Lipopolysaccharide (LPS), which consists of a lipid A anchor, a core oligosaccharide, and a highly variable O-antigen, plays an important role in maintaining membrane integrity and preventing harmful extracellular molecules from penetrating the membrane of Gram-negative bacteria. Although the roles of lipid A and O-antigen have been extensively studied, the role of the core oligosaccharide in envelope stress responses and antibiotic resistance remains relatively poorly understood. In this study, we analyzed the roles of ten enzymes involved in core biosynthesis and modification in envelope stress responses and antibiotic resistance. Our systematic analyses demonstrated that biosynthesis and modification of heptoses present in the inner core of LPS are important for resistance to bile salts and antibiotics. Notably, we found that phosphorylation of the first heptose in the inner core had a role distinct from that of phosphorylation of the second heptose. Defects in heptose biosynthesis resulted in increased membrane permeability. Finally, we found that SpeA/SpeB-dependent putrescine biosynthesis may be partially associated with the sensitivity of the heptose biosynthesis-defective mutant to clindamycin and erythromycin. Taken together, our results demonstrate that the biosynthesis and modification of heptoses in the inner core of LPS are strongly associated with the envelope stress response and antibiotic resistance.

Chronic stress is a major risk factor for depression and anxiety. However, individuals differ markedly in stress susceptibility and resilience. Accumulating preclinical and clinical evidence indicates that the gut microbiota is closely associated with stress-related phenotypes through the immune, endocrine, and neural pathways. Alterations in microbial diversity, short-chain fatty acid production, and tryptophan metabolism have been associated with stress-related neuroendocrine and immune regulation, whereas emerging preclinical evidence suggests potential links to neural circuits involved in reward processing. By integrating findings from microbiome research and systems neuroscience, this review proposes a microbiology-centered framework for understanding stress resilience and stress-induced anhedonia. Beyond merely summarizing the existing evidence, we critically evaluate the methodological challenges in current human and preclinical studies and highlight the critical need for standardized approaches and multi-omics integration to decipher causality and develop precise psychobiotic interventions.

Bradyrhizobium diazoefficiens USDA110 is an important soybean symbiont widely used as a nitrogen biofertilizer, but its capacity to solubilize inorganic phosphate remains largely unknown. This study evaluated its ability to solubilize insoluble tricalcium phosphate [Ca₃(PO₄)₂] and examined the effect of pyrroloquinoline quinone (PQQ) on this process. USDA110 solubilized Ca₃(PO₄)₂, increasing dissolved phosphate up to 69.5 ± 3.2 µg PO₄³⁻/ml. Phosphate release was accompanied by a decrease in culture pH from approximately 7.0 to 5.0. Supplementation with 10 µM PQQ significantly enhanced phosphate solubilization, resulting in the accumulation of up to 81.8 ± 4.3 µg PO₄³⁻/ml per 10⁹ cells by day 9. An apo-glucose dehydrogenase reconstitution assay detected extracellular PQQ under all carbon-source and phosphate conditions examined, with PQQ concentrations influenced by both factors. Expression of the pqqB-E genes was generally lower under high-P conditions than under low- and medium-P conditions, although pqqA, the first gene in the pqq operon, remained highly expressed across all conditions. RNA-seq analysis showed no transcriptional induction of genes encoding glucose or glycerol dehydrogenases following PQQ supplementation. However, this finding does not exclude their involvement through the PQQ-dependent activation of pre-existing enzymes. Alternative dehydrogenases, organic acid production, or membrane-associated proton/ion transport may contribute to the enhancement. Hence, the molecular mechanism underlying PQQ-enhanced phosphate solubilization requires further investigation. These findings demonstrate that B. diazoefficiens USDA110 possesses acidification-associated phosphate-solubilizing activity that is enhanced by exogenous PQQ, supporting its potential as a dual-function biofertilizer for nitrogen fixation and P mobilization in soybean cultivation.

