Environmental and genetic regulation of Streptococcus pneumoniae galactose catabolic pathways
Efficient utilization of nutrients is crucial for microbial survival and virulence. The same nutrient may be utilized by multiple catabolic pathways, indicating that the physical and chemical environments for induction as well as their functional roles may differ. Here, we study the tagatose and Leloir pathways for galactose catabolism of the human pathogen Streptococcus pneumoniae. We show that galactose utilization potentiates pneumococcal virulence, the induction of galactose catabolic pathways is influenced differentially by the concentration of galactose and temperature, and sialic acid downregulates galactose catabolism. Furthermore, the genetic regulation and in vivo induction of each pathway differ, and both galactose catabolic pathways can be turned off with a galactose analogue in a substrate-specific manner, indicating that galactose catabolic pathways can be potential drug targets.
Funding
NIH R01 AI139077-01A1
NIH R01 AI135060-01A1
History
Citation
Kareem, B.O., Gazioglu, O., Mueller Brown, K. et al. Environmental and genetic regulation of Streptococcus pneumoniae galactose catabolic pathways. Nat Commun 15, 5171 (2024). https://doi.org/10.1038/s41467-024-49619-wAuthor affiliation
College of Life Sciences,Genetics & Genome Biology and Respiratory SciencesVersion
- VoR (Version of Record)
Published in
Nature CommunicationsVolume
15Issue
1Pagination
5171Publisher
Springer Science and Business Media LLCissn
2041-1723eissn
2041-1723Acceptance date
2024-06-10Copyright date
2024Available date
2024-07-10Publisher DOI
Spatial coverage
EnglandLanguage
enPublisher version
Deposited by
Dr Hasan YesilkayaDeposit date
2024-07-09Data Access Statement
All data supporting the paper’s conclusions are included in the main text and supplementary material file. The RNA-seq data is available from the Gene Expression Omnibus (GEO) repository with the primary accession code GSE246424. Source data are provided with this paper.Rights Retention Statement
- No