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CDB Seminars
All welcome

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First Year CDB PhD Students: Mini Symposium

Tuesday 1 July, 1.30-4.10pm

Host: Yoshiyuki Yamamoto
Room 249, 2nd Floor, Medical Sciences Building
1.30pm  Lizzie Yates: "Messed up lysosomes: what’s their role in Parkinson’s disease?"

1.45pm  Francis Carpenter: “Neural Representations of Space in Connected, Perceptually Identical Compartments”

2.00pm  Chris Penny:  "The functional architecture of Two-Pore Channels" 

2.15pm  Amina Yonis: “The role of actin nucleators in the cellular actin cortex”

2.30pm  Lewis Brayshaw: ”Cadherin de-adhesion in cancer”

2.45pm  Agnieszka Piatkowska: “Mechanism of somite formation”

3.00pm  Interval

3.10pm  Alan Greig: “Pertussis vaccination and dysfunction of the blood brain barrier: an in vitro study”

3.25pm  Marina Teter: “The role of Wnt antagonists in synapse vulnerability”

3.40pm  Gauri Bhosale: “Investigating the mitochondrial permeability transition pore as a therapeutic target in human disease”

3.55pm  Lourdes Sri Raja: "Modelling Protein Signalling Pathways during Neutrophil Differentiation"

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Thursday July 3rd, 12pm
Dr Shmuel Muallem, National Institutes of Health
Title: Lysosomal ion channels: form, function and dysfunction
Host: Prof Sandip Patel
Venue: Room 249, Medical Sciences Building

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Professor Stephen Davies

Prof Steve Davies


Stephen Davies is Professor of Molecular Neuropathology

s.w.davies@ucl.ac.uk

Telephone:

Office - 020 7679 2677
(Int: 32677)

Lab - 020 7679 2126
(Int: 32126)

View Prof Davies' Lab Research website here and his Profile on the School of Life and Medical Sciences here

Research Interests

The ultrastructural and molecular organisation of the neuronal nucleus.

Research Description

The neuronal cell nucleus has a characteristic and highly specialised organisation. The nucleolus appears to act as a central organising region around which there is a complex organisation of subnuclear structures, such as the perinucleolar rosette and a large perinucleolar cap of heterochromatin. We are currently defining the molecular and ultrastructural composition of these domains. The rosette is made up of 1-2 domains containing the Cajal Body protein p80 coilin together with Nopp140 and the SMN complex, the remainder contain Nopp140. The heterochromatin caps contain large areas of MeCP2 and are associated with smaller domains containing the chromosome centromeres or the polycomb protein complex. All these areas are variably marked by trimethylated histones. We are further defining this complex organisation by comparing it with 1) the spatial patterns of gene expression occurring in neurons in vivo and 2) the 3d spatial arrangement of genes within the nucleus of defined neurons Why do we think that this complex arrangement of neuronal nuclear structure is of importance for human neurological disease? We have shown that in Huntington's disease the neuronal nucleus reorganises to accommodate a large intranuclear inclusion such that the perinucleolar rosette is disrupted to allow movement of the Cajal body like p80 coilin positve structure to attach to the newly formed inclusion. This results in a profound rearrangement of the nucleolar structure, dissociation away from defined chromosomal domains and transcriptional dysregulation. Similar disruption of these structures occurs in spinal muscular atrophy (SMA), fragile X tremor ataxia syndrome (FXTAS), frontotemporal dementia (FTD) and autism spectrum disorder (ASD). We are currently investigating the functional consequences of nuclear disruption in these conditions.

Page last modified on 25 may 10 14:50 by Glenda Young