BipA is a conserved ribosome-associated GTPase that supports bacterial stress adaptation. It participates in 50S ribosome assembly and envelope stress responses; however, it is not known whether both functions depend on its GTPase activity. In this study, we investigated Escherichia coli strains carrying chromosomal D74A or N128D substitutions in the conserved GTPase motifs of BipA. Both mutants displayed severe cold-sensitive growth defects that were similar to those of the ΔbipA strain. At low temperatures, 50S ribosome assembly was defective and immature ribosomal particles accumulated. Ribosome-binding analysis revealed that the mutant BipA had a lower association with ribosomal fractions. The mutants exhibited altered lipopolysaccharide profiles and envelope phenotypes, including increased capsule production, reduced biofilm formation and motility, and increased cell width and length. These phenotypes were most notable at low temperatures, indicating activation of the Rcs (Regulator of Capsule Synthesis) phosphorelay. We next examined the effects of BipA abundance on cellular physiology. BipA expression was influenced by both start-codon identity and the downstream coding context. BipA overexpression impaired growth and induced pronounced cell elongation at both optimal and low temperatures, indicating that proper control of BipA abundance is important for cellular homeostasis. Furthermore, the increased susceptibility of the ΔbipA strain to ampicillin at low temperatures suggested an association between BipA and peptidoglycan homeostasis. Together, these findings suggest that BipA GTPase function is required to maintain ribosome biogenesis and envelope homeostasis during cold adaptation, and that proper control of BipA abundance is also important for maintaining cellular physiology.

The discovery of influenza A viruses in bats has changed our understanding of viral circulation in nature. For years, wild aquatic birds were considered the primary natural reservoir for influenza A viruses. However, surveillance efforts in Neotropical bats have revealed highly divergent bat-derived lineages, including H17N10, H18N11, and H18N12. Researchers also isolated an avian-like H9N2 virus from Egyptian fruit bats. These findings show that bats do not carry a single influenza virus type; instead, they are associated with multiple lineages with distinct evolutionary backgrounds. The H17 and H18 viruses appear to be adapted to bat physiology. They infect cells via major histocompatibility complex class II (MHC-II) molecules rather than the usual sialic acid receptors; their neuraminidase-like proteins lack conventional sialidase activity; and they replicate poorly in non-bat mammalian models. In contrast, the bat-associated, avian-like H9N2 virus behaves differently. Although its surface proteins retain avian-like characteristics, it replicates efficiently and transmits readily in mammalian systems, together with reduced sensitivity to human MxA restriction. These observations raise the possibility that bats could act as ecological bridging hosts for avian influenza viruses. However, there is currently no direct field evidence that avian influenza viruses acquire mammalian-compatible traits in bats or are subsequently transmitted from bats to other host species. This review provides an overview of the current understanding of bat-associated influenza viruses and their potential implications for global health.

Gamma irradiation causes severe cellular damage through indirect oxidative stress generated by water radiolysis. Although carotenoids are well known as antioxidant pigments, their independent contribution to microbial resistance against highly penetrating ionizing radiation remains to be investigated. In this study, recombinant Escherichia coli was used as a controlled and radiation-sensitive host to evaluate whether engineered carotenoid accumulation improves gamma-radiation tolerance and protects DNA from irradiation-induced structural damage. Lycopene- and β-carotene-producing E. coli strains were compared with non-carotenoid-producing controls, including an empty-vector control grown under the same carotenoid-inducing conditions. Under carotenoid-producing conditions, the D₁₀ values of the lycopene- and β-carotene-producing strains significantly increased compared with the control strain. To examine the chemical contribution of carotenoids to DNA protection, purified pUC19 plasmid DNA was irradiated in the presence or absence of carotenoids. Agarose gel electrophoresis showed that lycopene and β-carotene reduced the conversion of supercoiled DNA to open-circular and linear forms, while AFM imaging confirmed improved preservation of intact plasmid morphology. These findings suggest that carotenoid biosynthesis may be applied as a metabolic engineering strategy to improve microbial robustness in irradiation-associated biotechnology, food microbiology, environmental applications, and stress-tolerant production platforms.