bioRxivMicrobiologyPreprint
Novel Streptococcus mitis subsp. mitis Picklauza buccal isolate from individual with idiopathic pulmonary fibrosis containing functional mobile qacG Gene.
Sydnie N KlauzaiD, Sophie M. P. PickelneriD, Kelyah SpurgeoniD, Souzane Ntamubano, Nicole R. Falkowski, Nisha Mohan, Jay H. Lipinski, Justin M. OldhamiD, David N. O’DwyeriD, Ariangela J. KozikiD
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease characterized by immune dysregulation, fibrosis, and eventual respiratory failure. While the etiology of IPF remains unclear, accumulating evidence implicates the oral and airway microbiome in disease progression, with elevated Streptococcal burden linked to increased mortality. Whether specific taxa actively contribute to IPF pathophysiology or arise secondarily from the damaged lung environment remains unresolved. Here, we characterize "Picklauza," a streptococcal strain isolated from the buccal mucosa of an individual with IPF. Although its average nucleotide identity to a Streptococcus mitis reference genome was 93.855%, analysis with Streptoquod supported classification as Streptococcus mitis subsp. mitis. Genomic analysis identified a 109-amino-acid qacG homolog predicted to encode a small multidrug resistance (SMR)-family efflux transporter. The locus was located near genes associated with mobile genetic elements, raising the possibility of horizontal acquisition. The predicted QacG protein retained residues conserved in the extensively characterized SMR transporter EmrE, and RT-qPCR detected qacG transcripts under standard culture conditions. Nevertheless, Picklauza did not display increased tolerance to benzalkonium chloride, benzethonium chloride, or ethidium bromide compared with S. mitis NCTC 12261. Picklauza also differed from the reference strain in growth kinetics, carbon utilization, and antimicrobial susceptibility. PCR screening detected qacG homologs in three additional oral isolates from patients with IPF. Together, these findings identify a transcriptionally active, putatively mobile qacG homolog in oral streptococci while revealing a disconnect between gene carriage and QAC susceptibility under the conditions tested. This work highlights the need to validate predicted resistance determinants phenotypically and to investigate the mobility and conditional activity of SMR-family genes across genus boundaries in host-associated microbial communities.
- organism: human
- assay: DNA methylation
- assay: whole-genome sequencing
- research focus: gene regulatory network inference
- approach: statistical model
- Citations
- 0
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