Dirk Schnappinger
· Professor of Microbiology and ImmunologyCornell University · Microbiology and Immunology
Active 1995–2026
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About
Dirk Schnappinger is a researcher with extensive contributions to the study of bacterial gene regulation, particularly focusing on the tetracycline repressor system and its applications. His work includes detailed investigations into the molecular mechanisms of antibiotic action, uptake, and resistance, as well as the structural basis of gene regulation by tetracycline-inducible systems. Schnappinger has contributed to understanding protein-protein recognition and dimerization specificity in regulatory proteins, as well as the conformational changes induced by tetracycline binding. His research extends into the field of infectious diseases, with a significant focus on Mycobacterium tuberculosis, exploring the bacterial response to hypoxia, gene expression regulation within macrophages, and the pathogen's survival strategies against host immune defenses. Schnappinger has also been involved in developing genetic tools for controlling gene expression in mycobacteria, including the use of tetracycline repressors for gene silencing. His work has provided insights into the adaptation of both the pathogen and host during infection, contributing to the broader understanding of host-pathogen interactions and bacterial persistence mechanisms.
Research topics
- Biology
- Genetics
- Computational biology
- Medicine
- Evolutionary biology
- Chemistry
- Virology
- Bioinformatics
- Microbiology
- Pharmacology
Selected publications
Genome-wide gene expression tuning reveals diverse vulnerabilities of M. tuberculosis
Cell · 2021 · 327 citations
Antibacterial agents target the products of essential genes but rarely achieve complete target inhibition. Thus, the all-or-none definition of essentiality afforded by traditional genetic approaches fails to discern the most attractive bacterial targets: those whose incomplete inhibition results in major fitness costs. In contrast, gene "vulnerability" is a continuous, quantifiable trait that relates the magnitude of gene inhibition to the effect on bacterial fitness. We developed a CRISPR inter…
Nature Microbiology · 2022 · 221 citations
Mycobacterium tuberculosis (Mtb) infection is notoriously difficult to treat. Treatment efficacy is limited by Mtb's intrinsic drug resistance, as well as its ability to evolve acquired resistance to all antituberculars in clinical use. A deeper understanding of the bacterial pathways that influence drug efficacy could facilitate the development of more effective therapies, identify new mechanisms of acquired resistance, and reveal overlooked therapeutic opportunities. Here we developed a CRISPR…
EMBO Molecular Medicine · 2020 · 95 citations
and the cytochrome bd oxidase protects M. tuberculosis from Q203-induced death, highlighting the attractiveness of the bd-type terminal oxidase for drug development. Here, we employed a facile whole-cell screen approach to identify the cytochrome bd inhibitor ND-011992. Although ND-011992 is ineffective on its own, it inhibits respiration and ATP homeostasis in combination with Q203. The drug combination was bactericidal against replicating and antibiotic-tolerant, non-replicating mycobacteria,…
eLife · 2023 · 24 citations
and cAMP as central mediators of intrinsic multidrug resistance and fatty acid metabolism in Mtb and highlights the potential utility of small molecule modulators of cAMP signaling.
SuFEx-based antitubercular compound irreversibly inhibits Pks13
Nature · 2025-07-30 · 15 citations
articleOpen access
Recent grants
NIH · $1.4M · 2010
Decoding the roles of critical genes of unknown function in M. tuberculosis
NIH · $21.4M · 2013–2019
NIH · $3.0M · 2016
Frequent coauthors
- 116 shared
Sabine Ehrt
Cornell University
- 47 shared
Kyu Y. Rhee
Weill Cornell Medicine
- 46 shared
Curtis A. Engelhart
Cornell University
- 36 shared
Véronique Dartois
Hackensack Meridian Health
- 28 shared
Helena I. Boshoff
National Institutes of Health
- 28 shared
Thomas R. Ioerger
- 26 shared
Carolina Trujillo
Hospital Nacional Cayetano Heredia
- 25 shared
Matthew Zimmerman
Center for Discovery
Labs
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