Faculty & Research
- Contact Information
- Contact Ankur Dalia by ankdalia [at] indiana [dot] edu
- By telephone: 812-856-1895 (office)
- By fax: 812-855-6055 (lab phone)
- JH 469A (ofc), JH 455 (lab)
- Research Areas
- Genomics and Bioinformatics
- Microbial Cell Biology and Environmental Responses
- Microbial Interactions and Pathogenesis
Ph.D., University of Pennsylvania, 2011
Postdoctoral Fellow, Tufts University, 2011-2015
Microbes can rapidly adapt and evolve in the face of clinical interventions and environmental insults. One mechanism that promotes this evolution is horizontal gene transfer (HGT) through natural competence and transformation. During this process, microorganisms take up DNA from the extracellular environment and integrate it into their genome by homologous recombination (Fig. 1). Natural transformation is a property of diverse microbial species and is often tightly regulated. In our lab, we study the mechanisms and regulation underlying this conserved evolutionary process.
One model organism we employ to study natural transformation is Vibrio cholerae - the causative agent of the diarrheal disease cholera. This pathogen naturally resides in the aquatic environment and causes disease when ingested in contaminated food or drinking water. In the environment, V. cholerae forms biofilms on the chitinous exoskeletons of crustacean zooplankton, which is critical for both the survival and waterborne transmission of this pathogen (Fig. 2). Chitin also induces natural competence in this organism. In our lab, we are studying the mechanisms and regulation of Vibrio-chitin interactions to gain insight into how V. cholerae evolves in the aquatic environment and transitions from this site to infect its human host. It was recently found that clinical isolates of V. cholerae are poorly transformed by this mechanism of HGT. So, we are also studying natural transformation in clinical isolates of V. cholerae to determine the mechanisms and role of HGT in strains from the ongoing 7th pandemic of cholera.
In addition to studying mechanisms of HGT, we have also exploited this process to develop a novel method for multiplexed genome editing by natural transformation (MuGENT) (Fig. 3). This method allows for “accelerated evolution” of microbes through the integration of multiple unlinked fragments of DNA into the bacterial genome in a single step. This increases the pace of genetic studies, but also allows us to probe biological questions that were previously genetically intractable. We are currently employing this method to dissect the biology of bacterial pathogens, including V. cholerae. MuGENT also allows for rapid metabolic and phenotypic engineering of microbes, which we will employ to develop non-pathogenic naturally competent species for novel biotechnology applications.
We use genome-wide approaches (Tn-seq, RNA-seq, ChIP-seq, etc.), comparative genomics, genetics, molecular biology, microscopy, flow activated cell sorting (FACS), and biochemistry to achieve these goals.
- Dalia AB. 2016. RpoS is required for natural transformation of Vibrio cholerae through regulation of chitinases. Environ Microbiol. Mar 21. doi: 10.1111/1462-2920.13302. [Epub ahead of print]
Dalia AB, Seed KD, Calderwood SB, Camilli A. 2015. A globally distributed mobile genetic element inhibits natural transformation of Vibrio cholerae. PNAS. 112(33):10485-90
Dalia AB, Lazinski DW, Camilli A. 2014. Identification of a membrane-bound transcriptional regulator that links chitin and natural competence in Vibrio cholerae. MBio. 5(1):e01028-13
Dalia AB, McDonough EK, Camilli A. 2014. Multiplex Genome Editing by Natural Transformation. PNAS. 111(24):8937-42
*Research Highlight in this issue of PNAS
Dalia AB, Lazinski DW, Camilli A. 2013. Characterization of undermethylated sites in Vibrio cholerae. Journal of Bacteriology. 195(10):2389-99
*Recommended by Faculty of 1000
Rodriguez JL, Dalia AB, Weiser JN. 2012. Increased chain length promotes pneumococcal adherence and colonization. Infection and Immunity. 80(10):3454-9
Nakamura S, Shchepetov M, Dalia AB, Murphy TF, Gilsdorf JR, Smith AL, and Weiser JN. 2011. Molecular Basis of Increased Serum Resistance Among Pulmonary Isolates of Non-typeable Haemophilus influenzae. PLoS Pathogens. 7(1):e1001247
Pluvinage B, Higgins MA, Abbott DW, Robb C, Dalia AB, Deng L, Weiser JN, Parsons TB, Fairbanks AJ, Vocadlo DJ, Boraston AB. 2011. Inhibition of the pneumococcal virulence factor StrH and molecular insights into N-glycan recognition and hydrolysis. Structure. 9(19):1603-14
Dalia AB and Weiser JN. 2011. Minimization of bacterial size allows for complement evasion and is overcome by the agglutinating effect of antibody. Cell Host & Microbe. 10(5):486-496
*Research Highlight in Nature Reviews Microbiology and 5-star rating on Faculty of 1000
Dalia AB, Standish AJ, Weiser JN. 2010. Three surface exoglycosidases from Streptococcus pneumoniae, NanA, BgaA, and StrH, promote resistance to opsonophagocytic killing by human neutrophils. Infection and Immunity. 78(5):2108–16.