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A. A.

Cambridge University Press

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National Academy of Sciences


TRP Channels


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A-L.


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PDN - Graduate Education - PhD Projects on Offer

www.pdn.cam.ac.uk [cached]

The work will be conducted and supervised jointly between PDN and Engineering.
The project is an interdisciplinary collaboration between the Departments of Engineering and Physiology, Development & Neuroscience, University of Cambridge, and the School of Engineering and Applied Sciences, Harvard University. To gain a mechanistic insight into these different responses we analyze the occupancy of the DNA-binding complex associated with Notch pathway activation over a similar time period (using ChIP). Combining these data will allow us to distinguish (1) genes with a high probability of being primary targets (2) different binding kinetics at different loci and how these correlate with specific patterns of transcriptional activity. From these combined data we aim to identify the underlying regulatory circuits and connectivity in the network (e.g., the presence of feedback loops), using a Bayesian analysis of stochastic models and their associated stochastic differential equations. Regulatory circuits and modules identified through these models will be tested by perturbing down the function of nodal components with RNAi, or by co-expressing specific factors, allowing us to further refine the models in light of these interventions. While the correct deployment of Notch is crucial, its incorrect activity is associated with many types of diseases including dimentias and cancers. Activation of Notch elicits a proteolytic cleavage, releasing the Notch intracellular domain (Nicd), which enters the nucleus and collaborates directly with the DNA-binding proteins to regulate transcription. However, we have recently demonstrated that the glands are an important source of nutrients for the conceptus during the first trimester. Burton , G.J., Jauniaux, E. and Charnock-Jones, D.S. (2007) Human early placental development: potential roles of the endometrial glands. Placenta, 28 Suppl. A, S64-69. We recenty showed that stem cell self-renewal and differentiation pathways in adult skin are controlled by post-transcriptional methylation of cytosine-5 in RNA. Funding is available for this project Heart disease is the greatest killer in the UK today, imposing a substantial burden on the nation's health and wealth. The concept that smoking and obesity increase the risk of heart disease is familiar to all of us. However, it does little to explain why some develop the disease and others do not. This will reduce the burden not only of IUGR, but also of early origins of cardiovascular disease, thereby having a major clinical, economic and social impact on health. For further information, please visit: http://www.pdn.cam.ac.uk/staff/giussani/ References: GIUSSANI, D.A. & GARDNER, D.S. (2004). Frontiers in Nutritional Sciences, No.2. Fetal Nutrition and Adult Disease: Programming of chronic disease through fetal exposure to undernutrition. Ed. LANGLEY-EVANS, S.C.pp. 55-85. Hypoxia, fetal growth and developmental origins of health and disease. In: Early Life Origins of Health and Disease, Springer Science + Business Media; Landes Bioscience/Eurekah.com. Ed. WINTOUR, E.M. & OWENS, J. 18: 221-224. ISBN: 1-58706-294-1. FOWDEN, A.L., GIUSSANI, D.A. & FORHEAD, A.J. (2006). FOWDEN, A.L., GIUSSANI, D.A. & FORHEAD, A.J. (2006). Intrauterine programming: Causes and consequences. Physiology 21:29-37. Prenatal hypoxia: Relevance to developmental origins of health and disease. In Developmental Origins of Health and Disease, Cambridge University Press. Ed. Gluckman, P.D. & Hanson, M.A. pp 178-190. GIUSSANI, D.A., SALINAS, C.E., VILLENA, M. & BLANCO, C.E. (2007). Drosophila photoreceptors represent an important genetic model for sensory transduction and G-protein coupled signaling in general. The light response is mediated by phospholipase C (PLC), which leads to the activation of Ca2+ permeable "TRP" channels via a mechanism that is still not fully