Journal of Basic Microbiology最新文献

Wastewater from a furfural plant in Argentina contains 791 mg L⁻¹ of furfural, posing toxicity risks if untreated. This study aimed to isolate actinobacteria from these furfural-contaminated sites, select tolerant strains, and assess their removal efficiency individually and in consortium. Six microorganisms with macroscopic characteristics corresponding to the phylum Actinomycetota were isolated. These microorganisms and Streptomyces sp. A5, A12 and M7, isolated from pesticide and heavy metal contaminated environments, showed tolerance to furfural 800 mg L⁻¹. The isolate L9 (identified as Nocardiopsis sp. L9) and Streptomyces sp. A12 and M7 were selected because they were the most efficient with respect to their growth capacity and furfural removal in MM supplemented with furfural 400 mg L⁻¹. The consortium formulated with the three actinobacteria (L9-A12-M7) exhibited significantly higher growth (123%) and furfural removal efficiency (58%) compared to individual cultures, when exposed to a pollutant concentration similar to that of the actual effluent (800 mg L⁻¹). Ecotoxicity tests using Raphanus sativus seeds showed that the toxic effects caused by furfural were reversed by the treatment, confirming the effectiveness of the bioremediation process. These results suggest that the actinobacterial consortium is a promising bioremediation tool for the treatment of industrial effluents contaminated with furfural.

Acinetobacter baylyi ADP1 has garnered attention as a promising synthetic biology chassis due to its compact genome, rapid growth, innate competence for horizontal gene transfer, and ease of genetic manipulation. To assess its potential for natural product biosynthesis, we engineered ADP1 for the production of l-leucine. First, feedback inhibition was relieved by overexpressing the endogenous leuA and ilvBN genes, alongside the replacement of transcriptional attenuation regions within the leuBCD operon. These interventions derepressed the native biosynthetic pathway, resulting in a substantial increase in l-leucine titers from 0.10 to 0.82 g/L. Next, we augmented the eda gene in the Entner–Doudoroff pathway, while disrupting poxB, which diverts carbon toward acetate, further promoting l-leucine biosynthesis. To resolve carbon competition between the tricarboxylic acid (TCA) cycle and l-leucine synthesis, an inducible sRNA-based system was developed to dynamically repress TCA cycle-associated genes. This balanced the cell growth with l-leucine anabolism, ultimately achieving a titer of 1.16 g/L with a yield of 0.08 g/g glucose. Interestingly, the l-leucine feedback regulation diverges markedly from classical prokaryotic chassis like Escherichia coli and Corynebacterium glutamicum, in which feedback-resistant variants of leuA and ilvBN are typically required to overcome repression. In contrast, in ADP1, overexpression of the native, wild-type genes was sufficient to drive efficient product synthesis. Moreover, the unique glucose catabolism network in ADP1 limits its pyruvate availability, supplementing pyruvate and minimizing carbon loss proved critical for optimizing l-leucine production. Collectively, our findings offer mechanistic insights into chassis-specific metabolic regulation and optimizing precursor supply in nonmodel organisms.

The putative two-component system (TCS) CgtRS5, encoded by the ncgl2572–ncgl2573 gene cluster, plays a critical role in environmental adaptation in Corynebacterium glutamicum. Comparative transcriptomic analysis between the wild-type strain and a ΔcgtRS5 mutant revealed three upregulated and 107 downregulated genes in the mutant. Among these, genes involved in iron metabolism (ncgl1959), aromatic compound degradation (ncgl2320), and drug resistance (cssR) were significantly downregulated. Phenotypic assays demonstrated that the ΔcgtRS5 mutant exhibited impaired growth in media supplemented with the divalent form of iron (Fe²⁺) or the alkylating agent iodoacetamide (IAM), but showed no significant differences under benzoate, resorcinol, or antibiotic stress. These results suggest that CgtRS5 specifically regulates the stress response to iron and IAM in C. glutamicum, providing new insights into TCS-mediated regulatory mechanisms in this organism.

The haloalkaliphilic archaea are a group of unique organisms that can thrive in environments with high salinity and alkaline pH. Theses microorganisms have developed various strategies to survive in polyextereme conditions, carotenoids production included as a one of defense mechanism. The ecological distribution of haloalkaliphilic archaea is in soda lakes. Haloalkaliphilic carotenoids producing archaea includes genera such as Natronococcus, Halostagnicola, Natrialba, Natronobacterium, Natronolimnobius, and Natronorubrum. The main carotenoids produce by haloalkaliphilic archea are bacterioruberin and its derivatives. In silico studies of bacterioruberin and its derivatives have shown potential results in binding to cancer-related proteins like MMP-9, ROS1, Bcl-2 cyclin D1. Bacterioruberin from haloalkophiles have higher antioxidanat potential compare to halophilic archea. Bacterioruberin able to inhibit the most importanat replicative enzyme of viruses. They have gained recent attention due to their antioxidant, anticancer, antiviral and antibacterial properties. The bacterioruberin applied in the field of biotechnological and industrial of these as natural colorants, Immunomodulants, feed additive. Extremozymes of these organisms have advantage due to their ability to active in such extreme condition.

