Address: Institut Pasteur of Shanghai, Chinese Academy of Sciences, Life Science Research Building ,320Yueyang Road, Xuhui District, 200031
Our current research is focusing on interactions between host and fungal pathogens with three specific aims: 1. identify key signals involved in fungal commensal-pathogen transition; 2. iIllustrate novel host anti-fungal immune mechanisms; 3. and unravel genetic networks driving the dynamics of host-pathogen interactions
We are working on two major fungal pathogens： Candida albicans and Cryptococcus neoformans
Our approaches include: 1. High-throughput genetics, taking advantage of the two homozygous gene deletion libraries; 2. Animal models including systemic murine infection model; GI tract commensal model; Vagina infection model; Skin Infection model; Oral infection model; Lung infection model
Molecular Genetics, MS, The Chinese Academy of Sciences 1995-1998
Biology, BA, Shanghai Fudan University, China 1990-1995
07/2011-06/2013 Assistant Specialist, Department of Microbiology & Immunology, The University of California, San Francisco
01/2010-06/2011 Postdoctoral Fellow, Department of Microbiology & Immunology, The University of California, San Francisco
07/2005-12/2010 Postdoctoral Fellow, Department of Biochemistry & Biophysics, The University of California, San Francisco
09/2004-06/2005 Research Technologist, Department of Plant Pathology, The University of Nebraska-Lincoln
Honors & Distinctions
2014 The "100 Talents" Program, Chinese Academy of Sciences
2006 Herbert Boyer Postdoctoral Fellowship, Department of Biochemistry & Biophysics, University of California, San Francisco
2002 Widaman Trust Distinguished Graduate Assistant Award, Institute of Agriculture and Natural Resources, University of Nebraska-Lincoln
1. Gao, N., and Chen, C. (2016) Candida Infections: an update on host immune defenses and anti-fungal drugs. IDTM. Review.
2. Pande, K., Chen, C. and Noble, S. M. (2013) Passage through the mammalian gut triggers a phenotypic switch required for Candida albicans commensalism. Nature Genetics. 45(9):1088-91
3. Chen, C. and Noble, S. M. (2012) Post-transcriptional regulation of the Sef1 transcription factor controls the virulence of Candida albicans in its mammalian host. PLOS Pathogens, 8(11): e1002956.
4. Chen, C*., Pande, K*., French, S. D., Tuch, B. B. and Noble, S. M. (2011) A unique iron homeostasis regulatory circuit with reciprocal roles in Candida albicans commensalism and pathogenesis. Cell Host & Microbe. 10(2): 118-35. (*equal contribution)
5. Dumesic, P., Natarajan, P., Chen, C., Drinnenberg, A., Schiller, B., Moresco, J., Thompson, J., Yates, J., Bartel, D., and Madhani H. (2013) Stalled spliceosomes are a signal for RNAimediated genome defense. Cell: 152(5):957-968.
6. Liu, O. W., Chun, C. D., Chow, E. D., Chen, C., Madhani, H. D. and Noble, S. M. (2008) Systematic gene deletion and analysis of virulence in the human fungal pathogen Cryptococcus neoformans. Cell 135(1): 174-188.
7. Chen, C. and Dickman, M. B. (2005) Proline suppresses apoptosis in the fungal pathogen Colletotrichum trifolii. PNAS 102(9): 3459-3464
8. Deng Z., Ma S., Zhou H., Zang A., Fang Y., Li T., Shi H., Liu M., Du M., Taylor P., Zhu H., Chen J., Meng G., Li F., Chen C., Zhang Y., Jia X., Lin X., Zhang X., Pearlman E., Li X., Feng G., and Xiao H. (2015) Shp2 mediates C-type lectin receptor-induced Syk activation and anti-fungal Th17 responses. Nature Immunology. 16(6):642-52.
9. Xie X., Li F., Wang Y., Lin Z., Cheng X., Liu J., Chen C., and Pan L. (2015) Molecular basis of ubiquitin recognition by the autophagy receptor CALCOCO2. Autophagy. 11(10):1775-89.
10. Chen M., Xing Y., Lu A., Fang W., Sun B., Chen C., Liao W., and Meng G. (2015) Internalized Cryptococcus neoformans activates the canonical Caspase-1 and the noncanonical Caspase-8 inflammasomes. J. Immunol. 195(10):4962-72.
