Dr Raphael Dias Teixeira

• 2015 PhD in Biochemistry, University of Sao Paulo, Brazil
• 2009 BSc in Biology, Federal University of Minas Gerais, Brazil

Raphael Dias Teixeira obtained his PhD from the University of São Paulo, Brazil, where he trained in the laboratory of Prof. Chuck Farah. His doctoral research focused on c-di-GMP signalling in the plant pathogen Xanthomonas citri, where he used structural biology and biophysics to study enzymes involved in this second messenger pathway.

He then moved to the Biozentrum, University of Basel, Switzerland, for postdoctoral research with Prof. Tilman Schirmer. There, he investigated diguanylate cyclases and uncovered the activation mechanism that regulate c-di-GMP synthesis.

He subsequently joined the laboratory of Prof. Urs Jenal at the University of Basel, where he shifted his focus to Pseudomonas aeruginosa and developed expertise in molecular microbiology. Using structural biology and biophysical approaches, he investigated the molecular mechanisms underlying surface colonisation and antibiotic tolerance in this pathogen. At the Biozentrum, he worked at the interface of structural biology and microbiology, in close collaboration with the laboratory of Prof. Sebastian Hiller.

If you are interested in joining the lab, please contact Raphael via email. Projects are available on bacterial antibiotic tolerance and mechanisms of biofilm formation, combining molecular microbiology and structural biology.

Bacterial infections often persist despite antibiotic treatment, posing a major challenge to modern medicine. While antimicrobial resistance is typically linked to genetic mutations, treatment failure frequently arises from antibiotic-tolerant persister cells, i.e., dormant bacteria that survive treatment and can reinitiate infection.

Research in the lab addresses how bacteria enter and maintain these tolerant states, with a focus on central metabolism. In particular, we study how perturbations in NAD⁺ homeostasis reshape cellular activity and promote antibiotic tolerance or bacterial growth. Toxin-antitoxin systems that deplete NAD⁺ can drive metabolic shutdown, highlighting a direct connection between metabolic control and persistence.

Bacteriophages can be used to probe metabolic vulnerabilities in bacteria, as their replication depends on host metabolism. This provides a way to challenge dormant cells and identify functions that remain active in non-growing states. The lab combines structural biology, biophysics, and molecular microbiology to study NAD⁺-modifying enzymes and their role in bacterial physiology. The goal is to define how metabolic pathways are rewired during stress and to identify strategies to eliminate persister cells.

The work focuses on clinically relevant pathogens, including Pseudomonas aeruginosa and Acinetobacter baumannii, allowing comparison of conserved and species-specific mechanisms of persistence.

NatT-NatR toxin-antitoxin complex bound to DNA. The system is involved in NAD depletion and persister formation in Pseudomonas aeruginosa