Troemel, Emily - University of California, San Diego

个人简介

Emily Troemel received her B.S. from the University of Wisconsin-Madison and then spent a year in Japan before receiving her Ph.D. in Cell Biology at UC-San Francisco. She worked for a start-up biotech company in the Bay Area before returning to academia to do a postdoc at Massachusetts General Hospital and then joined the UCSD faculty in 2008. Since joining UCSD, she has received a Searle Scholars Award, David & Lucile Packard Foundation Award and a Burroughs Wellcome Fund Investigators in the Pathogenesis of Infectious Disease Award.

研究领域

How do pathogens attack their hosts, and how do hosts defend themselves against these attacks? We are using the nematode C. elegans to study these questions of host/pathogen interactions in the intestine. The nematode C. elegans provides a wonderful system in which to study these questions. The worm has intestinal cells that are similar in structure to human intestinal cells, but C. elegans is transparent and easy to study in lab. C. elegans lacks a professional immune system, and instead relies solely on epithelial defense to fight off pathogen attack. It is being increasingly appreciated that epithelial cells in the intestine are involved in detecting and responding to pathogens in mammals, and are implicated in inflammatory disorders. It is critical to understand more about how these cells detect and respond to pathogens. What we find in C. elegans intestinal immunity may be directly applicable to host/pathogen interactions in the human intestine. Microsporidia infecting C. elegans intestine Microsporidia infecting C. elegans intestine – microsporidia are labeled in red, C. elegans intestine labeled in green, and DNA labeled in blue. Our research focuses on two different pathogens. The first pathogen is a natural intracellular pathogen isolated from a wild-caught C. elegans strain, which we have found defines a genus and species of microsporidia (intestinal infection of C. elegans intestine shown below). Microsporidia are poorly understood eukaryotic pathogens that are emerging pathogens of humans and can cause problems for immunocompromised patients. The second pathogen is an extracellular bacterial pathogen called Pseudomonas aeruginosa, which is a clinically relevant pathogen that causes opportunistic infections in humans.

近期论文

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In vivo mapping of tissue- and subcellular-specific proteomes in Caenorhabditis elegans. Reinke AW, Mak R, Troemel ER, Bennett EJ. Sci Adv. 2017 May 10;3(5):e1602426. doi: 10.1126/sciadv.1602426. eCollection 2017 May. Identification of microsporidia host-exposed proteins reveals a repertoire of rapidly evolving proteins. Reinke AW*, Balla, KM, Bennett EJ, Troemel ER. Nature Communications, 2017 Jan 9;8:14023. doi: 10.1038/ncomms14023. *corresponding author. A Large Collection of Novel Nematode-Infecting Microsporidia and Their Diverse Interactions with Caenorhabditis elegans and Other Related Nematodes. Zhang G, Sachse M, Prevost MC, Luallen RJ, Troemel ER, Félix MA. PLoS Pathog. 2016 Dec 12;12(12):e1006093. doi: 10.1371/journal.ppat.1006093. Cell-to-cell spread of microsporidia causes Caenorhabditis elegans organs to form syncytia. Balla KM, Luallen RJ, Bakowski MA, Troemel ER. Nature Microbiology 1, (2016) doi:10.1038/nmicrobiol.2016.144 Microsporidia Intracellular Development Relies on Myc Interaction Network Transcription Factors in the Host. Botts MR, Cohen LB, Probert CS, Wu F, Troemel ER. G3 (Bethesda). 2016 Jul 8. pii: g3.116.029983. doi: 10.1534/g3.116.029983. [Epub ahead of print] PMID: 27402359 Discovery of a Natural Microsporidian Pathogen with a Broad Tissue Tropism in Caenorhabditis elegans. Luallen RJ, Reinke AW, Tong L, Botts MR, Félix MA, Troemel ER. PLoS Pathog. 2016 Jun 30;12(6):e1005724. doi: 10.1371/journal.ppat.1005724. eCollection 2016 Jun. PMID: 27362540 The C. elegans CCAAT-Enhancer-Binding Protein Gamma Is Required for Surveillance Immunity. Reddy KC, Dunbar TL, Nargund AM, Haynes CM, Troemel ER. Cell Rep. 2016 Feb 10. pii: S2211-1247(16)30033-X. doi: 10.1016/j.celrep.2016.01.055. [Epub ahead of print] PMID:26876169 Small GTPases promote actin coat formation on microsporidian pathogens traversing the apical membrane of C. elegans intestinal cells. Szumowski SC, Estes KA, Popovich JJ, Botts MR, Sek G, Troemel ER. Cell Microbiol. 2015 Jul 6. doi: 10.1111/cmi.12481. [Epub ahead of print] PMID:26147591 Balla KM, Andersen EC, Kruglyak L, Troemel ER. A wild C. elegans strain has enhanced epithelial immunity to a natural microsporidian parasite. PLoS Pathogens. 2015 Feb 13;11(2):e1004583. doi: 10.1371/journal.ppat.1004583. PMID:25680197 Szumowski SC, Botts MR, Popovich JJ, Smelkinson MG, Troemel ER. The small GTPase RAB-11 directs polarized exocytosis of the intracellular pathogen N. parisii for fecal-oral transmission from C. elegans. Proc Natl Acad Sci U S A. 2014 May 19. PMCID: PMC4050618 Bakowski MA, Desjardins CA, Smelkinson MG, Dunbar TA, Lopez-Moyado IF, Rifkin SA, Cuomo CA, Troemel ER. Ubiquitin-Mediated Response to Microsporidia and Virus Infection in C. elegans. PLoS Pathog. 2014 Jun 19;10(6):e1004200. PMCID: PMC4063957 Cuomo CA, Desjardins CA, Bakowski MA, Goldberg J, Ma AT, Becnel JJ, Didier ES, Fan L, Heiman DI, Levin JZ, Young S, Zeng Q, Troemel ER. Microsporidian genome analysis reveals evolutionary strategies for obligate intracellular growth. Genome Research 2012 Dec;22(12):2478-88. PMCID: PMC3514677 Dunbar TL, Yan Z, Balla KM, Smelkinson MG, Troemel ER. C. elegans Detects Pathogen-Induced Translational Inhibition to Activate Immune Signaling. Cell Host Microbe. 2012 Apr 19;11(4):375-86. PMCID: PMC3334869