Dr. Chung-Yu Lan

Associate Professor
Institute of Molecular and Cellular Biology,
National Tsing Hua University, Taiwan

Education

Ph.D., Microbiology, University of California-Davis
M.S., National Taiwan University
B.S., National Chung Hsing University

Positions

Associate Professor
Institute of Molecular and Cellular Biology
National Tsing Hua University, Taiwan
Assistant Researcher
Department of Cell and Tissue Biology
University of California, San Francisco
Postgraduate Researcher
Department of Cell and Tissue Biology
University of California, San Francisco
Postdoctoral Scholar
Department of Cell and Tissue Biology
University of California, San Francisco
Assistant Research Fellow
Cell Biology and Immunology Division
Development Center for Biotechnology

Awards and Honors

2013
Teaching Award, National Tsing Hua University, Taiwan
(國立清華大學101學年度傑出教學獎)
2013
Outstanding Mentor Award, National Tsing Hua University, Taiwan
(國立清華大學第五屆傑出導師獎)
2013, 2012, 2011 & 2010
Research Paper Publication Award, National Tsing Hua University, Taiwan
(國立清華大學102、101、100及99年度學術研究出版獎勵)
2011 & 2008
Teaching Award, College of Life Science, National Tsing Hua University, Taiwan
(國立清華大學生命科學院100及97年度傑出教學獎)
2010
New Faculty Research Award, College of Life Science, National Tsing Hua University, Taiwan
(國立清華大學生命科學院99年度新進教師研究獎)

2013 Outstanding Mentor Award

Research Interests

The main focus in my lab is to study the biology and pathogenicity of a major fungal pathogen of humans, Candida albicans, and the interactions between C. albicans and its hosts. As a commensal, C. albicans frequently causes irritating and recurrent infections, including oral thrush and vaginal candidiasis. In immunocompromised patients, C. albicans can become invasive and causes life-threatening systemic infections. Moreover, C. albicans can also gain entry into the bloodstream (candidaemia) during procedures associated with the implantation of medical devices. As such, this organism has emerged as the fourth most common blood-bone infection in the US and candidaemia is a significant nosocomial infection. The projects currently underway include:

(1) Environmental sensing, signal integration and C. albicans pathogenesis.

During its natural history in the host, C. albicans encounters a wide variety of environmental conditions, including changing nutrients, pH, and antimicrobial mediators. One of the features that allow C. albicans to transition from a commensal organism to a successful pathogen is its ability to sense these complex environmental signals and respond by controlling cell growth/proliferation, hyphal morphogenesis and expression of associated virulence determinants. Our immediate objective is to characterize the roles of a new Rhb1-mediated signaling/regulatory pathway for integrating multiple environmental signals, cell growth/proliferation and virulence. (Tsao et al., 2009; Chen et al., in revision). In addition, we also study the response of C. albicans to human antimicrobial peptide LL-37 (Tsai et al., 2011a; Tsai et al., 2011b; Chang et al., 2011)

(2) Regulatory networks affected by iron availability.

Iron is important for the microbial pathogen-host interaction. The availability of iron serves as an important signal for the expression of virulence determinants in pathogens, and iron withholding is a defense mechanism of hosts against microbial infections. Using functional genomics and molecular genetics, we have identified genes whose expression is modulated by iron availability and also identified the transcriptional factors, Sfu1 and Hap43, involved in this regulation (Lan et al., 2004; Hsu et al., 2011).

(3) Interaction between C. albicans and host.

In collaboration with Dr. Y.-J. Chuang’s group (NTHU), we demonstrate that zebrafish can be a useful model to study C. albicans pathogenesis (Chao et al., 2010). Currently, using functional genomic and systems biological approaches, C. albicans-host interaction networks are investigated.