Fatih Çakar
[email protected]Dr. Fatih Cakar received his PhD from Prof. Stefan Schild’s lab at the Institute of Molecular Biosciences, University of Graz, Austria in 2018. His research focused on the mechanisms that enable the human pathogen Vibrio cholerae to adapt to host-associated and environmental conditions. He developed a new cell-based reporter system (TRIVET) to identify genes repressed during passage through the gastrointestinal tract and contributed to elucidating the roles of bacterial gene silencing in intestinal colonization and stress responses. He also investigated the biogenesis of outer membrane vesicles in Gram-negative bacteria and their contributions to bacterial surface remodeling and host adaptation.
After completing his graduate studies, he joined Prof. James Slauch’s lab in the Department of Microbiology at the University of Illinois Urbana–Champaign as a postdoctoral researcher. His research focused on the molecular regulation of Salmonella pathogenesis, particularly the control of the SPI 1-encoded type III secretion system. He investigated how small regulatory RNAs and post-transcriptional regulatory mechanisms influence bacterial virulence.
Dr. Cakar continues his research at the Health Sciences and Technologies Research Institute (SABITA), Istanbul Medipol University. His research focuses on understanding the regulatory mechanisms that enable human pathogens to adapt to their host environment, within the framework of molecular microbiology, bacterial genetics, and pathogenesis. His research utilizes bacterial genetics, small RNA-based regulation, cell-based reporter systems, gene expression, and post-transcriptional regulation approaches.
Dr. Cakar’s current research interests include:
• Molecular regulation of Salmonella virulence and pathogenesis • Small regulatory RNAs and post-transcriptional gene control in Salmonella • Adaptation of Vibrio cholerae to host and environmental conditions • Biogenesis of outer membrane vesicles in Gram-negative bacteria
Selected Publications;
The Salmonella pathogenicity island 1-encoded small RNA InvR mediates post-transcriptional feedback control of the activator HilA in Salmonella
The Salmonella pathogenicity island 1-encoded small RNA InvR mediates post-transcriptional feedback control of the activator HilA in Salmonella
Hou Y, Kim K, Cakar F, Golubeva YA, Slauch JM, Vanderpool CK. The Salmonella pathogenicity island 1-encoded small RNA InvR mediates post-transcriptional feedback control of the activator HilA in Salmonella. J Bacteriol. 2025 Mar 20;207(3):e0049124. doi: 10.1128/jb.00491-24. Epub 2025 Feb 27. PMID: 40013798; PMCID: PMC11925239.
Small RNAs Activate Salmonella Pathogenicity Island 1 by Modulating mRNA Stability through the hilD mRNA 3' Untranslated Region
Small RNAs Activate Salmonella Pathogenicity Island 1 by Modulating mRNA Stability through the hilD mRNA 3' Untranslated Region
Abdulla SZ, Kim K, Azam MS, Golubeva YA, Cakar F, Slauch JM, Vanderpool CK. Small RNAs Activate Salmonella Pathogenicity Island 1 by Modulating mRNA Stability through the hilD mRNA 3' Untranslated Region. J Bacteriol. 2023 Jan 26;205(1):e0033322. doi: 10.1128/jb.00333-22. Epub 2022 Dec 6. PMID: 36472436; PMCID: PMC9879128.
The Small RNA MicC Downregulates hilD Translation To Control the Salmonella Pathogenicity Island 1 Type III Secretion System in Salmonella enterica Serovar Typhimurium
The Small RNA MicC Downregulates hilD Translation To Control the Salmonella Pathogenicity Island 1 Type III Secretion System in Salmonella enterica Serovar Typhimurium
Cakar F, Golubeva YA, Vanderpool CK, Slauch JM. The Small RNA MicC Downregulates hilD Translation To Control the Salmonella Pathogenicity Island 1 Type III Secretion System in Salmonella enterica Serovar Typhimurium. J Bacteriol. 2022 Jan 18;204(1):e0037821. doi: 10.1128/JB.00378-21. Epub 2021 Oct 25. PMID: 34694902; PMCID: PMC8765453.
The activity of the quorum sensing regulator HapR is modulated by the bacterial extracellular vesicle (BEV)-associated protein ObfA of Vibrio cholerae
The activity of the quorum sensing regulator HapR is modulated by the bacterial extracellular vesicle (BEV)-associated protein ObfA of Vibrio cholerae
Ebenberger SP, Cakar F, Chen YC, Pressler K, Eberl L, Schild S. The activity of the quorum sensing regulator HapR is modulated by the bacterial extracellular vesicle (BEV)-associated protein ObfA of Vibrio cholerae. J Extracell Vesicles. 2024 Sep;13(9):e12507. doi: 10.1002/jev2.12507. PMID: 39252550; PMCID: PMC11386269.
Silence is golden: gene silencing of V. cholerae during intestinal colonization delivers new aspects to the acid tolerance response
Silence is golden: gene silencing of V. cholerae during intestinal colonization delivers new aspects to the acid tolerance response
Cakar F, Zingl FG, Schild S. Silence is golden: gene silencing of V. cholerae during intestinal colonization delivers new aspects to the acid tolerance response. Gut Microbes. 2019;10(2):228-234. doi: 10.1080/19490976.2018.1502538. Epub 2018 Aug 15. PMID: 30110191; PMCID: PMC6546326.
Bacterial outer membrane vesicle biogenesis: a new mechanism and its implications
Bacterial outer membrane vesicle biogenesis: a new mechanism and its implications
Roier S, Zingl FG, Cakar F, Schild S. Bacterial outer membrane vesicle biogenesis: a new mechanism and its implications. Microb Cell. 2016 May 10;3(6):257-259. doi: 10.15698/mic2016.06.508. PMID: 28357362; PMCID: PMC5348994.
A novel mechanism for the biogenesis of outer membrane vesicles in Gram-negative bacteria
A novel mechanism for the biogenesis of outer membrane vesicles in Gram-negative bacteria
Roier S, Zingl FG, Cakar F, Durakovic S, Kohl P, Eichmann TO, Klug L, Gadermaier B, Weinzerl K, Prassl R, Lass A, Daum G, Reidl J, Feldman MF, Schild S. A novel mechanism for the biogenesis of outer membrane vesicles in Gram-negative bacteria. Nat Commun. 2016 Jan 25;7:10515. doi: 10.1038/ncomms10515. PMID: 26806181; PMCID: PMC4737802.

