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Pathogen Interaction Laboratory PhD scholarship in live cell imaging and electron microscopy of intracellular pathogens Tull D, Heng J, Gooley PR, Naderer T, McConville MJ.

Acylation dependent and independent membrane targeting and distinct functions of small myristoylated proteins (SMPs) in Leishmania major. Int J Parasitol. He worked as a post doctoral scientist in the laboratory of Prof Malcolm McConville (University of Melbourne) before joining the NHMRC Program on Cellular Microbiology headed by Prof Trevor Lithgow, Monash University. In 2012 he established the does amazon sell real louis vuitton macrophage pathogen interaction group with funding from the NHMRC. Aim: The aim of the laboratory is to discover the molecular and cellular interactions that allow human pathogens to survive in macrophages. Perspective: Macrophages are phagocytic (to engulf and digest) immune cells designed to kill invading microorganisms by employing a diverse arsenal of anti microbial agents. They are part of the first line defence (innate immune response) but also initiate adaptive immunity. Despite that, several important human pathogens, including Legionella, Burkholderia, Mycobacteria and Leishmania survive long term within specialized compartments or the cytosol of macrophages. Intracellular replication depends on efficient scavenging of essential nutrients, expression of diverse virulence factors and subversion of host cellular processes. Understanding the molecular interactions between macrophages and pathogens in more detail promises the discovery of novel anti microbial drug targets.1. Characterization of effector molecules: Intracellular pathogens express sophisticated machineries that facilitate the transfer of unique effector proteins into the cytoplasm of host macrophages. In particular, gram negative bacteria have evolved several secretion systems that cross bacterial outer membranes. A major aim louis vuitton damier ebene bracelet in the laboratory is to determine their localization and function using state of the art plat form technologies, including live cell imaging, in close collaboration with other members of the host pathogen unit. In particular, Legionella pneumophila exports around 10% (300 proteins) of its proteome into the cytoplasm of host macrophages. We have recently louis vuitton belt amazon uk shown that one of these effectors is targeted to the inner membrane of mitochondria as an ATP carrier protein. The aim of this project is louis vuitton shoes men to characterize other effectors and to determine their role during infection. 2. Regulation of macrophage cell death pathways by bacteria Macrophages are able to sense several pathogen associated patterns resulting in the activation of cell death pathways and secretion of pro inflammatory cytokines. Conversely, bacterial pathogens have developed molecular mechanisms to subvert these pathways during intracellular growth. In the case of Legionella pneumophila at least two effectors have been shown to target cell death factors. The aim of this project is to determine how Legionella control cell death pathways and which pathways are required for successful replication in macrophages. For this, we utilize an array of transgenic mice that overexpress or lack individual cell death factors. 3. Bacterial escape from macrophages Little is known how intracellular pathogens (trigger) escape from its host cells after completing their growth phase. While some pathogens express pore forming toxins to facilitate rupture of the host membranes, others rely on host pathways for successful egress. Legionella infected macrophages have been shown to become increasingly apoptotic, suggesting that these bacteria activate distinct cell death pathway during escape. The aim of this project is to determine which cell death pathways are activated during Legionella egress by follow bacterial infections with live cell imaging. Legionella pneumophila secretes a mitochondrial carrier protein during infection. PLoS Pathog. 2012 Jan;8(1):e1002459. Naderer T, Dandash O, McConville MJ. Calcineurin is required for Leishmania major stress response pathways and for virulence in the mammalian host. Mol Microbiol. 2011 Feb 14. McConville MJ, Naderer T. Metabolic pathways required for the intracellular survival of Leishmania. Annu Rev Microbiol. 2011;65:543 61. Naderer T, Heng J, McConville MJ. Evidence that intracellular stages of Leishmania major utilize amino sugars as a major carbon source. PLoS Pathog. 2010 Dec 23;6(12):e1001245. Saunders EC, DE Souza DP, Naderer T, Sernee MF, Ralton JE, Doyle MA, Macrae JI, Chambers JL, Heng J, Nahid A, Likic VA, McConville MJ. Central carbon metabolism of Leishmania parasites. Parasitology. 2010 Aug;137(9):1303 13. Tull D, Naderer T, Spurck T, Mertens HD, Heng J, McFadden GI, Gooley PR, McConville MJ. Membrane protein SMP 1 is required for normal flagellum function in Leishmania. J Cell Sci. 2010 Feb 15;123(Pt 4):544 54. Naderer T, Wee E, McConville MJ. Role of hexosamine biosynthesis in Leishmania growth and virulence. Mol Microbiol. 2008 Aug;69(4):858 69. PMID: 18532982 Naderer T, McConville MJ. The Leishmania macrophage interaction: a metabolic perspective. Cell Microbiol. 2008 Feb;10(2):301 8. Epub 2007 Dec 9. Review. PMID: 18070117 Naderer T, Ellis MA, Sernee MF, De Souza DP, Curtis J, Handman E, McConville MJ. Virulence of Leishmania major in macrophages and mice requires the gluconeogenic enzyme fructose 1,6 bisphosphatase.

Proc Natl Acad Sci U S A. 2006 Apr 4;103(14):5502 7. PMID:16569701.


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