resolved. TRP channels, first discovered in our lab as the phototransduction channels in Drosophila, are now recognized as a major cation channel family with 28 mammalian isoforms playing vital roles in Ca2+ signaling throughout the body. In the photoreceptors TRP-mediated Ca2+ influx acts at multiple molecular targets, directly shaping the kinetics of the light response and mediating light adaptation, as well as regulating a range of cellular responses. Mutations of the TRP channel and other proteins involved in Ca2+ homeostasis lead to retinal degeneration and cell death. Activation of TRP Channels by Protons and Phosphoinositide Depletion in Drosophila Photoreceptors. Yau, K.W., and Hardie, R.C. (2009). Yau, K.W., and Hardie, R.C. (2009). The visual systems of Xenopus and zebrafish are ideal for such questions because of their embryological, molecular and genetic accessibility to experimentation, combined with the possibility of in vivo time-lapse imaging. References: Norden C, Young S, Link BA, Harris WA. 2009 Actomyosin is the main driver of interkinetic nuclear migration in the retina. Cell. 138(6):1195-208. Agathocleous M, Iordanova I, Willardsen MI, Xue XY, Vetter ML, Harris WA, Moore KB. 2009 A directional Wnt/beta-catenin-Sox2-proneural pathway regulates the transition from proliferation to differentiation in the Xenopus retina. Development. 136(19):3289-99. 1) Lei, M., Goddard, C., Liu, J., Léoni, A-L., Royer, A., Fung, S. S. M., Xiao, G., Ma, A., Zhang, H., Charpentier, F., Vandenberg, J. I., Colledge, W. H., Grace, A. A. & Huang, C. L-H. (2005). Sinus node dysfunction following targeted disruption of the murine cardiac sodium channel gene, SCN5A. Journal of Physiology. 567(Pt 2):387-400. 2) van Veen, T. A. B., Stein, M., Royer, A., Quang, K. L., Charpentier, F., Colledge, W. H., Huang , C. L-H., Grace, A. A., Escande, D., de Bakker, J. M. T., van Rijen , H. V. M. (2005). 2) van Veen, T. A. B., Stein, M., Royer, A., Quang, K. L., Charpentier, F., Colledge, W. H., Huang , C. L-H., Grace, A. A., Escande, D., de Bakker, J. M. T., van Rijen , H. V. M. (2005). Circulation. 112(13):1927-1935. 3) Lei, M., Zhang, H., Grace, A. A. Huang, C. L-H. (2007). SCN5a and sinoatrial node pacemaker function. Cardiovascular Research. 74, 356-365. Heart failure is characterized by systemically high plasma free fatty acids, systemic and local hypoxia and oxidative stress. The exact role of each of these stresses in the progression of heart failure, and the development of mitochondrial dysfunction in heart and skeletal muscle is not yet clearly established. In models of heart failure it is difficult to tease apart the effects of hypoxia from those of an altered metabolic milieu and it is impossible, therefore, to establish cause and effect, in the context of failure, or to identify what constitutes an adaptation or maladaption. Mitochondria are the end-consumers of oxygen in the body, and likely modulate the metabolic adaptation to cellular hypoxia by decreasing oxygen dependency at the electron transport chain. This adaptation could involve metabolic switches towards the use of more oxygen-efficient substrates (e.g. glucose instead of fatty acids), improved coupling of the processes of oxidation and phosphorylation at the inner membrane or redistribution of mitochondrial populations within the cell to minimize oxygen concentration gradients. Such changes may be brought about via alterations in the transcription of genes controlled by the hypoxia-inducible factor (HIF) transcription factors. This project will use chamber-induced hypoxia in whole animals and muscle samples from humans acclimatising to high altitude as part of the second Xtreme Everest expeditions (www.xtreme-everest.co.uk) to investigate mechanisms of adaptation. Techniques will include isolated, working heart perfusions, mitochondrial respiration, western blotting and RT-PCR. Students with experience of these techniques are particularly encouraged to apply. Invited Review: Mitochondria in Heart Failure. Curr Opin Clin Nutr Metab Care 10: 704-711, 2007. AJ Murray. Metabolic adaptation of skeletal muscle to high altitude hypoxia: how new technologies could resolve the controversies. Genome Medicine In Press 2009 Fear


