ArticleJournal of bacteriology2012
SMU.152 acts as an immunity protein for mutacin IV.
Article in Journal of bacteriology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 26 citations in OpenAlex.
- Fluoride triggers lysis inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- SepM mutation in Streptococcus mutans clinical isolates and related function analysis.BMC oral health · 2024Article
- Expanding the genetic toolbox for the obligate human pathogenFrontiers in bioengineering and biotechnology · 2024Article
- Genomic and phenotypic characterization ofFrontiers in microbiology · 2022Article
- The bacteriocin Angicin interferes with bacterial membrane integrity through interaction with the mannose phosphotransferase system.Frontiers in microbiology · 2022Article
- Article
- The membrane topology of immunity proteins for the two-peptide bacteriocins carnobacteriocin XY, lactococcin G, and lactococcin MN shows structural diversity.MicrobiologyOpen · 2020Article
- Genome mining unveils widespread natural product biosynthetic capacity in human oral microbe Streptococcus mutans.Scientific reports · 2016Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Streptococcus mutans, a principal causative agent of dental caries, secretes antimicrobial peptides known as mutacins to suppress the growth of competing species to establish a successful colonization. S. mutans UA159, a sequenced strain, produces at least two major mutacins, mutacins IV and V. Mutacin IV is a two-peptide mutacin encoded by nlmAB genes, which are mapped just upstream of a putative immunity-encoding gene SMU.152. Here we explored the function of SMU.152 as an immunity protein. We observed that overexpression of SMU.152 in two sensitive host strains converted the strains to become immune to mutacin IV. To identify the residues that are important for immunity function, we sequentially deleted residues from the C-terminal region of SMU.152. We observed that deletion of as few as seven amino acids, all of which are highly charged (KRRSKNK), drastically reduced the immunity function of the protein. Furthermore, we identified two other putative immunity proteins, SMU.1909 and SMU.925, which lack the last four charged residues (SKNK) that are present in SMU.152 but contain the KRR residues. Synthetic addition of SKNK residues to either SMU.1909 or SMU.925 to reconstitute the KRRSKNK motif and expressing these constructs in sensitive cells rendered the cells resistant to mutacin IV. We also demonstrated that deletion of Man-PTS system from a sensitive strain made the cells partially resistant to mutacin IV, indicating that the Man-PTS system plays a role in mutacin IV recognition.
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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.