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Dr B Mueller
No more applications being accepted
Competition Funded PhD Project (European/UK Students Only)
About the Project
Medical Research Scotland
PhD Studentship Awards
This project is one of six four-year PhD Studentships funded by Medical Research Scotland (http://www.medicalresearchscotland.org.uk) to be delivered jointly by the named University and Company. The Studentships will provide the first-class academic and commercial training needed to equip the successful student for a science career in an increasingly competitive market.
Identifying and correcting neuronal defects caused by deregulation of the novel autism susceptibility gene EIF4E - an opportunity to develop treatments for autism. Delivered by the University of Aberdeen and Dundee Cell Products (http://www.dundeecellproducts.com). Academic Supervisors: Dr Berndt Müller & Professor Colin McCaig; Industrial Supervisor: Dr Paul Ajuh, Director.
Autism is a neurodevelopmental disorder characterised by severe and sustained impairments of social interaction and communicative abilities, and a restricted repertoire of activities and interests. This lifelong disability starts in early childhood, affecting 1 out of every 200 individuals.
Autism is caused by genetic defects that are complex and poorly understood. We recently identified the EIF4E gene as an autism susceptibility gene (1). eIF4E protein is a key regulator of mRNA translation. Tight control of mRNA translation is important for neuron function, specifically for synaptic signalling and plasticity (see e.g. (2)). Importantly, mutations in several genes that regulate the activity of eIF4E protein also pre-dispose to autism. Our findings fit with an emerging theme in autism research, namely that deregulation of translation, especially locally at the neuronal synapse, contributes to the development of autism.
The aim of this project is to identify neuronal abnormalities caused by eIF4E deregulation. A cellular model will be used to identify abnormalities in neuron differentiation and behaviour caused by eIF4E deregulation, using live cell microscopy and immunocytochemistry. Changes in neuronal protein components caused by eIF4E deregulation will be identified using state of the art protein profiling methods. Recent evidence indicates that control of eIF4E activity could form the basis of effective treatment of autism (3;4), and this model will be exploited to identify compounds that correct the effects of eIF4E deregulation. This project will provide insight into the underlying molecular changes in neurons contributing to the development of autism.
The successful candidate will be trained in molecular cell biology and neurobiology in the facilities at the Institute of Medical Sciences of Aberdeen University. The project will be undertaken in collaboration with Dundee Cell Products, a company specialised in molecular and cell biology research including protein profiling.
The ideal candidate for this position is expected to obtain or has already obtained at least an upper second class honours degree (or equivalent) in Genetics, Neurobiology, Biochemistry or a related area. He/She should be highly motivated to work on a project important for understanding the causes of autism.
Further information can be obtained from Dr Berndt Müller ([Email Address Removed])
PhD Studentship Awards
This project is one of six four-year PhD Studentships funded by Medical Research Scotland (http://www.medicalresearchscotland.org.uk) to be delivered jointly by the named University and Company. The Studentships will provide the first-class academic and commercial training needed to equip the successful student for a science career in an increasingly competitive market.
Identifying and correcting neuronal defects caused by deregulation of the novel autism susceptibility gene EIF4E - an opportunity to develop treatments for autism. Delivered by the University of Aberdeen and Dundee Cell Products (http://www.dundeecellproducts.com). Academic Supervisors: Dr Berndt Müller & Professor Colin McCaig; Industrial Supervisor: Dr Paul Ajuh, Director.
Autism is a neurodevelopmental disorder characterised by severe and sustained impairments of social interaction and communicative abilities, and a restricted repertoire of activities and interests. This lifelong disability starts in early childhood, affecting 1 out of every 200 individuals.
Autism is caused by genetic defects that are complex and poorly understood. We recently identified the EIF4E gene as an autism susceptibility gene (1). eIF4E protein is a key regulator of mRNA translation. Tight control of mRNA translation is important for neuron function, specifically for synaptic signalling and plasticity (see e.g. (2)). Importantly, mutations in several genes that regulate the activity of eIF4E protein also pre-dispose to autism. Our findings fit with an emerging theme in autism research, namely that deregulation of translation, especially locally at the neuronal synapse, contributes to the development of autism.
The aim of this project is to identify neuronal abnormalities caused by eIF4E deregulation. A cellular model will be used to identify abnormalities in neuron differentiation and behaviour caused by eIF4E deregulation, using live cell microscopy and immunocytochemistry. Changes in neuronal protein components caused by eIF4E deregulation will be identified using state of the art protein profiling methods. Recent evidence indicates that control of eIF4E activity could form the basis of effective treatment of autism (3;4), and this model will be exploited to identify compounds that correct the effects of eIF4E deregulation. This project will provide insight into the underlying molecular changes in neurons contributing to the development of autism.
The successful candidate will be trained in molecular cell biology and neurobiology in the facilities at the Institute of Medical Sciences of Aberdeen University. The project will be undertaken in collaboration with Dundee Cell Products, a company specialised in molecular and cell biology research including protein profiling.
The ideal candidate for this position is expected to obtain or has already obtained at least an upper second class honours degree (or equivalent) in Genetics, Neurobiology, Biochemistry or a related area. He/She should be highly motivated to work on a project important for understanding the causes of autism.
Further information can be obtained from Dr Berndt Müller ([Email Address Removed])
Funding Notes
The PhD Studentship provides: an annual tax-free stipend of £16,000, increasing to £16,500 over the four years; tuition fees at UK/EU rates only; and consumables. Please note international fees are not covered.
Applicants for a studentships must have obtained, or be about to obtain, an upper second class UK honours degree, or the equivalent qualifications gained outside the UK, in neurobiology, biochemistry, genetics or a related area.
Applicants for a studentships must have obtained, or be about to obtain, an upper second class UK honours degree, or the equivalent qualifications gained outside the UK, in neurobiology, biochemistry, genetics or a related area.
References
References
1. Neves-Pereira, et al (2009) Deregulation of EIF4E: a novel mechanism for autism. J Med Genet, 46, 759-765.
2. Liu-Yesucevitz,et al (2011) Local RNA Translation at the Synapse and in Disease. J Neurosci, 31, 16086-16093.
3. Santini, et al (2013) Exaggerated translation causes synaptic and behavioural aberrations associated with autism. Nature, 493, 411-415.
4. Gkogkas et al. (2013) Autism-related deficits via dysregulated eIF4E-dependent translational control. Nature, 493, 371-377.
1. Neves-Pereira, et al (2009) Deregulation of EIF4E: a novel mechanism for autism. J Med Genet, 46, 759-765.
2. Liu-Yesucevitz,et al (2011) Local RNA Translation at the Synapse and in Disease. J Neurosci, 31, 16086-16093.
3. Santini, et al (2013) Exaggerated translation causes synaptic and behavioural aberrations associated with autism. Nature, 493, 411-415.
4. Gkogkas et al. (2013) Autism-related deficits via dysregulated eIF4E-dependent translational control. Nature, 493, 371-377.
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