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Overproduction of the AlgT Sigma Factor Is Lethal to Mucoid Pseudomonas aeruginosa. | LitMetric

Overproduction of the AlgT Sigma Factor Is Lethal to Mucoid Pseudomonas aeruginosa.

J Bacteriol

Division of Pulmonary, Allergy and Immunology, Cystic Fibrosis, and Sleep, Department of Pediatrics, Emory University School of Medicine, Atlanta, Georgia, USA

Published: September 2020

AI Article Synopsis

  • Chronic lung infections can lead to the overproduction of alginate by mucoid bacterial strains, which is linked to worse patient outcomes.
  • A common mutation causes a dysfunctional form of the anti-sigma factor MucA, resulting in unchecked activity of the sigma factor AlgT and excessive alginate production.
  • The study suggests that mutations in the protease MucP stabilize the truncated MucA, helping to regulate AlgT and potentially reducing the toxicity associated with its overproduction, which is crucial for understanding chronic infections caused by opportunistic bacteria.

Article Abstract

isolates from chronic lung infections often overproduce alginate, giving rise to the mucoid phenotype. Isolation of mucoid strains from chronic lung infections correlates with a poor patient outcome. The most common mutation that causes the mucoid phenotype is called and results in a truncated form of the anti-sigma factor MucA that is continuously subjected to proteolysis. When a functional MucA is absent, the cognate sigma factor, AlgT, is no longer sequestered and continuously transcribes the alginate biosynthesis operon, leading to alginate overproduction. In this work, we report that in the absence of wild-type MucA, providing exogenous AlgT is toxic. This is intriguing, since mucoid strains endogenously possess high levels of AlgT. Furthermore, we show that suppressors of toxic AlgT production have mutations in , a protease involved in MucA degradation, and provide the first atomistic model of MucP. Based on our findings, we speculate that mutations in stabilize the truncated form of MucA22, rendering it functional and therefore able to reduce toxicity by properly sequestering AlgT. is an opportunistic bacterial pathogen capable of causing chronic lung infections. Phenotypes important for the long-term persistence and adaption to this unique lung ecosystem are largely regulated by the AlgT sigma factor. Chronic infection isolates often contain mutations in the anti-sigma factor , resulting in uncontrolled AlgT and continuous production of alginate in addition to the expression of ∼300 additional genes. Here, we report that in the absence of wild-type MucA, AlgT overproduction is lethal and that suppressors of toxic AlgT production have mutations in the MucA protease, MucP. Since AlgT contributes to the establishment of chronic infections, understanding how AlgT is regulated will provide vital information on how is capable of causing long-term infections.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7515251PMC
http://dx.doi.org/10.1128/JB.00445-20DOI Listing

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