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BS in Biology - Denison University, Granville, OH (2001-2004)
PhD in Microbiology & Molecular Genetics - Emory University, Atlanta, GA (2005-2011)
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Postdoctoral Researcher - National Institutes of Health (NIH), Bethesda, MD (2012-2013)
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(2 – Undergraduate SJU student, 3 – Graduate SJU student, C – Corresponding author)
- Muche S2, El-Fenej J2, Mihaita A2, Mrozek Z2, Cleary S3, Critelli B2, Marino M2, Yu W3, Amos B2, Hunter T2, Riga M2, Buerkert T2, and Bhatt SC. The Two sRNAs OmrA and OmrB Indirectly Repress Transcription from the LEE1 promoter of enteropathogenic Escherichia coli. Folia Microbiol (Praha). Dec. 2023.
- Raina M, Aoyama JJ, Bhatt S, Paul BJ, Zhang A, Updegrove TB, Miranda-Rios J, and Storz G. Dual-function AzuCR RNA modulates carbon metabolism. Proc. Nat. Acad. Sci. 2022.
- Bhatt S. Atypical Enteropathogenic Escherichia coli: From Kittens to Humans and Beyond! Infection & Immunity. 2020.
- Egan M2, Critelli B2, Cleary S3, Marino M2, Upreti C, Kalman D, and Bhatt SC. Transcriptional and Posttranscriptional Regulation of the Locus of Enterocyte Effacement in Escherichia albertii. Microbial Pathogenesis. 2019. 135: Oct. 2019, 103643.
- Bhatt SC, Egan M2, Kouse A, Kalman D, and Upreti C. The Evasive Enemy: Insights into the Virulence and Epidemiology of the Emerging Attaching and Effacing pathogen, Escherichia albertii. Infection & Immunity. 2018. Dec 19;87(1). pii: e00254-18. doi: 10.1128/IAI.00254-18.
- Bhatt SC, Jenkins V2, Mason E2, and Muche S2. 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.
- 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.
- Bhatt SC, Egan M2, Ramirez J3, Xander C2, Jenkins V2, Muche S2, El-Fenej J3, Palmer J2, Mason E2, Storm E2, and Buerkert T2. 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.
- Bhatt SC, Egan M2, Jenkins V2, Muche S2, and El-Fenej J3. 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. 6:105. doi: 10.3389/fcimb.2016.00105
- Bhatt SC, Egan M2, Ramirez J3, Xander C2, 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
- Egan M2, Ramirez J3, Xander C2, Upreti C, and Bhatt SC. Lambda Red-mediated Recombineering In The Attaching And Effacing Pathogen Escherichia albertii. Biological Procedures Online. 2016; Feb 3; 18:3. doi: 10.1186/s12575-015-0032-8
- 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). Journal of Bacteriology. 2013 Aug; 195(16): 3640-50
- 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
- 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. Journal of Bacteriology. 2011 Sep; 193 (17): 4516-4522
- Bhatt S, Romeo T, and Kalman D. Honing the message: posttranscriptional and post-translational control in attaching and effacing pathogens. Trends in Microbiology. 2011 May; 19(5): 217-224.
- 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. Infection and Immunity. 2009 Sep; 77(9): 3552-68.
- 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.
- Bhatt S, and Weingart CL. Identification of sodium chloride-regulated genes in Burkholderia cenocepacia. Current Microbiology. 2008 May; 56(5):418-422.
- 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. Proceedings of the National Academy of Science (PNAS) USA. 2007 Jan; 104 (3): 1003-1008.
- Bhatt S. 2017. Cracking the code on drug resistant microbes. Association of Jesuit Colleges and Universities Connections. (Invited manuscript)
- Bhatt S. 2012. Investigation of the role of the RNA binding protein CsrA in the virulence of enteropathogenic Escherichia coli. ProQuest-UMI. (Dissertation)
Italics - SJU student
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Enteropathogenic E. coli (EPEC) and Escherichia albertii are bacterial pathogens that are major public health concerns in developing countries, where they cause significant morbidity and mortality in infants. These bacteria belong to the attaching and effacing (A/E) family of pathogens, 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. Furthermore, the attached bacterium recruits structural proteins from the disintegrated 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. This histopathological structure is commonly referred to as attaching and effacing (A/E) pedestal. The ability of these pathogens 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 the bacterium 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, both proteins and regulatory small RNAs (sRNAs) that control the LEE and modulate the resulting virulence of EPEC and E. albertii. Identification of such virulence factors and their mechanisms of action is essential for the development of effective therapeutic measures to combat A/E pathogens, especially in light of the emergence of highly drug-resistant strains of EPEC and E. albertii. We use a highly interdisciplinary approach by incorporating tools and techniques from bioinformatics, genetics, and biochemistry to interrogate and characterize such virulence factors.