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Events

Details of any upcoming colloquia, seminars or public lectures will be posted here when they become available.

Upcoming events

Wed
4
Mar

Diamond Light Source

Dr Chris Christou, Head of Radiofrequency Group, Diamond Light Source

Fri
20
Mar

Schools Space Conference with Tim Peake

Astronaut Tim Peake will meet students at a schools' conference hosted by the University of York.

Fri
20
Mar

Seminar

Part of the Biological Physics seminar series

Fri
27
Mar

Seminar: Neurotrophin-mediated regulation of axonal transport is perturbed in genetic peripheral neuropathy

Charcot-Marie-Tooth disease type 2D (CMT2D) is a peripheral neuropathy caused by dominant mutations in the widely expressed housekeeping gene GARS, which encodes the non-redundant glycyl-tRNA synthetase (GlyRS). The cause of this neuronal selectivity remains unresolved and there is no available treatment for this debilitating condition. We recently identified that dominant, CMT2D-linked GARS mutations cause the encoded mutant GlyRS protein to aberrantly interact with extracellular regions of tropomyosin receptor kinase (Trk) receptors (1). These largely neuron-specific, receptor tyrosine kinases mediate the survival, development, and differentiation of motor and sensory neurons by binding with differential affinity to neurotrophins secreted by distal target cells. The rogue interaction of mutant GlyRS with Trk/neurotrophin receptors provides a rationale for neuronal selectivity in CMT2D, implies a non-cell autonomous disease mechanism, and likely accounts for the pre-natal perturbation of sensory neuron fate that we observed in mutant CMT2D mice. The main aim of our latest research is to assess the in vivo axonal transport dynamics of neurotrophin/Trk receptor-loaded signalling endosomes in CMT2D mice. In unpublished work, we have used a fluorescently-labelled probe (2) to interrogate the impact of neurotrophins on signalling endosome trafficking in healthy and CMT2D axons in live, anaesthetised mice. We have identified that CMT2D mice display early and persistent impairments in retrograde axonal transport of signalling endosomes in vivo, and that perturbations in neurotrophin signalling account for this deficit. Moreover, through recombinant neurotrophin administration directly into CMT2D muscle, we are able to effectively reverse the deficit in axonal transport across timepoints. Through these experiments, we have uncovered an unappreciated role for neurotrophins in regulating the dynamics of axonal transport, and discovered a neuropathic pathway that may be broadly amenable to therapeutic intervention. (1) Sleigh et al. (2017) Trk receptor signaling and sensory neuron fate are perturbed in human neuropathy caused by Gars mutations. Proc Natl Acad Sci U S A 114: E3324-E3333. (2) Gibbs et al. (2016) In vivo imaging of axonal transport in murine motor and sensory neurons. J Neurosci Methods 257: 26-33. Part of the Biological Physics seminar series

Fri
17
Apr

Lecture

Part of the "Essentials of Physics of Life" lecture series.

Fri
24
Apr

Ten-minute seminars

Part of the "Essentials of Physics of Life" lecture series.

Fri
1
May

Ten-minute seminars

Part of the "Essentials of Physics of Life" lecture series.

Fri
22
May

Opening Genesis 3

Official opening of the new Physics of Life Building at Genesis 3

Events by type

Seminars in the Department of Chemistry

Seminars in the Department of Electronics