PDN: Graduate Education

www.pdn.cam.ac.uk [cached]

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The work will be conducted and supervised jointly between PDN and Engineering. The project is an interdisciplinary collaboration between the Departments of Engineering and Physiology, Development & Neuroscience, University of Cambridge, and the School of Engineering and Applied Sciences, Harvard University. To gain a mechanistic insight into these different responses we analyze the occupancy of the DNA-binding complex associated with Notch pathway activation over a similar time period (using ChIP). Combining these data will allow us to distinguish (1) genes with a high probability of being primary targets (2) different binding kinetics at different loci and how these correlate with specific patterns of transcriptional activity. From these combined data we aim to identify the underlying regulatory circuits and connectivity in the network ( e.g., the presence of feedback loops), using a Bayesian analysis of stochastic models and their associated stochastic differential equations. Regulatory circuits and modules identified through these models will be tested by perturbing down the function of nodal components with RNAi, or by co-expressing specific factors, allowing us to further refine the models in light of these interventions. While the correct deployment of Notch is crucial, its incorrect activity is associated with many types of diseases including dimentias and cancers. Activation of Notch elicits a proteolytic cleavage, releasing the Notch intracellular domain (Nicd), which enters the nucleus and collaborates directly with the DNA-binding proteins to regulate transcription. The molecular mechanisms underlying these changes are only just beginning to be explored, but may involve signalling pathways activated by the hypoxia inducible (HIF) family of transcription factors and also the Unfolded Protein Response (UPR). The project will use various transgenic mutants in the HIF and UPR pathways to dissect the mechanisms, and will involve assessing placental and fetal development stereologically using the NewCAST system to quantify end-points. This will be a CASE studentship sponsored by Visiopharm Ltd., and will involve spending some time at their headquarters in Denmark developing application protocols for mouse placental and fetal stereological assessment. This project has attracted partial funding from an industrial sponsor as a CASE proposal. The successful applicant will be entered into a departmental competition 'Genes to Organisms (G2O)' for the remaining funds. For full information on how to apply go to: http://www.pdn.cam.ac.uk/g2o/info/apply.shtml The closing date for receipt of all documentation is Friday 13 January 2012 Interviews for shortlisted candidates will take place on Thursday 9 February 2012 This studentship is open only to UK or EU candidates satisfying the BBSRC's policy on eligibility for funding http://www.bbsrc.ac.uk/web/FILES/Guidelines/studentship_eligibility.pdf However, we have recently demonstrated that the glands are an important source of nutrients for the conceptus during the first trimester. Burton , G.J., Jauniaux, E. and Charnock-Jones, D.S. (2007) Human early placental development: potential roles of the endometrial glands. Placenta, 28 Suppl. A, S64-69. Using a genetic mouse model, we have recently shown that the imprinted atypical Notch ligand delta-like homologue 1, DLK1, is required for normal adult neurogenesis. DLK1 is expressed in two major isoforms – a memebrane-bound form and a secreted form. Dlk1 mutant mice have compromised neurogenesis. Our results have shown that the secreted form is an important factor in the neurogenic niche. In contrast, the membrane-bound isoform acts in the stem cell compartment where, unusually, the gene is expressed from both parental chromosomes. This absence of imprinting is important for the normal neurogenic potential of the stem cells. In the proposed project, the student will consider (a) the mechanism through which secreted DLK1in the niche influences the neural stem cell population and the signalling pathway through which membrane-bound DLK1 in the stem cell acts. (b) In