11. Guo C, Chen M, Fa Z, Lu A, Fang W, Sun B, Chen C, Liao W, Meng G. (2014) Acapsular Cryptococcus neoformans activates the NLRP3 inflammasome. Microbes Infect. 16(10): 845-54.
12. Georgette, C., Chen, C., Shih, S., et al., (2011) A site specific acetylation mark on the essential RSC chromatin remodeling complexpromotes resistance to replication stress. PNAS 108(26):10620-10625
13. Chen, C. and Dickman, M. B. (2005) cAMP blocks MAPK activation and sclerotial development via Rap-1 in a PKA-independent manner in Sclerotinia sclerotiorum. Molecular Microbiology 55(1): 299-311.
14. Chen, C., and Dickman, M. B. (2004) Dominant active Rac and dominant negative Rac revert the dominant active Ras phenotype in Colletotrichum trifolii by distinct signaling pathways. Molecular Microbiolology 51: 1493-1507.
15. Chen, C., Ha, Y-S., Min, J-Y., Memmott, S. D., and Dickman, M. B.. (2006) Cdc42 is required for proper growth and development in the fungal pathogen Colletotrichum trifolii. Eukaryotic Cell 5(1): 155-166.
16. Scheffer, J., Chen, C., Heidrich, P., Dickman, M. B., and Tudzynski, P. (2005) A CDC42 homologue in Claviceps purpurea is involved in vegetative differentiation and is essential for pathogenicity. Eukaryotic Cell 4(7): 1228-1238.
17. Chen, C., and Dickman, M. B. (2002) Colletotrichum trifolii TB3 kinase, a COT1 homolog, is light inducible and becomes localized in the nucleus during hyphal elongation. Eukaryotic Cell 1: 626-633.
18. Chen, C., Harel, A., Gorovoits, R., Yarden, O., and Dickman, M. B. (2004) MAPK regulation of sclerotial development in Sclerotinia sclerotiorum is linked with pH and cAMP sensing. Molecular Plant-Microbe Interactions 17: 404-413.
19. Kim, H.J., Chen, C., Kabbage, M. and Dickman, M.B. (2011) Identification and Characterization of Sclerotinia sclerotiorum NADPH Oxidases. Applied and Environmental Microbiology 77(21):7721-9.
20. Chen, C., Wanduragala, S., Becker, D. F., and Dickman, M. B. (2006) A tomato QM-like protein protects Saccharomyces cerevisiae cells against oxidative stress by regulating intracellular proline levels. Applied and Environmental Microbiology 72(6): 4001-6.
Our laboratory aims to dissect molecular mechanisms of virulence and commensalism during C. albicans infection, to understand how host immune systems act during C. albicans transitions from being a commensal to being a pathogen, and to decipher mechanisms of how the opportunistic fungal pathogen Cryptococcus neoformans crosses blood-brain barrier.
Current research is mainly focusing on the following directions:
1. Key signal transduction pathways regulating C. albicans commensal-pathogen transition.
2. Interplay between fungal secreted effectors and host anti-fungal immune responses.
3. Mechanisms of how fungal pathogens cross host blood-brain barrier.
4. Effect of GI microbiome on fungal infection and host immune responses.
5. High throughput screening for novel anti-fungal drugs and potential action modes of candidate drugs
6. Epigenetic regulation of fungal anti-drug resistance
1. Tsinghua University
2. Institute of Genomics, CAS
3. Institute of Microbiology, CAS
4. Institute of Zoology, CAS
5. Shanghai East Hospital
6. Shanghai Changhai Hospital
7. Shanghai No.1 People's Hospital
8. Shanghai Ruijin Hospital
9. Shanghai Fudan Women & Children Hospital
10. Guanzhou No. 8 Hospital
11. Rutgers University
12. South Carolina Medical University
13. Institut of Pasteur
14. University of California, San Francisco
Graduate students under supervision
1. Yongmin He，M.S. , Bio-engineering
2. Xiaoqing Chen, M.S., Biology
1. Yinhe Mao, Ph.D. program, Microbiology
2. Yuanyuan Wang, Ph.D. program, Microbiology
3. Xianwei Wu, Ph.D. program, Microbiology