this novel perspective\, the dynamics of calcium
 \, representing neural activity during wakefulness\, can be integrated and
  converted into the auto-phosphorylation status of CaMKIIα/CaMKIIβ\, whi
 ch induces and sustains sleep (Tone et al.\, 2022). Concerning sleep funct
 ions\, we conducted computational studies to examine synaptic efficacy dyn
 amics during sleep and wakefulness. Our findings led to the formulation of
  the Wake-Inhibition-Sleep-Enhancement (WISE) hypothesis\, suggesting that
  wakefulness inhibits synaptic efficacy\, while sleep enhances it.\n\nDuri
 ng this talk\, we will also present our discoveries regarding the identifi
 cation of muscarinic acetylcholine receptors (Chrm1 and Chrm3) as essentia
 l genes of REM sleep. Furthermore\, we will discuss new insights into psyc
 hiatric disorders\, neurodevelopmental disorders\, and neurodegenerative d
 isorders derived from the phosphorylation hypothesis of sleep.\n\nThis tal
 k is hosted by Dr Keita Tamura and Dr Christian Wood.\n\nYou can join the 
 talk via Zoom using the following link:\nhttps://cam-ac-uk.zoom.us/j/89822
 382715?pwd=eExMZlpERkRJM1R0d2NmUEZxU1ZEZz09\nMeeting ID: 898 2238 2715\nPa
 sscode: 112932
LOCATION:Hodgkin Huxley Seminar Room\, Physiology builiding\, Downing Site
  CB2 3EG
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