Skip to content
DraconiticResearch
Search Sources API
201,818 studies31 sourcesUpdated 4 min ago
Peer-reviewedCC BY 4.0Microbiology Spectrum

Salmonella Typhimurium vitamin B12-dependent methionine metabolism regulates Caenorhabditis elegans development and vitellogenesis

  1. 1Department of Biological Sciences, Indian Institute of Science Education and Research (IISER) Mohali, SAS Nagar, Punjab, India

Abstract

Host-microbe interactions extend beyond infection, involving microbial metabolites, such as short-chain fatty acids, vitamins, and other bioactive compounds, that influence host physiology and development. Using Caenorhabditis elegans, an excellent model organism for host-microbe interactions, we demonstrate that Salmonella Typhimurium significantly accelerates C. elegans growth through a vitamin B12-dependent mechanism affecting methionine metabolism. We measured the reproductive maturity of C. elegans via embryo and oocyte production in response to various Salmonella virulence factor mutants and Salmonella strains deficient in cobalamin, folate, and methionine synthesis pathways. We found that the Salmonella cbiB and metH genes are essential for rapid development in C. elegans. Moreover, the C. elegans metr-1 mutant, which lacks functional methionine synthase, did not exhibit increased reproductive maturity when fed on S. Typhimurium or Escherichia coli OP50 supplemented with vitamin B12. However, methionine supplementation rescued this phenotype, indicating that C. elegans obtains vitamin B12 from S. Typhimurium, enhancing the methionine/S-adenosylmethionine (MET/SAM) cycle. We further observed that the C. elegans sams-1 mutant, deficient in SAM synthase, showed growth defects and reduced oocyte production when fed on Salmonella or OP50 supplemented with vitamin B12 or methionine, respectively. Thus, SAM emerges as a key link between bacterial vitamin B12 metabolism and host reproduction. Additionally, Salmonella increases vitellogenin-2 expression, reduces glutathione S-transferase activity, and decreases mitochondrial function. However, ΔcbiB and ΔmetH reversed the beneficial effects of vitamin B12-dependent methionine on vitellogenesis and oxidative stress, suggesting that Salmonella promotes vitellogenesis and reduces oxidative stress through vitamin B12-dependent mitochondrial regulation, linking microbial metabolism to host development.IMPORTANCEUnderstanding the interactions between hosts and pathogens is essential for improving host health. Caenorhabditis elegans obtains micronutrients from diet, gut microbiota, and supplements, but the contribution of microbiota in nutrient absorption is not fully understood. Bacterial metabolism may influence micronutrient status and pathogenicity, resulting in both positive and adverse health effects on the host. This study demonstrates that pathogenic Salmonella can serve as a nutritional source for C. elegans when the two organisms coexist in the same environment. The findings suggest that, rather than being solely detrimental, Salmonella can alter the metabolism of C. elegans, highlighting a complex interaction between the pathogen and its host. This relationship may provide insights into the ecological dynamics of microbial communities and their influence on host physiology and development.

