The growing global plastic waste crisis demands the development of urgent, effective, and sustainable solutions. While conventional recycling methods present intrinsic limitations, microbial biodegradation of plastic waste has emerged as a promising alternative. In this review, we explore the potential of using microorganisms to degrade major hydrocarbon-based plastic polymers and discuss key aspects of this rapidly advancing field, including (i) isolation and characterization of novel microorganisms and enzymes in hydrocarbon-based plastic biodegradation, (ii) development and streamlining of microbial consortia to improve hydrocarbon-based plastic biodegradation efficiency, and (iii) investigation of natural biodegradation processes to illustrate the relationship between plastic degradation and environmental influence. We highlight practical biotechnological approaches and advanced computational tools in hydrocarbon-based plastic degradation, as hydrocarbon-based plastic represents the highest proportion of plastic waste while still lacking effective conversion strategies. Our ultimate goal is to integrate microbial biodegradation strategies into modern waste-management systems and offer a feasible pathway toward a circular bioeconomy, one in which persistent plastic polymers are no longer treated as waste but are converted into renewable feedstocks that support sustainable resource recovery.

The land−sea interface is a vital component of global biogeochemical cycles, where microorganisms drive the cycling of carbon, nitrogen, and sulfur. This review synthesizes the research progress from representative land−sea interfaces to elucidate how the microbial community structure and metabolic function influence the mobilization, transformation, and retention of organic carbon. Here, we also review the mechanisms underlying carbon cycle dynamics and emphasize the role of coupled biogeochemical cycles and climate change. A key focus is the synergistic interaction among the marine microbial carbon pump (MCP), the soil MCP, and the mineral-associated carbon pump, hereafter referred to as the land−sea MCP framework. We further propose an integrated study framework, based on measurable parameters such as carbon use efficiency and bacterial growth efficiency, to link microbial processes to long-term carbon sequestration at the land−sea interface.

Toxin–antitoxin (TA) systems found in diverse bacteria play important roles in their adaptation to changing environments. The toxin of the Fic-1–AntF TA pair from Pseudomonas bijieensis strain 2P24 inhibits bacterial DNA replication by attacking the subunit B of DNA gyrase (GyrB) via AMPylation, while the antitoxin AntF blocks its enzymatic activity by forming a stable protein complex. Although many proteins, including bacterial toxins, have been found to catalyze AMPylation, few enzymes involved in reversing this modification have been described. In this study, we found that the Fic-1–AntF complex functions as a deAMPylase to reverse GyrB modification imposed by Fic-1. Structural and genetic analyses of the Fic-1–AntF complex revealed that Glu28 of AntF is critical for catalysis. Thus, AntF not only functions to inhibit the activity of Fic-1 but also cooperates with the toxin to return the modified substrate to its native form by de-modification. Our results reveal a novel regulatory mechanism for bacterial toxin, which sheds light on the evolution of such enzymes, particularly those of multiple subunits.

Biological nitrogen fixation in symbiotic diazotrophs is subject to oxygen regulation by an oxygen-sensing FixLJ two-component system under micro-oxic conditions. However, it remains unclear whether this mechanism is conserved in free-living diazotrophs. In this study, we discovered for the first time that FixLJ strongly inhibits the expression of nifHDK genes that encode molybdenum nitrogenase in response to oxygen. The deletion of fixLJ genes, whose expression was stimulated by oxygen, allowed a free-living photosynthetic diazotroph Rhodopseudomonas palustris to express active nitrogenase and grow diazotrophically even under oxic conditions. The unphosphorylated FixJ protein showed high-affinity binding to the promoter of nitrogenase gene cluster (P_nifH) and strongly repressed the nitrogenase expression in response to oxygen. The transcriptional repression of nifHDK by FixJ reveals a new regulatory role for the FixLJ system. In addition, transcriptome analysis suggested that the FixLJ regulatory system also plays a role in the energy metabolism of R. palustris, probably through FixK regulation. This newly identified mechanism is speculated to allow R. palustris to rapidly shut down the synthesis of nitrogenase when exposed to oxygen, avoiding the build-up of nitrogenase with impaired activity due to the lack of protection from oxygen damage.

The elongasome, or the Rod complex, orchestrates lateral peptidoglycan (PG) synthesis in many rod-shaped bacteria. It consists of the actin-like protein MreB, the PG synthase RodA-PBP2 complex, as well as MreCD and RodZ. Although the loss or disruption of any elongasome component results in a loss of rod shape, previous studies found that a constitutively active RodA-PBP2 complex can partially bypass the requirement of MreCD and RodZ for lateral PG synthesis and restore rod shape. However, how MreB is connected to RodA-PBP2 under this situation and whether this linkage is important for elongasome activity in wild-type cells remain unknown. Here, we report the isolation of additional RodA and PBP2 variants that can partially compensate for the absence of MreCD and RodZ in lateral PG synthesis. Taking advantage of these mutants and guided by an AlphaFold 3 structural model of the elongasome complex, we discover that both the cytoplasmic region of PBP2 and the C-terminal tail of RodA interact with MreB. Moreover, disruption of these interactions results in a loss of rod shape, indicating that the interaction between MreB and RodA-PBP2 is critical for elongasome function. Taken together, our results uncover how the MreB cytoskeleton is coupled to RodA-PBP2 to organize lateral PG synthesis. These findings provide mechanistic insights into cell wall biogenesis in bacteria and offer strategies for the development of new antibiotics targeting the elongasome.

