SroA links SigS-dependent stress signaling to metabolic remodeling in Staphylococcus aureus
- 1Howard University College of Medicine
Abstract
Staphylococcus aureus encounters diverse environmental conditions during colonization and infection, including fluctuations in nutrient availability, oxidative stress, and oxygen limitation. Adaptation to these environments requires regulatory systems that coordinate stress responses with metabolic physiology. The extracytoplasmic function sigma factor SigS contributes to stress adaptation and virulence in S. aureus and directly activates expression of the sroAB operon, which encodes the small proteins SroA and SroB. Previous work demonstrated that SroA participates in feedback regulation of sigS expression, but the broader physiological role of SroA has remained unclear. To further define the regulatory functions of SroA, we performed RNA sequencing following inducible overexpression of sroA in S. aureus. Transcriptome analysis identified altered expression of genes associated with nitrate respiration, nucleotide biosynthesis, stress responses, and nutrient acquisition. Northern blot and quantitative RT-PCR analysis confirmed repression of narG and narJ transcripts following SroA overexpression. Consistent with these transcriptional changes, SroA overexpression impaired nitrate reduction and produced a modest but significant growth disadvantage under anaerobic conditions in chemically defined medium supplemented with glucose and nitrate. In addition to repression of nitrate respiration genes, SroA overexpression reduced expression of genes involved in de novo purine and pyrimidine biosynthesis, while transcripts associated with stress responses and nutrient acquisition, including sosA and pstS, were increased. Together, these findings support a role for SroA in modulating nitrate respiration-associated pathways and growth under conditions supporting anaerobic respiration, linking SigS-dependent stress signaling to metabolic adaptation in S. aureus.
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BibTeX
@misc{alqahtani2026sroa,
title = {{SroA links SigS-dependent stress signaling to metabolic remodeling in Staphylococcus aureus}},
author = {S. A. Alqahtani and S. Pasham and J. Alsulami and A. Al Ali and J. I. Aubee and B. R. Tomlinson and S. Kennedy and E. A. Felton and L. N. Shaw and K. M. Thompson},
howpublished = {bioRxiv},
year = {2026},
month = may,
doi = {10.64898/2026.05.15.725384},
url = {https://www.biorxiv.org/content/10.64898/2026.05.15.725384v2},
note = {CC BY},
}
RIS
TY - UNPB
TI - SroA links SigS-dependent stress signaling to metabolic remodeling in Staphylococcus aureus
AU - S. A. Alqahtani
AU - S. Pasham
AU - J. Alsulami
AU - A. Al Ali
AU - J. I. Aubee
AU - B. R. Tomlinson
AU - S. Kennedy
AU - E. A. Felton
AU - L. N. Shaw
AU - K. M. Thompson
PY - 2026
DA - 2026/05/15
PB - bioRxiv
DO - 10.64898/2026.05.15.725384
UR - https://www.biorxiv.org/content/10.64898/2026.05.15.725384v2
AB - Staphylococcus aureus encounters diverse environmental conditions during colonization and infection, including fluctuations in nutrient availability, oxidative stress, and oxygen limitation. Adaptation to these environments requires regulatory systems that coordinate stress responses with metabolic physiology. The extracytoplasmic function sigma factor SigS contributes to stress adaptation and virulence in S. aureus and directly activates expression of the sroAB operon, which encodes the small proteins SroA and SroB. Previous work demonstrated that SroA participates in feedback regulation of sigS expression, but the broader physiological role of SroA has remained unclear. To further define the regulatory functions of SroA, we performed RNA sequencing following inducible overexpression of sroA in S. aureus. Transcriptome analysis identified altered expression of genes associated with nitrate respiration, nucleotide biosynthesis, stress responses, and nutrient acquisition. Northern blot and quantitative RT-PCR analysis confirmed repression of narG and narJ transcripts following SroA overexpression. Consistent with these transcriptional changes, SroA overexpression impaired nitrate reduction and produced a modest but significant growth disadvantage under anaerobic conditions in chemically defined medium supplemented with glucose and nitrate. In addition to repression of nitrate respiration genes, SroA overexpression reduced expression of genes involved in de novo purine and pyrimidine biosynthesis, while transcripts associated with stress responses and nutrient acquisition, including sosA and pstS, were increased. Together, these findings support a role for SroA in modulating nitrate respiration-associated pathways and growth under conditions supporting anaerobic respiration, linking SigS-dependent stress signaling to metabolic adaptation in S. aureus.
ER -