addition, the student will consider the epigenetic regulatory mechanisms through which biallelic expression/absence of imprinting is regulated in the stem cells and monoallelic expression is established in the differentiated population of astrocytes in the niche. (c) Finally, the student will participate in behavioural studies using this genetic mouse model to determine the functional correlates of compromised adult neurogenesis in vivo Heart disease is the greatest killer in the UK today, imposing a substantial burden on the nation's health and wealth. The concept that smoking and obesity increase the risk of heart disease is familiar to all of us. However, it does little to explain why some develop the disease and others do not. This will reduce the burden not only of IUGR, but also of early origins of cardiovascular disease, thereby having a major clinical, economic and social impact on health. For further information, please visit: http://www.pdn.cam.ac.uk/staff/giussani/ References: GIUSSANI, D.A. & GARDNER, D.S. (2004). Frontiers in Nutritional Sciences, No.2. Fetal Nutrition and Adult Disease: Programming of chronic disease through fetal exposure to undernutrition. Ed. LANGLEY-EVANS, S.C.pp. 55-85. Hypoxia, fetal growth and developmental origins of health and disease. In: Early Life Origins of Health and Disease, Springer Science + Business Media; Landes Bioscience/Eurekah.com. Ed. WINTOUR, E.M. & OWENS, J. 18: 221-224. ISBN: 1-58706-294-1. FOWDEN, A.L., GIUSSANI, D.A. & FORHEAD, A.J. (2006). FOWDEN, A.L., GIUSSANI, D.A. & FORHEAD, A.J. (2006). Intrauterine programming: Causes and consequences. Physiology 21:29-37. Prenatal hypoxia: Relevance to developmental origins of health and disease. In Developmental Origins of Health and Disease, Cambridge University Press. Ed. Gluckman, P.D. & Hanson, M.A. pp 178-190. GIUSSANI, D.A., SALINAS, C.E., VILLENA, M. & BLANCO, C.E. (2007). Drosophila photoreceptors represent an important genetic model for sensory transduction and G-protein coupled signaling in general. The light response is mediated by phospholipase C (PLC), which leads to the activation of Ca2+ permeable "TRP" channels via a mechanism that is still not fully resolved. TRP channels, first discovered in our lab as the phototransduction channels in Drosophila, are now recognized as a major cation channel family with 28 mammalian isoforms playing vital roles in Ca2+ signaling throughout the body. In the photoreceptors TRP-mediated Ca2+ influx acts at multiple molecular targets, directly shaping the kinetics of the light response and mediating light adaptation, as well as regulating a range of cellular responses. Mutations of the TRP channel and other proteins involved in Ca2+ homeostasis lead to retinal degeneration and cell death. Yau, K.W., and Hardie, R.C. (2009). Yau, K.W., and Hardie, R.C. (2009). The visual systems of Xenopus and zebrafish are ideal for such questions because of their embryological, molecular and genetic accessibility to experimentation, combined with the possibility of in vivo time-lapse imaging. References: Norden C, Young S, Link BA, Harris WA. 2009 Actomyosin is the main driver of interkinetic nuclear migration in the retina. Cell. 138(6):1195-208. Agathocleous M, Iordanova I, Willardsen MI, Xue XY, Vetter ML, Harris WA, Moore KB. 2009 A directional Wnt/beta-catenin-Sox2-proneural pathway regulates the transition from proliferation to differentiation in the Xenopus retina. Development. 136(19):3289-99. 1) Lei, M., Goddard, C., Liu, J., Léoni, A-L., Royer, A., Fung, S. S. M., Xiao, G., Ma, A., Zhang, H., Charpentier, F., Vandenberg, J. I., Colledge, W. H., Grace, A. A. & Huang, C. L-H. (2005). Sinus node dysfunction following targeted disruption of the murine cardiac sodium channel gene, SCN5A. Journal of Physiology. 567(Pt 2):387-400. 2) van Veen , T. A. B.,Stein, M., Royer, A., Quang, K. L., Charpentier, F., Colledge, W. H., Huang , C. L-H., Grace, A. A., Escande, D., de Bakker, J. M. T., van Rijen , H. V. M. (2005). 2) van Veen , T. A. B.,Stein, M., Royer, A., Quang, K. L., Charpentier, F., Colledge, W. H., Huang , C. L-H., Grace, A. A., Escande, D., de Bakker, J.


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