Abstract:
:Pseudomonas aeruginosa 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 mucA22 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 mucP, a protease involved in MucA degradation, and provide the first atomistic model of MucP. Based on our findings, we speculate that mutations in mucP stabilize the truncated form of MucA22, rendering it functional and therefore able to reduce toxicity by properly sequestering AlgT.IMPORTANCEPseudomonas aeruginosa 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 mucA, 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 P. aeruginosa is capable of causing long-term infections.
journal_name
J Bacterioljournal_title
Journal of bacteriologyauthors
Cross AR,Raghuram V,Wang Z,Dey D,Goldberg JBdoi
10.1128/JB.00445-20subject
Has Abstractpub_date
2020-09-23 00:00:00issue
20eissn
0021-9193issn
1098-5530pii
JB.00445-20journal_volume
202pub_type
杂志文章abstract::The structural gene for histidyl-tRNA synthetase was localized to 53.8 min on the Escherichia coli genome. The gene order in this region was determined to be dapE-purC-upp-purG-(guaA, guaB)-hisS-glyA. ...
journal_title:Journal of bacteriology
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doi:10.1128/JB.138.1.264-267.1979
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更新日期:1972-10-01 00:00:00
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journal_title:Journal of bacteriology
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journal_title:Journal of bacteriology
pub_type: 杂志文章
doi:10.1128/jb.177.8.2021-2032.1995
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pub_type: 杂志文章
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pub_type: 杂志文章
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pub_type: 杂志文章
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更新日期:2005-12-01 00:00:00
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journal_title:Journal of bacteriology
pub_type: 杂志文章
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journal_title:Journal of bacteriology
pub_type: 杂志文章
doi:10.1128/JB.181.20.6238-6246.1999
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journal_title:Journal of bacteriology
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journal_title:Journal of bacteriology
pub_type: 杂志文章
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journal_title:Journal of bacteriology
pub_type: 杂志文章
doi:10.1128/jb.176.21.6672-6676.1994
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journal_title:Journal of bacteriology
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journal_title:Journal of bacteriology
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journal_title:Journal of bacteriology
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journal_title:Journal of bacteriology
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journal_title:Journal of bacteriology
pub_type: 杂志文章
doi:10.1128/JB.149.2.798-799.1982
更新日期:1982-02-01 00:00:00
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journal_title:Journal of bacteriology
pub_type: 杂志文章
doi:10.1128/jb.171.8.4410-4416.1989
更新日期:1989-08-01 00:00:00
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journal_title:Journal of bacteriology
pub_type: 杂志文章
doi:10.1128/jb.176.18.5861-5863.1994
更新日期:1994-09-01 00:00:00