Bateman:Research

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Signal transduction in the nervous system
We are interested in how the insulin and Ras/MAPK signal transduction pathways control cell fate in the Drosophila nervous system. Both of these pathways are highly conserved and perform critical functions in both the developing and adult CNS. Aberrant activity of insulin or Ras/MAPK signalling can lead to disease and so understanding how these two pathways act in the CNS will provide insight into pathogenic states such as neurodegeneration and brain cancer.

Insulin signalling in neurogenesis
Insulin signalling is best known for its role in glucose homeostasis and diabetes. However, this pathway also 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 shown that insulin signalling interacts with the EGFR pathway in controlling PR cell fate (McNeill et al., 2008). Our current aim is to identify novel genes that are regulated by insulin signalling to control PR neurogenesis.

Ras/MAPK signalling in glial maintenance and proliferation
Ras/MAPK signalling is used reiteratively to control fundamental processes such cell maintenance, differentiation and proliferation. We have shown that the Ras/MAPK and insulin pathway interact to control PR cell fate in the developing eye (McNeill et al., 2008). In the developing CNS Ras/MAPK signalling is essential for controlling glial maintenance in both Drosophila and vertebrates. We are currently interested in the role of Ras/MAPK signalling in glia in the Drosophila post-embryonic CNS.



Mitochondrial DNA inheritance in the nervous system
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 correct mitochondrial DNA (mtDNA) is maintained. Maintenance of correct mtDNA copy number is essential for mitochondrial respiratory function and defects in mtDNA maintenance can cause a group of disorders known as mitochondrial DNA depletion syndrome (MDS). We have recently shown that the mitochondrial inner membrane translocase Tim17 can prevent mitochondrial DNA loss in a cellular model of mitochondrial disease (Iacovino et al., 2009).



We are currently interested in understanding the mechanism and determining the therapeutic potential of Tim17 in preventing mitochondrial DNA loss. In addition, we are studying how mitochondrial DNA is maintained in the Drosophila CNS.