ArticleInfection and immunity2011
The Streptococcus iniae transcriptional regulator CpsY is required for protection from neutrophil-mediated killing and proper growth in vitro.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Determinants of bacterial survival and proliferation in blood.FEMS microbiology reviews · 2024Review
- Functional Analysis of Two NovelMicroorganisms · 2020Article
- Remodeling of the Streptococcus mutans proteome in response to LrgAB and external stresses.Scientific reports · 2017Article
- From bacterial killing to immune modulation: Recent insights into the functions of lysozyme.PLoS pathogens · 2017Review
- The Transcriptional Regulator CpsY Is Important for Innate Immune Evasion in Streptococcus pyogenes.Infection and immunity · 2017Article
- Article
- Zebrafish as a model for zoonotic aquatic pathogens.Developmental and comparative immunology · 2014Review
- Positive feedback regulation of stgR expression for secondary metabolism in Streptomyces coelicolor.Journal of bacteriology · 2013Article
- Genome-wide identification of genes required for fitness of group A Streptococcus in human blood.Infection and immunity · 2013Article
- Evolution of the capsular operon of Streptococcus iniae in response to vaccination.Applied and environmental microbiology · 2012Article
- CpsY influences Streptococcus iniae cell wall adaptations important for neutrophil intracellular survival.Infection and immunity · 2012Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ability of a pathogen to metabolically adapt to the local environment for optimal expression of virulence determinants is a continued area of research. Orthologs of the Streptococcus iniae LysR family regulator CpsY have been shown to regulate methionine biosynthesis and uptake pathways but appear to influence expression of several virulence genes as well. An S. iniae mutant with an in-frame deletion of cpsY (ΔcpsY mutant) is highly attenuated in a zebrafish infection model. The ΔcpsY mutant displays a methionine-independent growth defect in serum, which differs from the methionine-dependent defect observed for orthologous mutants of Streptococcus mutans and Streptococcus agalactiae. On the contrary, the ΔcpsY mutant can grow in excess of the wild type (WT) when supplemented with proteose peptone, suggesting an inability to properly regulate growth. CpsY is critical for protection of S. iniae from clearance by neutrophils in whole blood but is dispensable for intracellular survival in macrophages. Susceptibility of the ΔcpsY mutant to killing in whole blood is not due to a growth defect, because inhibition of neutrophil phagocytosis rescues the mutant to WT levels. Thus, CpsY appears to have a pleiotropic regulatory role for S. iniae, integrating metabolism and virulence. Furthermore, S. iniae provides a unique model to investigate the paradigm of CpsY-dependent regulation during systemic streptococcal infection.
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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.