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Lei He

Publications and source records attributed to Lei He.

2 recordsLinked to original sources

Streptomyces songxianensis sp. nov. SX92T: biocontrol of tobacco black shank and modulation of the rhizosphere microbiome.

Streptomyces species are well-known for their potential in biocontrol and plant growth promotion, with the rhizosphere serving a rich reservoir for novel isolates. In this study, a Streptomyces strain (SX92T) was isolated from the rhizosphere of healthy tobacco plants. In dual-culture assays, SX92T displayed broad-spectrum antagonistic activity against six major fungal pathogens of tobacco, with the highest inhibition (59.22%) against Phytophthora nicotianae, the causal agent of tobacco black shank. Polyphasic taxonomic characterization, combining 16S rRNA gene phylogeny, distinctive physiological traits, chemotaxonomic markers (LL-diaminopimelic acid, major menaquinones MK-10(H₄) and MK-9(H₈), and predominant fatty acids anteiso-C₁₅:₀ and C₁₆:₀), and genome-based metrics (ANI and dDDH), clearly distinguished SX92T from its closest relatives. Accordingly, strain SX92T is proposed as the type strain of a novel species, Streptomyces songxianensis sp. nov. The genome of SX92T is 9.69 Mb in size with a G + C content of 71% and contains 26 biosynthetic gene clusters, including one showing 100% similarity to the albaflavenone cluster. In field trials, application of SX92T fermentation broth significantly improved tobacco agronomic traits and reduced black shank incidence by 44.97%. Furthermore, SX92T treatment reshaped the rhizosphere microbiome by enriching beneficial bacteria such as Flavobacterium and altering the relative abundance of specific fungi, including a reduction in the arbuscular mycorrhizal fungus Rhizophagus irregularis. It also shifted soil enzyme activities, with increased cellulase and decreased catalase levels. These findings establish Streptomyces songxianensis SX92T as a promising multifunctional biocontrol agent for sustainable tobacco production.

Streptomyces

Fe-S cluster deficiency drives small colony variant formation in persistent infections.

INTRODUCTION: Small colony variants (SCVs) of Staphylococcus aureus (S. aureus) are associated with persistent infections and poor clinical outcomes. The mechanisms driving stable SCV formation remain poorly understood, particularly concerning metabolic adaptations. This study explores the in-host evolutionary dynamics of S. aureus and identifies a novel genetic determinant linked to SCV formation. OBJECTIVES: To investigate the genetic mutations and phenotypic adaptations underlying SCV formation, with a focus on the role of a novel mutation in the sufB gene, which is critical for Fe-S cluster biosynthesis. METHODS: Sequential isolates from a patient with recurrent infections were analyzed using whole-genome sequencing, antimicrobial susceptibility testing, and functional assays. The phylogenetic relationship of the isolates was determined, and specific mutations were identified. Functional assays included aconitase and glutamate synthase activity measurements, ATP level quantification, reactive oxygen species (ROS) production, and biofilm formation assays. In vivo pathogenesis was assessed using a murine catheter infection model. RESULTS: A novel frameshift mutation in sufB was identified, disrupting Fe-S cluster biosynthesis and impairing the TCA cycle and electron transport chain, leading to reduced ATP and ROS production. This metabolic reprogramming promoted stable SCV formation, characterized by slow growth, enhanced tolerance to antibiotics and neutrophil-mediated killing, and persistent inflammation in vivo. Restoration of sufB reversed these phenotypes, confirming its pivotal role in SCV-associated persistence. CONCLUSION: sufB is a novel genetic determinant of stable SCV formation through Fe-S cluster deficiency, driving metabolic shifts that enhance immune evasion and chronic infection. Our findings highlight antibiotic stewardship and suggest potential therapeutic strategies for managing persistent SCV-associated infections.

Staphylococcus aureus