Related

  1. Comparative transcriptomics of outbreak-associated Salmonella Heidelberg, Typhimurium, and monophasic Typhimurium reveals differential expression of stress tolerance, virulence, and biofilm-associated genes
    Chelsey A. Patch, Andrea J. Etter
    Frontiers in MicrobiologyPeer-reviewedCC BY 4.0Full textMicrobiologyPMCCrossrefEurope PMC
  2. The contribution of LepA to virulence and host cell invasion in Salmonella Typhimurium.
    Sebastian Braetz, Andreas Nerlich, Marcus Fulde
    BMC microbiologyPeer-reviewedCC BYFull textMicrobiologyEurope PMCDOAJ
  3. WISH-barcoding of Salmonella Typhimurium ATCC14028s strains for population dynamics studies in vivo
    Christopher Schubert, Jeongmin Kim, Nicolas Näpflin +4
    PLOS OnePeer-reviewedCC BY 4.0Full textEcologyGenetics & genomicsPLOS
  4. Human-targeted drugs extensively reshape regulatory networks controlling virulence and antibiotic resistance in Salmonella Typhimurium
    M. K. Amstalden, R. Olayo-Alarcon, S. Brenzinger +10
    bioRxivPreprintCC BY-NC-NDFull textMicrobiologybioRxiv
  5. The chemoreceptor McpA mediates aerotaxis and redox taxis in Salmonella Typhimurium
    K. Franco, K. Cooper, C. H. Shin +2
    bioRxivPreprintCC BYFull textMicrobiologybioRxiv
BibTeX
@article{daimai2026salmonella,
  title = {{Salmonella Typhimurium vitamin B12-dependent methionine metabolism regulates Caenorhabditis elegans development and vitellogenesis}},
  author = {Chamjailiu Daimai and Vidya Devi Negi},
  journal = {Microbiology Spectrum},
  year = {2026},
  month = sep,
  doi = {10.1128/spectrum.00827-26},
  url = {https://doi.org/10.1128/spectrum.00827-26},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Salmonella Typhimurium vitamin B12-dependent methionine metabolism regulates Caenorhabditis elegans development and vitellogenesis
AU  - Chamjailiu Daimai
AU  - Vidya Devi Negi
PY  - 2026
DA  - 2026/09/29
JO  - Microbiology Spectrum
DO  - 10.1128/spectrum.00827-26
UR  - https://doi.org/10.1128/spectrum.00827-26
AB  - Host-microbe interactions extend beyond infection, involving microbial metabolites, such as short-chain fatty acids, vitamins, and other bioactive compounds, that influence host physiology and development. Using Caenorhabditis elegans, an excellent model organism for host-microbe interactions, we demonstrate that Salmonella Typhimurium significantly accelerates C. elegans growth through a vitamin B12-dependent mechanism affecting methionine metabolism. We measured the reproductive maturity of C. elegans via embryo and oocyte production in response to various Salmonella virulence factor mutants and Salmonella strains deficient in cobalamin, folate, and methionine synthesis pathways. We found that the Salmonella cbiB and metH genes are essential for rapid development in C. elegans. Moreover, the C. elegans metr-1 mutant, which lacks functional methionine synthase, did not exhibit increased reproductive maturity when fed on S. Typhimurium or Escherichia coli OP50 supplemented with vitamin B12. However, methionine supplementation rescued this phenotype, indicating that C. elegans obtains vitamin B12 from S. Typhimurium, enhancing the methionine/S-adenosylmethionine (MET/SAM) cycle. We further observed that the C. elegans sams-1 mutant, deficient in SAM synthase, showed growth defects and reduced oocyte production when fed on Salmonella or OP50 supplemented with vitamin B12 or methionine, respectively. Thus, SAM emerges as a key link between bacterial vitamin B12 metabolism and host reproduction. Additionally, Salmonella increases vitellogenin-2 expression, reduces glutathione S-transferase activity, and decreases mitochondrial function. However, ΔcbiB and ΔmetH reversed the beneficial effects of vitamin B12-dependent methionine on vitellogenesis and oxidative stress, suggesting that Salmonella promotes vitellogenesis and reduces oxidative stress through vitamin B12-dependent mitochondrial regulation, linking microbial metabolism to host development.IMPORTANCEUnderstanding the interactions between hosts and pathogens is essential for improving host health. Caenorhabditis elegans obtains micronutrients from diet, gut microbiota, and supplements, but the contribution of microbiota in nutrient absorption is not fully understood. Bacterial metabolism may influence micronutrient status and pathogenicity, resulting in both positive and adverse health effects on the host. This study demonstrates that pathogenic Salmonella can serve as a nutritional source for C. elegans when the two organisms coexist in the same environment. The findings suggest that, rather than being solely detrimental, Salmonella can alter the metabolism of C. elegans, highlighting a complex interaction between the pathogen and its host. This relationship may provide insights into the ecological dynamics of microbial communities and their influence on host physiology and development.
SN  - 2165-0497
ER  -