Houston Methodist Research Institute, Houston, TX (United States). Center for Molecular and Translational Human Infectious Diseases Research;
Houston Methodist Research Institute, Houston, TX (United States). Dept. of Pathology and Genomic Medicine; DOE/OSTI
Houston Methodist Research Institute, Houston, TX (United States). Center for Molecular and Translational Human Infectious Diseases Research; Houston Methodist Research Institute, Houston, TX (United States). Dept. of Pathology and Genomic Medicine
Houston Methodist Research Institute, Houston, TX (United States). Center for Molecular and Translational Human Infectious Diseases Research;
Houston Methodist Research Institute, Houston, TX (United States). Dept. of Pathology and Genomic Medicine;
Weill Medical College of Cornell University, New York, NY (United States). Dept. of Pathology and Laboratory Medicine
Houston Methodist Research Institute, Houston, TX (United States). Center for Molecular and Translational Human Infectious Diseases Research;
Houston Methodist Research Institute, Houston, TX (United States). Dept. of Pathology and Genomic Medicine;
Weill Medical College of Cornell University, New York, NY (United States). Dept. of Pathology and Laboratory Medicine
Houston Methodist Research Institute, Houston, TX (United States). Center for Molecular and Translational Human Infectious Diseases Research;
Houston Methodist Research Institute, Houston, TX (United States). Dept. of Pathology and Genomic Medicine
Bacteria control gene expression in concert with their population density by a process called quorum sensing, which is modulated by bacterial chemical signals and environmental factors. In the human pathogen Streptococcus pyogenes, production of secreted virulence factor SpeB is controlled by a quorum-sensing pathway and environmental pH. The quorum-sensing pathway consists of a secreted leaderless peptide signal (SIP), and its cognate receptor RopB. Here, we report that the SIP quorum-sensing pathway has a pH-sensing mechanism operative through a pH-sensitive histidine switch located at the base of the SIP-binding pocket of RopB. Environmental acidification induces protonation of His144 and reorganization of hydrogen bonding networks in RopB, which facilitates SIP recognition. The convergence of two disparate signals in the SIP signaling pathway results in induction of SpeB production and increased bacterial virulence. Our findings provide a model for investigating analogous crosstalk in other microorganisms.
Do, Hackwon, et al. "Environmental pH and peptide signaling control virulence of <em>Streptococcus pyogenes</em> via a quorum-sensing pathway." Nature Communications, vol. 10, no. 1, Jun. 2019. https://doi.org/10.1038/s41467-019-10556-8
Do, Hackwon, Makthal, Nishanth, VanderWal, Arica R., Saavedra, Matthew Ojeda, Olsen, Randall J., Musser, James M., & Kumaraswami, Muthiah (2019). Environmental pH and peptide signaling control virulence of <em>Streptococcus pyogenes</em> via a quorum-sensing pathway. Nature Communications, 10(1). https://doi.org/10.1038/s41467-019-10556-8
Do, Hackwon, Makthal, Nishanth, VanderWal, Arica R., et al., "Environmental pH and peptide signaling control virulence of <em>Streptococcus pyogenes</em> via a quorum-sensing pathway," Nature Communications 10, no. 1 (2019), https://doi.org/10.1038/s41467-019-10556-8
@article{osti_1624160,
author = {Do, Hackwon and Makthal, Nishanth and VanderWal, Arica R. and Saavedra, Matthew Ojeda and Olsen, Randall J. and Musser, James M. and Kumaraswami, Muthiah},
title = {Environmental pH and peptide signaling control virulence of <em>Streptococcus pyogenes</em> via a quorum-sensing pathway},
annote = {Bacteria control gene expression in concert with their population density by a process called quorum sensing, which is modulated by bacterial chemical signals and environmental factors. In the human pathogen Streptococcus pyogenes, production of secreted virulence factor SpeB is controlled by a quorum-sensing pathway and environmental pH. The quorum-sensing pathway consists of a secreted leaderless peptide signal (SIP), and its cognate receptor RopB. Here, we report that the SIP quorum-sensing pathway has a pH-sensing mechanism operative through a pH-sensitive histidine switch located at the base of the SIP-binding pocket of RopB. Environmental acidification induces protonation of His144 and reorganization of hydrogen bonding networks in RopB, which facilitates SIP recognition. The convergence of two disparate signals in the SIP signaling pathway results in induction of SpeB production and increased bacterial virulence. Our findings provide a model for investigating analogous crosstalk in other microorganisms.},
doi = {10.1038/s41467-019-10556-8},
url = {https://www.osti.gov/biblio/1624160},
journal = {Nature Communications},
issn = {ISSN 2041-1723},
number = {1},
volume = {10},
place = {United States},
publisher = {Nature Publishing Group},
year = {2019},
month = {06}}
Zentralblatt für Bakteriologie, Mikrobiologie und Hygiene. 1. Abt. Originale. A, Medizinische Mikrobiologie, Infektionskrankheiten und Parasitologie, Vol. 255, Issue 2-3https://doi.org/10.1016/s0174-3031(83)80161-9
