Bateman:Research: Difference between revisions
No edit summary |
|||
| Line 15: | Line 15: | ||
The overall focus of my laboratory is to understand basic processes in neural development by identifying the key pathways and genes involved and to use this information to provide novel insight into neuropathological disease. Our work will in the long term contribute to improving quality of life by providing new knowledge about nervous system development that can be used to develop strategies to regenerate neural cells and combat neuropathological disease. | The overall focus of my laboratory is to understand basic processes in neural development by identifying the key pathways and genes involved and to use this information to provide novel insight into neuropathological disease. Our work will in the long term contribute to improving quality of life by providing new knowledge about nervous system development that can be used to develop strategies to regenerate neural cells and combat neuropathological disease. | ||
== | == Regulation of neurogenesis by mTOR signalling and its role in epilepsy == | ||
We are interested in how the | We are interested in how the mTOR signal transduction pathway controls neuronal differentiation. Hyperactivation of mTOR signalling causes the disease Tuberous Sclerosis Complex (TSC). TSC patients frequently suffer from neurodevelopmental disorders such as epilepsy and autism. | ||
=== | === mTOR signalling in neurogenesis === | ||
mTOR signalling has critical roles in controlling processes such as cell growth, autophagy and ageing. We have discovered a novel role for the insulin pathway in the temporal control of neurogenesis in Drosophila photoreceptor (PR) neurons (Bateman & McNeill, 2004). | |||
[[Image:Inr.jpg|400px|none|thumb|Photoreceptor differentiation (red) is delayed in insulin receptor clones (marked by the absence of GFP expression]] | [[Image:Inr.jpg|400px|none|thumb|Photoreceptor differentiation (red) is delayed in insulin receptor clones (marked by the absence of GFP expression]] | ||
More recently we have | More recently we have identified a novel complex of two proteins, Unkempt and Headcase, that act downstream of mTOR to regulate photoreceptor differentiation in Drosophila (Avet-Rochex et al., 2014). We are currently study the role of the Unkempt and Headcase in the CNS in Drosophila and mammalian models systems. Understanding the function of these factors and how they are regulated by mTOR will provide novel insight into how mTOR signalling contributes to neurological disorders like epilepsy and autism. | ||
== Mitochondrial dysfunction in the nervous system and its role in neurodegenerative disease == | |||
== Mitochondrial | |||
Mitochondria play critical roles in the generation of cellular energy, apoptosis, cellular calcium buffering and the generation of reactive oxygen species. Mitochondria also have important functions in normal ageing. Given these critical roles in cellular function and physiology, it is not surprising that mitochondria also contribute to a large number of pathogenenic states ranging from cancer to neurodegenerative diseases such as Parkinson’s. | Mitochondria play critical roles in the generation of cellular energy, apoptosis, cellular calcium buffering and the generation of reactive oxygen species. Mitochondria also have important functions in normal ageing. Given these critical roles in cellular function and physiology, it is not surprising that mitochondria also contribute to a large number of pathogenenic states ranging from cancer to neurodegenerative diseases such as Parkinson’s. | ||
We are interested in how | We are interested in how neurons respond to mitochondrial dysfunction and how this process can be modified as a treatment for neurodegenerative disease. We have previously used a genetic screen in yeast to identify genes that can prevent mitochondrial DNA loss in yeast and a cellular model of mitochondrial disease (Iacovino et al., 2009). | ||
We are currently | We are currently developing a Drosophila model of neuronal mitochondrial dysfunction and using this to understand how neurons respond. | ||
We also use human neurodegenerative disease tissue to study the changes that result from mitochondrial dysfunction in diseases like Parkinson's (Gatt et al., 2013). | |||
Revision as of 23:17, 5 September 2014
Overview
The overall focus of my laboratory is to understand basic processes in neural development by identifying the key pathways and genes involved and to use this information to provide novel insight into neuropathological disease. Our work will in the long term contribute to improving quality of life by providing new knowledge about nervous system development that can be used to develop strategies to regenerate neural cells and combat neuropathological disease.
Regulation of neurogenesis by mTOR signalling and its role in epilepsy
We are interested in how the mTOR signal transduction pathway controls neuronal differentiation. Hyperactivation of mTOR signalling causes the disease Tuberous Sclerosis Complex (TSC). TSC patients frequently suffer from neurodevelopmental disorders such as epilepsy and autism.
mTOR signalling in neurogenesis
mTOR signalling has critical roles in controlling processes such as cell growth, autophagy and ageing. We have discovered a novel role for the insulin pathway in the temporal control of neurogenesis in Drosophila photoreceptor (PR) neurons (Bateman & McNeill, 2004).
More recently we have identified a novel complex of two proteins, Unkempt and Headcase, that act downstream of mTOR to regulate photoreceptor differentiation in Drosophila (Avet-Rochex et al., 2014). We are currently study the role of the Unkempt and Headcase in the CNS in Drosophila and mammalian models systems. Understanding the function of these factors and how they are regulated by mTOR will provide novel insight into how mTOR signalling contributes to neurological disorders like epilepsy and autism.
Mitochondrial dysfunction in the nervous system and its role in neurodegenerative disease
Mitochondria play critical roles in the generation of cellular energy, apoptosis, cellular calcium buffering and the generation of reactive oxygen species. Mitochondria also have important functions in normal ageing. Given these critical roles in cellular function and physiology, it is not surprising that mitochondria also contribute to a large number of pathogenenic states ranging from cancer to neurodegenerative diseases such as Parkinson’s.
We are interested in how neurons respond to mitochondrial dysfunction and how this process can be modified as a treatment for neurodegenerative disease. We have previously used a genetic screen in yeast to identify genes that can prevent mitochondrial DNA loss in yeast and a cellular model of mitochondrial disease (Iacovino et al., 2009).
We are currently developing a Drosophila model of neuronal mitochondrial dysfunction and using this to understand how neurons respond.
We also use human neurodegenerative disease tissue to study the changes that result from mitochondrial dysfunction in diseases like Parkinson's (Gatt et al., 2013).