Antibiotic resistance has escalated globally, affecting not only commonly used antibiotics but also last-resort agents such as carbapenems and colistin. The rise of antibiotic-resistant bacteria has prompted microbiologists to devise new strategies, with bacteriophages emerging as one of the most promising options. Nevertheless, certain mechanisms have been identified in bacteria that confer resistance to phages. While phage resistance is currently less widespread than antibiotic resistance, challenges such as biofilm formation, newly emerging resistance mechanisms against phages, and the natural limitations of unmodified phages have driven the advancement of engineered phages. This study aims to examine the efficacy of engineered phages and both engineered and recombinant endolysins against carbapenem-resistant Gram-negative bacteria (CR-GNB). We performed a literature review through PubMed, Scopus, Web of Science, and Google Scholar, concentrating on studies that utilized these agents against carbapenem-resistant Gram-negative bacteria (CR-GNB). Reviewed studies indicate potential antibacterial activity of these agents against CR-GNB. By engineering and modifying phages, these agents exhibit improved antimicrobial efficacy, temperature stability, and membrane permeability. Furthermore, they demonstrate the ability to eliminate bacteria with multidrug-resistant (MDR) and extensively drug-resistant (XDR) profiles. These findings suggest the promising potential of engineered phages and endolysins for future clinical applications against CR-GNB.

Multidrug-resistant Pseudomonas aeruginosa poses escalating threats in healthcare settings. This review highlights AmpC β-lactamase's key role in conferring β-lactam resistance. We investigate the regulatory network of ampR, ampD, and ampG genes that control AmpC expression, specifically how mutations cause enzyme overproduction. The study explores AmpC structural characteristics and mutations in conserved regions that improve catalytic performance against newer cephalosporins and carbapenems. The review covers the interaction between penicillin-binding proteins (PBPs) and AmpC β-lactamases, highlighting how PBP alteration affects enzyme production and resistance patterns. To combat resistant P. aeruginosa, we evaluate alternative therapeutic approaches, including collateral sensitivity strategies and phytochemicals as novel antimicrobials or antibiotic adjuvants. This review elucidates the complicated mechanisms that drive AmpC-mediated resistance, providing critical information that is directly applicable to healthcare practice. The findings help to develop personalized therapeutic methods, improve antimicrobial stewardship protocols, and design diagnostic tools for rapid resistance detection. By bridging molecular research to clinical practice, this study explains therapy failures and proposes new intervention techniques, such as phytochemical-enhanced combination therapies and collateral sensitivity methods. This comprehensive understanding promotes the development of precision treatment strategies, ultimately improving patient outcomes and preventing the spread of multidrug-resistant P. aeruginosa in healthcare facilities and communities.

Sesame phyllody, a destructive disease caused by phytoplasma infection, induces severe morphological abnormalities, including floral virescence, phyllody, witches' broom, leaf deformation, and stunted growth. This study aimed to characterize phytoplasma isolates from diverse regions of India, identifying them as Candidatus Phytoplasma asteris (16Sr-I), Candidatus Phytoplasma citri (16Sr-II), and Candidatus Phytoplasma australasia (16Sr-II). Whole-genome sequencing of Candidatus Phytoplasma asteris isolate SPGN revealed a genome size of 563,754 bp, encoding 542 proteins, including several genes associated with antibiotic resistance. Effector prediction analysis identified key virulence-associated proteins, such as SAP50-like, SAP34-like, TENGU-su inducer, and immunodominant membrane proteins, which manipulate host development and immune responses. Transcriptomic analysis of infected sesame plants revealed significant gene expression alterations, with upregulated genes linked to floral malformation, vascular tissue modifications, and stress responses, while the downregulated genes were associated with flavonoid metabolism and immune signaling. Phytoplasma infection disrupted hormonal pathways, leading to increased expression of auxin, cytokinin, and gibberellin-related genes, suggesting hormonal dysregulation as a key factor in symptom development. Furthermore, immune suppression was evident through the downregulation of key defense-related genes, including those involved in MAPK signaling and pathogenesis-related protein families. These findings enhance our understanding of phytoplasma pathogenesis in sesame and provide potential targets for developing effective disease management strategies.