Strains Mo2-6T, S9, KG4-3T, and 50Mo3-2, identified as coagulase-negative, Gram-stain-positive, halotolerant, non-motile coccoid bacteria, were isolated from traditional Korean soybean foods. Strains Mo2-6T and S9 were both catalase- and oxidase-negative, whereas KG4-3T and 50Mo3-2 were catalase-positive but oxidase-negative. The optimal growth conditions for Mo2-6T and S9 were 30°C, 2% NaCl, and pH 7.0, while KG4-3T and 50Mo3-2 grew best at 35°C, 2% NaCl, and pH 7.0. All strains contained menaquinone-7 as the predominant isoprenoid quinone, with anteiso-C15:0 and iso-C15:0 as the major cellular fatty acids (> 10%). Additionally, anteiso-C13:0 was a major fatty acid in strain KG4-3T. The DNA G + C contents of strains Mo2-6T, S9, KG4-3T, and 50Mo3-2 were 33.4%, 33.3%, 32.5%, and 32.7%, respectively. Phylogenetic analyses based on the 16S rRNA gene and whole-genome sequences revealed that strains Mo2-6T and S9, as well as KG4-3T and 50Mo3-2, formed distinct lineages within the genus Staphylococcus. Digital DNA-DNA hybridization (dDDH) and average nucleotide identity (ANI) analyses confirmed that strains Mo2-6T and S9, as well as KG4-3T and 50Mo3-2, belonged to the same species. Meanwhile, dDDH and ANI values between strains Mo2-6T and KG4-3T, as well as comparisons with other Staphylococcus type strains, were below the species delineation thresholds, indicating they represent novel species. Based on phenotypic, chemotaxonomic, and molecular data, we propose strain Mo2-6T as the type strain of Staphylococcus parequorum sp. nov. (=KACC 23685T =JCM 37038T) and strain KG4-3T as the type strain of Staphylococcus halotolerans sp. nov. (=KACC 23684T =JCM 37037T).
The escalating antibiotic resistance crisis poses a significant challenge to global public health, threatening the efficacy of current treatments and driving the emergence of multidrug-resistant pathogens. Among the various factors associated with bacterial antibiotic resistance, small regulatory RNAs (sRNAs) have emerged as pivotal post-transcriptional regulators which orchestrate bacterial adaptation to antibiotic pressure via diverse mechanisms. This review consolidates the current knowledge on sRNA-mediated mechanisms, focusing on drug uptake, drug efflux systems, lipopolysaccharides, cell wall modification, biofilm formation, and mutagenesis. Recent advances in transcriptomics and functional analyses have revealed novel sRNAs and their regulatory networks, expanding our understanding of resistance mechanisms. These findings highlight the potential of targeting sRNA-mediated pathways as an innovative therapeutic strategy to combat antibiotic resistance, and offer promising avenues for managing challenging bacterial infections.
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