skip to content

Department of Physiology, Development and Neuroscience

 

Thu 09 May 16:00: Behavioural and mechanical heterogeneities underpin cell migration essential for mouse anterior patterning

https://talks.cam.ac.uk/show/rss/6283 - Fri, 12/04/2024 - 09:03
Behavioural and mechanical heterogeneities underpin cell migration essential for mouse anterior patterning

Abstract not available

Add to your calendar or Include in your list

Thu 14 Mar 16:00: Epigenetic priming of embryonic cell lineages in the mammalian epiblast

https://talks.cam.ac.uk/show/rss/6283 - Mon, 04/03/2024 - 13:23
Epigenetic priming of embryonic cell lineages in the mammalian epiblast

Miguel Torres trained in Drosophila Genetics during his PhD (1991) with Dr. Lucas Sánchez (CIB-CSIC, Madrid) and later in Mouse Developmental Genetics during his Postdoc at the MPI with Dr Peter Gruss. He established an independent research group at the National Center for Biotechnology, CSIC , Madrid in 1996 and moved in 2007 to CNIC where he now coordinates the Cardiovascular Regeneration Program. His group has a strong focus on understanding organ development and regeneration. Dr Torres group characterized the role of homeobox genes and signaling pathways in establishing positional information along the limb proximo-distal axis during development and regeneration. A second topic of interest has been understanding the role of cell death in embryonic development. The group demonstrated the conservation of cell death pathways in metazoan evolution and demonstrated the relevance of cell death and cell competition in mammalian tissue homeostasis and regeneration. The group has also developed clonal analysis strategies and live imaging tools that allowed defining new lineage relationships and tissue dynamics in limb and cardiovascular development.

Add to your calendar or Include in your list

Thu 15 Feb 16:00: Towards Human Systems Biology of Sleep/Wake Cycles: Phosphorylation Hypothesis of Sleep

https://talks.cam.ac.uk/show/rss/6283 - Thu, 15/02/2024 - 09:14
Towards Human Systems Biology of Sleep/Wake Cycles: Phosphorylation Hypothesis of Sleep

The field of human biology faces three major technological challenges. Firstly, the causation problem is difficult to address in humans compared to model animals. Secondly, the complexity problem arises due to the lack of a comprehensive cell atlas for the human body, despite its cellular composition. Lastly, the heterogeneity problem arises from significant variations in both genetic and environmental factors among individuals. To tackle these challenges, we have developed innovative approaches. These include 1) mammalian next-generation genetics, such as Triple CRISPR for knockout (KO) mice and ES mice for knock-in (KI) mice, which enables causation studies without traditional breeding methods; 2) whole-body/brain cell profiling techniques, such as CUBIC , to unravel the complexity of cellular composition; and 3) accurate and user-friendly technologies for measuring sleep and awake states, exemplified by ACCEL , to facilitate the monitoring of fundamental brain states in real-world settings and thus address heterogeneity in human.

By integrating these three technologies, we have made significant progress in addressing two major scientific challenges in sleep research: 1) understanding sleep regulation (sleep mechanisms) and 2) determining the role of sleep (sleep functions). With regard to sleep mechanisms, we have recently proposed the phosphorylation hypothesis of sleep, which emphasizes the role of the sleep-promoting kinase 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, which induces and sustains sleep (Tone et al., 2022). Concerning sleep functions, we conducted computational studies to examine synaptic efficacy dynamics 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.

During this talk, we will also present our discoveries regarding the identification of muscarinic acetylcholine receptors (Chrm1 and Chrm3) as essential genes of REM sleep. Furthermore, we will discuss new insights into psychiatric disorders, neurodevelopmental disorders, and neurodegenerative disorders derived from the phosphorylation hypothesis of sleep.

This talk is hosted by Dr Keita Tamura and Dr Christian Wood.

