ArticlePLoS pathogens2015
Identification of a Novel Lipoprotein Regulator of Clostridium difficile Spore Germination.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 76 citations in OpenAlex.
- A programmed reset mechanism primesScience advances · 2026Article
- Advances in understanding the Clostridial spore inner membrane.Archives of microbiology · 2026Review
- Penicillin-binding proteins exhibit functional redundancy during asymmetric cell division inJournal of bacteriology · 2025Article
- Unique growth and morphology properties of Clade 5bioRxiv : the preprint server for biology · 2025Article
- Unique growth and morphology properties of Clade 5 Clostridioides difficile strains revealed by single-cell time-lapse microscopy.PLoS pathogens · 2025Article
- Bile acids as germinants for Clostridioides difficile spores, evidence of adaptation to the gut?FEMS microbiology reviews · 2025Review
- Review
- Clostridioides difficile Sporulation.Advances in experimental medicine and biology · 2024Review
- Diversification of division mechanisms in endospore-forming bacteria revealed by analyses of peptidoglycan synthesis in Clostridioides difficile.Nature communications · 2023Article
- A sporulation signature protease is required for assembly of the spore surface layers, germination and host colonization in Clostridioides difficile.PLoS pathogens · 2023Article
- A dual-action antibiotic that killsProceedings of the National Academy of Sciences of the United States of America · 2023Article
- VanG- and D-Ala-D-Ser-dependent peptidoglycan synthesis and vancomycin resistance in Clostridioides difficile.Molecular microbiology · 2022Article
- Imaging Clostridioides difficile Spore Germination and Germination Proteins.Journal of bacteriology · 2022Article
- The Stickland Reaction PrecursormSphere · 2022Article
- Identification of ClpP Dual Isoform Disruption as an Antisporulation Strategy for Clostridioides difficile.Journal of bacteriology · 2022Article
- Clostridioides difficile spore germination: initiation to DPA release.Current opinion in microbiology · 2022Review
- A lipoprotein allosterically activates the CwlD amidase during Clostridioides difficile spore formation.PLoS genetics · 2021Article
- Opportunities for Nanomedicine inAntibiotics (Basel, Switzerland) · 2021Review
- Article
- Structural, Metabolic and Evolutionary Comparison of Bacterial Endospore and Exospore Formation.Frontiers in microbiology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Clostridium difficile is a Gram-positive spore-forming pathogen and a leading cause of nosocomial diarrhea. C. difficile infections are transmitted when ingested spores germinate in the gastrointestinal tract and transform into vegetative cells. Germination begins when the germinant receptor CspC detects bile salts in the gut. CspC is a subtilisin-like serine pseudoprotease that activates the related CspB serine protease through an unknown mechanism. Activated CspB cleaves the pro-SleC zymogen, which allows the activated SleC cortex hydrolase to degrade the protective cortex layer. While these regulators are essential for C. difficile spores to outgrow and form toxin-secreting vegetative cells, the mechanisms controlling their function have only been partially characterized. In this study, we identify the lipoprotein GerS as a novel regulator of C. difficile spore germination using targeted mutagenesis. A gerS mutant has a severe germination defect and fails to degrade cortex even though it processes SleC at wildtype levels. Using complementation analyses, we demonstrate that GerS secretion, but not lipidation, is necessary for GerS to activate SleC. Importantly, loss of GerS attenuates the virulence of C. difficile in a hamster model of infection. Since GerS appears to be conserved exclusively in related Peptostreptococcaeace family members, our results contribute to a growing body of work indicating that C. difficile has evolved distinct mechanisms for controlling the exit from dormancy relative to B. subtilis and other spore-forming organisms.
Indexed as
Identifiers
What OpenQuestion holds
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.