ArticlePloS one2012
Response of methicillin-resistant Staphylococcus aureus to amicoumacin A.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
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- Isolation and characterization of an antimicrobial Bacillus subtilis strain O-741 against Vibrio parahaemolyticus.PloS one · 2024Article
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- AntimicrobialAntibiotics (Basel, Switzerland) · 2022Review
- Multifaceted Mechanism of Amicoumacin A Inhibition of Bacterial Translation.Frontiers in microbiology · 2021Article
- Deep Functional Profiling Facilitates the Evaluation of the Antibacterial Potential of the Antibiotic Amicoumacin.Antibiotics (Basel, Switzerland) · 2020Article
- Mechanism of the Potential Therapeutic CandidateFrontiers in microbiology · 2020Article
- Antimicrobial Activity and Mechanism of Action ofFrontiers in microbiology · 2019Article
- Mechanism of anti-Vibrio activity of marine probiotic strain Bacillus pumilus H2, and characterization of the active substance.AMB Express · 2017Article
- Identification of Staphylococcus aureus Cellular Pathways Affected by the Stilbenoid Lead Drug SK-03-92 Using a Microarray.Antibiotics (Basel, Switzerland) · 2017Article
- Sorting Out Antibiotics' Mechanisms of Action: a Double Fluorescent Protein Reporter for High-Throughput Screening of Ribosome and DNA Biosynthesis Inhibitors.Antimicrobial agents and chemotherapy · 2016Article
- Activating and Attenuating the Amicoumacin Antibiotics.Molecules (Basel, Switzerland) · 2016Article
- Directed natural product biosynthesis gene cluster capture and expression in the model bacterium Bacillus subtilis.Scientific reports · 2015Article
- Amicoumacin a inhibits translation by stabilizing mRNA interaction with the ribosome.Molecular cell · 2014Article
- Extraction and Identification of Antibacterial Secondary Metabolites from Marine Streptomyces sp. VITBRK2.International journal of molecular and cellular medicine · 2014Article
- StaphyloBase: a specialized genomic resource for the staphylococcal research community.Database : the journal of biological databases and curation · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
Abstract
Amicoumacin A exhibits strong antimicrobial activity against methicillin-resistant Staphylococcus aureus (MRSA), hence we sought to uncover its mechanism of action. Genome-wide transcriptome analysis of S. aureus COL in response to amicoumacin A showed alteration in transcription of genes specifying several cellular processes including cell envelope turnover, cross-membrane transport, virulence, metabolism, and general stress response. The most highly induced gene was lrgA, encoding an antiholin-like product, which is induced in cells undergoing a collapse of Δψ. Consistent with the notion that LrgA modulates murein hydrolase activity, COL grown in the presence of amicoumacin A showed reduced autolysis, which was primarily caused by lower hydrolase activity. To gain further insight into the mechanism of action of amicoumacin A, a whole genome comparison of wild-type COL and amicoumacin A-resistant mutants isolated by a serial passage method was carried out. Single point mutations generating codon substitutions were uncovered in ksgA (encoding RNA dimethyltransferase), fusA (elongation factor G), dnaG (primase), lacD (tagatose 1,6-bisphosphate aldolase), and SACOL0611 (a putative glycosyl transferase). The codon substitutions in EF-G that cause amicoumacin A resistance and fusidic acid resistance reside in separate domains and do not bring about cross resistance. Taken together, these results suggest that amicoumacin A might cause perturbation of the cell membrane and lead to energy dissipation. Decreased rates of cellular metabolism including protein synthesis and DNA replication in resistant strains might allow cells to compensate for membrane dysfunction and thus increase cell survivability.
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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.