You can join the talk via Zoom using the following link: https://cam-ac-uk.zoom.us/j/89822382715?pwd=eExMZlpERkRJM1R0d2NmUEZxU1ZEZz09 Meeting ID: 898 2238 2715 Passcode: 112932

Add to your calendar or Include in your list

Thu 15 Feb 16:00: Towards Human Systems Biology of Sleep/Wake Cycles: Phosphorylation Hypothesis of Sleep

https://talks.cam.ac.uk/show/rss/6283 - Mon, 12/02/2024 - 09:28
Towards Human Systems Biology of Sleep/Wake Cycles: Phosphorylation Hypothesis of Sleep

The field of human biology faces three major technological challenges. Firstly, the causation problem is difficult to address in humans compared to model animals. Secondly, the complexity problem arises due to the lack of a comprehensive cell atlas for the human body, despite its cellular composition. Lastly, the heterogeneity problem arises from significant variations in both genetic and environmental factors among individuals. To tackle these challenges, we have developed innovative approaches. These include 1) mammalian next-generation genetics, such as Triple CRISPR for knockout (KO) mice and ES mice for knock-in (KI) mice, which enables causation studies without traditional breeding methods; 2) whole-body/brain cell profiling techniques, such as CUBIC , to unravel the complexity of cellular composition; and 3) accurate and user-friendly technologies for measuring sleep and awake states, exemplified by ACCEL , to facilitate the monitoring of fundamental brain states in real-world settings and thus address heterogeneity in human.

By integrating these three technologies, we have made significant progress in addressing two major scientific challenges in sleep research: 1) understanding sleep regulation (sleep mechanisms) and 2) determining the role of sleep (sleep functions). With regard to sleep mechanisms, we have recently proposed the phosphorylation hypothesis of sleep, which emphasizes the role of the sleep-promoting kinase 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, which induces and sustains sleep (Tone et al., 2022). Concerning sleep functions, we conducted computational studies to examine synaptic efficacy dynamics 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.

During this talk, we will also present our discoveries regarding the identification of muscarinic acetylcholine receptors (Chrm1 and Chrm3) as essential genes of REM sleep. Furthermore, we will discuss new insights into psychiatric disorders, neurodevelopmental disorders, and neurodegenerative disorders derived from the phosphorylation hypothesis of sleep.

This talk is hosted by Dr Keita Tamura and Dr Christian Wood

Add to your calendar or Include in your list

Thu 15 Feb 16:00: Towards Human Systems Biology of Sleep/Wake Cycles: Phosphorylation Hypothesis of Sleep

https://talks.cam.ac.uk/show/rss/6283 - Mon, 05/02/2024 - 09:27
Towards Human Systems Biology of Sleep/Wake Cycles: Phosphorylation Hypothesis of Sleep

The field of human biology faces three major technological challenges. Firstly, the causation problem is difficult to address in humans compared to model animals. Secondly, the complexity problem arises due to the lack of a comprehensive cell atlas for the human body, despite its cellular composition. Lastly, the heterogeneity problem arises from significant variations in both genetic and environmental factors among individuals. To tackle these challenges, we have developed innovative approaches. These include 1) mammalian next-generation genetics, such as Triple CRISPR for knockout (KO) mice and ES mice for knock-in (KI) mice, which enables causation studies without traditional breeding methods; 2) whole-body/brain cell profiling techniques, such as CUBIC , to unravel the complexity of cellular composition; and 3) accurate and user-friendly technologies for measuring sleep and awake states, exemplified by ACCEL , to facilitate the monitoring of fundamental brain states in real-world settings and thus address heterogeneity in human.

By integrating these three technologies, we have made significant progress in addressing two major scientific challenges in sleep research: 1) understanding sleep regulation (sleep mechanisms) and 2) determining the role of sleep (sleep functions). With regard to sleep mechanisms, we have recently proposed the phosphorylation hypothesis of sleep, which emphasizes the role of the sleep-promoting kinase 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, which induces and sustains sleep (Tone et al., 2022). Concerning sleep functions, we conducted computational studies to examine synaptic efficacy dynamics 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.

During this talk, we will also present our discoveries regarding the identification of muscarinic acetylcholine receptors (Chrm1 and Chrm3) as essential genes of REM sleep. Furthermore, we will discuss new insights into psychiatric disorders, neurodevelopmental disorders, and neurodegenerative disorders derived from the phosphorylation hypothesis of sleep.

