ArticlePloS one2008
Protein translation and cell death: the role of rare tRNAs in biofilm formation and in activating dormant phage killer genes.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
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Who cites it
76 citing papers in PubMed, 123 citations in OpenAlex.
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- YmoA functions as a molecular stress sensor in Yersinia.Communications biology · 2025Article
- Conformational change as a mechanism for toxin activation in bacterial toxin-antitoxin systems.Journal of virology · 2024Review
- The unique Legionella longbeachae capsule favors intracellular replication and immune evasion.PLoS pathogens · 2024Article
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- Characterization of a Filamentous Phage, Vaf1, fromApplied and environmental microbiology · 2023Article
- Bacterial Toxin-Antitoxin Systems' Cross-Interactions-Implications for Practical Use in Medicine and Biotechnology.Toxins · 2023Review
- Toxin-antitoxin systems in bacterial pathogenesis.Heliyon · 2023Review
- A dual functional Ti-Ga alloy: inhibiting biofilm formation and osteoclastogenesis differentiation via disturbing iron metabolism.Biomaterials research · 2023Article
- eDNA-stimulated cell dispersion fromeLife · 2023Article
- Biofilm Formation Ability of ESBL/pAmpC-ProducingAntibiotics (Basel, Switzerland) · 2023Article
- CRISPR-Cas Controls Cryptic Prophages.International journal of molecular sciences · 2022Article
- Deconstructing the Phage-Bacterial Biofilm Interaction as a Basis to Establish New Antibiofilm Strategies.Viruses · 2022Review
- Biofilm Maintenance as an Active Process: Evidence that Biofilms Work Hard to Stay Put.Journal of bacteriology · 2022Review
- Characterization of toxin-antitoxin systems from public sequencing data: A case study inFrontiers in microbiology · 2022Article
- Bacterial toxin-antitoxin modules: classification, functions, and association with persistence.Current research in microbial sciences · 2021Review
- Massively parallel transposon mutagenesis identifies temporally essential genes for biofilm formation inMicrobial genomics · 2021Article
- Wolf in Sheep's Clothing:Microorganisms · 2021Review
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We discovered previously that the small Escherichia coli proteins Hha (hemolysin expression modulating protein) and the adjacent, poorly-characterized YbaJ are important for biofilm formation; however, their roles have been nebulous. Biofilms are intricate communities in which cell signaling often converts single cells into primitive tissues. Here we show that Hha decreases biofilm formation dramatically by repressing the transcription of rare codon tRNAs which serves to inhibit fimbriae production and by repressing to some extent transcription of fimbrial genes fimA and ihfA. In vivo binding studies show Hha binds to the rare codon tRNAs argU, ileX, ileY, and proL and to two prophage clusters D1P12 and CP4-57. Real-time PCR corroborated that Hha represses argU and proL, and Hha type I fimbriae repression is abolished by the addition of extra copies of argU, ileY, and proL. The repression of transcription of rare codon tRNAs by Hha also leads to cell lysis and biofilm dispersal due to activation of prophage lytic genes rzpD, yfjZ, appY, and alpA and due to induction of ClpP/ClpX proteases which activate toxins by degrading antitoxins. YbaJ serves to mediate the toxicity of Hha. Hence, we have identified that a single protein (Hha) can control biofilm formation by limiting fimbriae production as well as by controlling cell death. The mechanism used by Hha is the control of translation via the availability of rare codon tRNAs which reduces fimbriae production and activates prophage lytic genes. Therefore, Hha acts as a toxin in conjunction with co-transcribed YbaJ (TomB) that attenuates Hha toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.