What is it about?

Infectious diseases are a leading cause of global mortality. During an infection, bacteria experience many different stresses — some from the host itself, some from co-colonizing microbes and others from therapies employed to treat the infection. In this arms race to outwit their competition, bacteria have evolved mechanisms to stay alive in the face of adversities. One such mechanism is the stringent response pathway. In this study, we show that the cell wall of the human pathogen Streptococcus pneumoniae can be used to divert the accumulation of toxic compounds, and in doing so buffer entry into the stringent response.

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Why is it important?

This collaborative work sets the framework for exploring the molecular connection between two fundamental cell processes, translation and cell wall synthesis, and stress responses. The pivotal position of the stringent response in survival to stresses and to antibiotics, suggests these findings may shed light on pathways associated with bacterial drug resistance, a major challenge for this century.


This project, linking cell wall to the stringent response and translational fidelity in pneumococcus, has been one of the most fun and exciting projects in my career. It is the result of a very productive collaboration between our lab at Carnegie Mellon University (US), the Filipe lab at Universidade NOVA de Lisboa (Portugal) and the Dowson, Roper, Lloyd group at the University of Warwick (UK).

Associate Professor N. Luisa Hiller
Carnegie Mellon University

Read the Original

This page is a summary of: A molecular link between cell wall biosynthesis, translation fidelity, and stringent response inStreptococcus pneumoniae, Proceedings of the National Academy of Sciences, March 2021, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2018089118.
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