Add to your calendar or Include in your list

Thu 06 Jun 16:00: Title to be confirmed

https://talks.cam.ac.uk/show/rss/6283 - Tue, 30/01/2024 - 09:27
Title to be confirmed

Abstract not available

Add to your calendar or Include in your list

Thu 23 May 16:00: Title to be confirmed

https://talks.cam.ac.uk/show/rss/6283 - Tue, 30/01/2024 - 09:26
Title to be confirmed

Abstract not available

Add to your calendar or Include in your list

Thu 09 May 16:00: Title to be confirmed

https://talks.cam.ac.uk/show/rss/6283 - Tue, 30/01/2024 - 09:25
Title to be confirmed

Abstract not available

Add to your calendar or Include in your list

Thu 25 Apr 16:00: Title to be confirmed

https://talks.cam.ac.uk/show/rss/6283 - Tue, 30/01/2024 - 09:24
Title to be confirmed

Abstract not available

Add to your calendar or Include in your list

Thu 14 Mar 16:00: Title to be confirmed

https://talks.cam.ac.uk/show/rss/6283 - Tue, 30/01/2024 - 09:23
Title to be confirmed

Abstract not available

Add to your calendar or Include in your list

Thu 14 Mar 16:00: Title to be confirmed

https://talks.cam.ac.uk/show/rss/6283 - Tue, 30/01/2024 - 09:23
Title to be confirmed

Abstract not available

Add to your calendar or Include in your list

Thu 29 Feb 16:00: Title to be confirmed

https://talks.cam.ac.uk/show/rss/6283 - Tue, 30/01/2024 - 09:12
Title to be confirmed

Abstract not available

Add to your calendar or Include in your list

Thu 29 Feb 16:00: Title to be confirmed

https://talks.cam.ac.uk/show/rss/6283 - Tue, 30/01/2024 - 09:12
Title to be confirmed

Abstract not available

Add to your calendar or Include in your list

Thu 15 Feb 16:00: Towards Human Systems Biology of Sleep/Wake Cycles: Phosphorylation Hypothesis of Sleep

https://talks.cam.ac.uk/show/rss/6283 - Tue, 30/01/2024 - 09:09
Towards Human Systems Biology of Sleep/Wake Cycles: Phosphorylation Hypothesis of Sleep

The field of human biology faces three major technological challenges. Firstly, the causation problem is difficult to address in humans compared to model animals. Secondly, the complexity problem arises due to the lack of a comprehensive cell atlas for the human body, despite its cellular composition. Lastly, the heterogeneity problem arises from significant variations in both genetic and environmental factors among individuals. To tackle these challenges, we have developed innovative approaches. These include 1) mammalian next-generation genetics, such as Triple CRISPR for knockout (KO) mice and ES mice for knock-in (KI) mice, which enables causation studies without traditional breeding methods; 2) whole-body/brain cell profiling techniques, such as CUBIC , to unravel the complexity of cellular composition; and 3) accurate and user-friendly technologies for measuring sleep and awake states, exemplified by ACCEL , to facilitate the monitoring of fundamental brain states in real-world settings and thus address heterogeneity in human.

By integrating these three technologies, we have made significant progress in addressing two major scientific challenges in sleep research: 1) understanding sleep regulation (sleep mechanisms) and 2) determining the role of sleep (sleep functions). With regard to sleep mechanisms, we have recently proposed the phosphorylation hypothesis of sleep, which emphasizes the role of the sleep-promoting kinase 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, which induces and sustains sleep (Tone et al., 2022). Concerning sleep functions, we conducted computational studies to examine synaptic efficacy dynamics 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.

During this talk, we will also present our discoveries regarding the identification of muscarinic acetylcholine receptors (Chrm1 and Chrm3) as essential genes of REM sleep. Furthermore, we will discuss new insights into psychiatric disorders, neurodevelopmental disorders, and neurodegenerative disorders derived from the phosphorylation hypothesis of sleep.

Add to your calendar or Include in your list