Shantanu Bhatt, Ph.D.

Assistant Professor
Office: Science Center 124
Phone: 610-660-3440
Fax: 610-660-1832
Email: sbhatt@sju.edu


Education

B.S. in Biology - Denison University, Granville, OH (2001-2004)

PhD in Microbiology & Molecular Genetics - Emory University, Atlanta, GA (2005-2011)

Professional Experience

Postdoctoral Researcher - National Institutes of Health (NIH), Bethesda, MD (2012-2013)

Courses Taught

Cells

Microbiology

Publications

  1. Bhatt S, Jenkins V, Mason E, and Muche S. The small regulatory RNA Spot42 inhibits indole biosynthesis to negatively regulate the locus of enterocyte effacement of enteropathogenic Escherichia coli. Microorganisms, 2017. 5(4) 78;1-12.
  2. Lee-Soety JY, Bhatt S, Adair TL, Bonilla JA, Klyczek KK, Harrison M, Garlena RA, Bowman CA, Russell DA, Pope WH, Jacobs-Sera D, Cresawn SG, and Hatfull G. Genome sequences of twelve Cluster AN Arthrobacter phages. Genome Announcements. 2017.
  3. Bhatt S, Egan M, Jenkins V, Ramirez J, Xander C, Valerie Jenkins, Sarah Muche, Jihad El-Fenej, Jamie Palmer, Elisabeth Mason, Elizabeth Storm, and Thomas Buerkert. Hfq and Three Hfq-dependent sRNAs – RyhB, MgrR, and McaS – Coregulate the Locus of Enterocyte Effacement Pathogenicity Island in Enteropathogenic Escherichia coli. FEMS Pathogens and Disease. 2017.
  4. Bhatt S, Egan M, Jenkins V, Muche S, and El-Fenej J. The Tip of the Iceberg: On the Roles of Regulatory Small RNAs in the virulence of Enterohemorrhagic and Enteropathogenic Escherichia coli. Frontiers in Cellular and Infection Microbiology. 2016. Sept. 21; 6:
  5. Bhatt S, Egan M, Ramirez J, Xander C, and Upreti C. Harnessing the Power of Recombineering to Interrogate the Virulome of Escherichia albertii. Gene and Translational Bioinformatics. 2016; 2: e1294. doi: 10.14800/gtb.1294
  6. Egan M, Ramirez J, Xander C, Upreti C, and Bhatt S. Lambda Red-mediated Recombineering In The Attaching And Effacing Pathogen Escherichia albertii. Biological Procedures Online (BPRO). 2016; Feb 3; 18:3. doi: 10.1186/s12575-015-0032-8
  7. VanOrsdel CE*, Bhatt S*, Allen RJ, Brenner EP, Hobson JJ, Jamil A, Haynes BM, Genson AM, Hemm MR. The Escherichia coli CydX protein is a member of the CydAB cytochrome bd oxidase complex and is required for cytochrome bd oxidase activity. (*-co-first authors). J.Bacteriol. 2013 Aug; 195(16): 3640-50
  8. Bommarius B, Anyanful A, Izrayelit Y, Bhatt S, Wang W, Cartwright E, Swimm A, Benian G, Schroeder F, and Kalman D. A family of indoles regulates virulence and shiga toxin production in pathogenic E. coli. PLoS ONE. 2013;8(1):e54456.doi: 10.1371/journal.pone.0054456
  9. Bhatt S, Anyanful A, and Kalman D. CsrA and TnaB coregulate tryptophanase activity to promote exotoxin-mediated killing of Caenorhabditis elegans by enteropathogenic Escherichia coli. J Bacteriol. 2011 Sep; 193 (17): 4516-4522
  10. Bhatt S, Romeo T, and Kalman D. Honing the message: posttranscriptional and post-translational control in attaching and effacing pathogens. Trends Microbiol. 2011 May; 19(5): 217-224.
  11. Bhatt S, Edwards AN, Nguyen HTT, Merlin D, Romeo T, and Kalman D. The RNA-binding protein CsrA is a pleiotropic regulator of the locus of enterocyte effacement pathogenicity island of enteropathogenic Escherichia coli. Infect. Immun. 2009 Sep; 77(9): 3552-68.
  12. Nguyen HT, Dalmasso G, Powell KR, Yan Y, Bhatt S, Kalman D, Sitaraman S, and Merlin D. Pathogenic bacteria induce colonic PepT1 expression: An implication in host defense response. Gastroenterology. 2009 Oct; 137(4): 1435-47.  
  13. Bhatt S, and Weingart CL. Identification of sodium chloride-regulated genes in Burkholderia cenocepacia. Curr Microbiol. 2008 May; 56(5):418-422.
  14. Stevenson LG, Strisovsky K, Clemmer KM, Bhatt S, Freeman M, and Rather PN. Rhomboid protease AarA mediates quorum-sensing in Providencia stuartii by activating TatA of the twin-arginine translocase. Proc Natl Acad Sci USA. 2007 Jan; 104 (3): 1003-1008.

Italics - SJU student

 

Research

Enteropathogenic E. coli (EPEC) is a major public health concern in developing countries where it causes significant morbidity and mortality in infants. EPEC, along with a few other related pathogens namely enterohemorrhagic E. coli (EHEC), Citrobacter rodentium, rabbit enteropathogenic E. coli (REPEC), and Escherichia albertii constitute a group collectively referred to as attaching and effacing (A/E) pathogens. They are so called because upon infection these pathogens attach intimately to intestinal cells and destroy cellular microvilli. Destruction of the microvilli reduces the ability of the cells to absorb water and nutrients, which ultimately leads to diarrhea. Upon destruction, the infected bacterium recruits the structural proteins from the microvilli and remodels them to form filament-like protrusions that extend out of the infected cell and are crowned on top by the infecting bacterium (Fig. 1). This histopathological structure is commonly referred to as attaching and effacing (A/E) pedestal. The ability of EPEC to form A/E lesions and cause disease depends on the presence of a pathogenicity island called locus of enterocyte effacement (LEE). The LEE encodes a type 3-secretion system that connects the cytoplasm of the bacteria to that of the host and enables EPEC to traffic a constellation of factors directly into the host, which aid bacterial colonization and cause disease. My lab is interested in identifying bacterial factors that regulate the LEE and modulate the resulting pathogenicity of EPEC. Identification of such virulence factors and their mechanism of action is essential for the development of effective therapeutic measures to combat EPEC infections, especially in light of the emergence of highly drug-resistant strains of EPEC. We use a highly interdisciplinary approach by incorporating tools and techniques from bioinformatics, genetics, and biochemistry to interrogate and characterize such virulence factors.

Figure 1A – Cartoon depicting the formation of pedestals by EPEC and EHEC - Under inducible conditions EPEC upregulates the expression of its Type III Secretion System (T3SS) that links the bacterial cytoplasm to that of the host cell (a). After the maturation of the translocon, effectors are trafficked into the host’s cytoplasm (a). One of these effectors, Tir, is inserted into the host plasma membrane where it interacts with its ligand, intimin, located on the outer bacterial membrane. Tir-intimin interactions promote the clustering of Tir and initiate a signal transduction cascade that culminates with recruitment and remodeling of actin to form fibrillar protrusions, termed “attaching and effacing (A/E) pedestals”, underneath adherent bacteria (b).

1B - Scanning electron micrographic (SEM) image of EPEC forming pedestals on infected mammalian cells. Inset – Pseudocolored image of two EPEC bacteria (green) infecting HeLa cells (purple). EM Image courtesy of Jorge Giron (University of Florida).