Kalai Mathee is the first founding faculty member and founding chair of the Department of Molecular Microbiology and Infectious Diseases. A native of Malaysia, Dr. Mathee is a dedicated and demanding teacher. She received BS (Genetics) and MS (Microbial Genetics) degrees from the University of Malaya and went on to complete her PhD in Molecular Microbiology at the University of Tennessee, Memphis. Her fascination with Pseudomonas aeruginosa and cystic fibrosis (CF) started in 1993. This led her to spend time in Copenhagen working on various aspects of the infections. In 1999, she joined the Department of Biological Sciences at FIU as an Assistant Professor. She was promoted to Associate Professor in 2005 and spent a productive sabbatical in Harvard Medical School in 2006-2007. She joined FIU Herbert Wertheim College of Medicine in 2007. In 2010 she was promoted to a full Professor. With continuous NIH funding since 2000, Dr. Mathee has established a multi-faceted research program focused on molecular pathogenesis of P. aeruginosa that is responsible for the high morbidity and mortality in CF patients. She is very passionate about her research and how it might contribute to increasing CF patient quality of life. She is well respected nationally and internationally by researchers in multiple fields, including comparative genomics, Pseudomonas pathogenesis, alternate therapy using botanicals, microbial biofilm development, and regulation of prokaryotic transcription. She has published more than 60 articles (in and several book chapters in the fields of molecular microbiology, forensic science and bioinformatics - many of which are recognized as seminal and have been selected for journal highlights. In 2008, one of her papers in the Proceedings of National Academy of Sciences was selected by the Faculty of 1000 Biology members, a much-coveted honor. She has mentored over 60 individuals at all levels, and in 2011, she received the Mentor of the year award. In addition, she was bestowed the highest honor of her career in FIU, the 2011 Faculty of the Year (President’s Council Worlds Ahead Faculty Award) in recognition of outstanding achievement as a student-centered professor who makes an impact and exceeds expectations. She serves as an Editor of Journal of Medical Microbiology and BMC Microbiology.


Bacteria rapidly respond and adapt to changing environmental conditions by altering gene expression. A Gram-negative opportunistic bacterium, Pseudomonas aeruginosa is a major human pathogen implicated in a number of acute and chronic infections. Of particular concern is the wide prevalence of antibiotic resistant P. aeruginosa in hospitals. Expression of virulence factors that contribute to P. aeruginosa pathogenicity is tightly regulated. Regulators make up ~8-10% of the P. aeruginosa genome. A transcriptional regulator of the LysR family, AmpR plays a major role in conferring resistance to ß-lactams by positively regulating ampC encoding a lactamase. Whole genome approaches such as microarrays, deep RNA sequencing, CHIP-Seq and proteomics analyses of the P. aeruginosa prototypic strain PAO1 and its isogenic ampR in-frame deletion mutant, PAO∆ampR, in the absence and presence of ß-lactams, revealed that the regulatory repertoire of AmpR is extensive and includes over 500 genes. AmpR regulates diverse phenotypes such as ß-lactam and non-ß-lactam resistance, many virulence processes and metabolism. AmpR regulated positively and negatively, phenotypes associated with acute and chronic infections, respectively. Furthermore, RNA-Seq and ChIP-Seq studies identified lasR, encoding the quorum-sensing regulator, to be a direct target of AmpR regulation. In silico comparative transcriptomics analyses further identified genes that are exclusively regulated by AmpR and core set are involved in bacterial homeostasis. In summary, AmpR is identified as a critical regulator of pathogenesis and metabolism in P. aeruginosa and is a potential therapeutic target.