The mechanism of SARS-CoV-2 egress predominantly governs the quantity and quality of progeny viruses, thereby significantly contributing to viral pathogenicity. However, the key factors influencing viral egress remain largely unclear. In this study, using transcription- and replication-competent SARS-CoV-2 virus-like-particle (SARS-CoV-2 trVLP), electron microscopy, drug inhibition assays, and cellular pH-sensitive fluorescent probes, we demonstrate that increased lysosomal exocytosis efficiency and lysosome deacidification play a pivotal role in facilitating SARS-CoV-2 egress. Specifically, SARS-CoV-2 may use multiple egress pathways, with lysosomal exocytosis as the primary mechanism and the biosynthetic secretory pathway as a less efficient route. Viral infection enhances lysosomal exocytosis via the ORF3a protein, thus facilitating viral release. SARS-CoV-2 infection also induces lysosome deacidification; moreover, treatment with bafilomycin A1, which induces lysosome deacidification, further enhances viral egress. Furthermore, we systematically investigate how viral proteins affect lysosomal pH and enzymatic activities. Our findings reveal that ORF3a and E proteins induce lysosome deacidification and diminish lysosomal enzyme activities, probably protecting progeny viruses from premature cleavage and degradation. This study provides mechanistic insight into how SARS-CoV-2 promotes lysosomal exocytosis and triggers lysosome deacidification for viral release.

Multidrug-resistant (MDR) bacteria pose a critical global health threat, urgently requiring solutions. Cefdinir, the highest-selling third-generation cephalosporin but one now facing clinical obsolescence due to escalating resistance, is conventionally classified as a nascent cell wall synthesis inhibitor. This study challenges this understanding by demonstrating that cefdinir renders existing cell walls negatively charged, thereby synergizing with ubiquitous lysozyme and simultaneously restoring both agents' efficacy against a broad spectrum of MDR Gram-positive superbugs without driving resistance. Specifically, cefdinir is unexpectedly shown to post-transcriptionally increase the levels of clustered enzymes in lipoteichoic acid (LTA) and wall teichoic acid (WTA) synthesis pathways, including TarA, TarB, TarD, TarF, TarH, TarK, TarL, TarS, and FmtA, thereby enhancing cell wall electronegativity to remodel existing cell wall into a lysozyme-susceptible state, in which TarS is identified for the first time by mass spectrometry. The combination of cefdinir and lysozyme also significantly suppresses biofilm formation and minimizes de novo resistance mutations. Antibacterial efficacy of combination therapy is validated in both cell-based infection models and rat skin infection models, demonstrating strong translational potential. Given the established safety profiles of both agents, this sensitization strategy can be applied to human clinical research to combat MDR Gram-positive bacterial infections.

Antimicrobial resistance poses an escalating global threat, renewing interest in bacteriophage therapy as a precision alternative to antibiotics. However, clinical translation remains hindered by the lack of rapid and quantitative phage susceptibility testing (PST) platforms capable of evaluating host range, infection potency, and effective multiplicity of infection (MOI). Here, we present a ramanome-based phage susceptibility test (RPST), a phenotypic platform that captures infection-induced remodeling of bacterial macromolecular composition to unify these diagnostic requirements within a single workflow. RPST integrates four Raman biomarkers into a Composite Infection Index (CII), enabling rapid and lysis-independent discrimination between susceptible and resistant bacterial populations within ~1 h, with 96.0% categorical concordance (24/25) to plaque assays. As a continuous population-level metric, CII quantifies the proportion of infected cells, allowing quantitative ranking of phage potency against shared hosts. By resolving CII trajectories across the MOI and time, RPST further determines the minimal effective MOI, which is the lowest phage-to-bacterium ratio sustaining self-propagating infection, thereby defining the lower boundary for therapeutic feasibility. Together, these capabilities transform PST from static compatibility assays into a dynamic and quantitative framework that bridges in vitro infectivity assessment and infection dynamics relevant to phage therapy.

Antibiotic resistance in plant pathogens threatens sustainable crop protection, and yet, its molecular basis remains incompletely understood. We report that streptomycin resistance in Clavibacter michiganensis strain TX-0702 is mediated by a plasmid-borne aminoglycoside phosphotransferase, APH(3), encoded on an uncharacterized plasmid, pCM3. Functional and biochemical analyses demonstrate that APH(3) inactivates streptomycin through phosphorylation, establishing a phosphorylation-driven resistance mechanism in Gram-positive plant pathogens. Sequence analyses reveal that pCM3 carries mobile genetic elements, suggesting environmental dissemination of resistance genes in plant-associated microbes. These findings expand understanding of phytopathogen antibiotic resistance and plant microbiomes as potential resistance gene sources for agricultural, food, and human health safety.

Protists are an underexplored but functionally important component of aerobic-activated granular sludge under pollution stress. Using metagenomics, we profiled protistan responses to ciprofloxacin, triclosan, and Cu²⁺ (alone or in combination). Protists remained a stable 6.35%–7.88% of the bacterial community, and the consumers were the most abundant groups. Ciprofloxacin showed little effect on protist abundance, while Cu²⁺ increased protist abundance, especially consumers. Stress conditions also strengthened predominantly positive protist–bacteria associations, suggesting cross-domain interactions that may enhance community resilience. These results demonstrate that protists are key determinants in stabilizing microbial communities under multiple stressors.