Most bacterial pathogens are polylysogens, harboring multiple vertically transmitted prophages. These prophages enhance bacterial pathogenicity and survival by encoding virulence factors and antiphage defence systems while retaining the capacity for horizontal transfer. Thus, prophage-encoded anti-phage defences must block propagation of external phages without inhibiting the spread of the prophages that encode them. Here we identify HepS—an abortive infection system encoded on the Gifsy-1 prophage constituted of a single HEPN domain protein—which restricts phages of the Siphoviridae family. We demonstrate that in its native host context of Salmonella enterica serovar Typhimurium, HepS both senses phage infection and enacts abortive infection. Structures of HepS reveal a tetrameric nuclease complex that undergoes allosteric activation upon recognition of Siphoviridae tail tip proteins during production of new phage particles. Once activated, HepS cleaves specific transfer RNA anticodon loops and arrests phage replication. Gifsy-1, a Siphoviridae itself, evades self-targeting by expressing a tail tip variant that does not trigger HepS, as do co-resident Siphoviridae prophages Gifsy-2 and Gifsy-3. This evasion permits Gifsy-1 to spread despite encoding HepS. These findings reveal a mechanism by which a prophage defends the host while maintaining its propagation abilities. A Gifsy-1 prophage–encoded higher eukaryotes and prokaryotes nucleotide-binding protein, HepS, senses Siphoviridae infection, activates abortive defence by cleaving host transfer RNAs, blocks rival phages and avoids self-targeting via tail-tip variation.

De novo genes generally refer to genes that arise from previously non-coding sequences. This evolutionary path — when randomly expressed sequences become folded and active proteins — challenges our understanding of genetic innovation and has prompted studies to address the evolutionary and mechanistic knowledge gaps. More specifically, prior work has illuminated the mechanisms underlying the origin of de novo genes, their potential functional roles in the cell and the evolutionary processes that lead to these functions. Recent advances in both experimental and computational approaches have contributed to insights into the emergence of de novo genes and the broader implications for our understanding of biological complexity. In this Review, we place particular emphasis on efforts to quantify the likelihood of de novo gene emergence in eukaryotes given genomic characteristics, as well as the mechanisms by which de novo protein structures that are not actively selected against become amenable to selection-driven changes. De novo gene evolution entails the birth of new genes from previously non-coding DNA. In this Review, Bornberg-Bauer and Eicholt overview how protein-coding de novo genes are identified, the mechanistic and evolutionary processes underlying their emergence and evolution, and the patterns in their encoded protein structures.

Pesticides are widely distributed in soils, yet their effects on soil biodiversity remain poorly understood. Here we examined the effects of 63 pesticides on soil archaea, bacteria, fungi, protists, nematodes, arthropods and key functional gene groups across 373 sites spanning woodlands, grasslands and croplands in 26 European countries. Pesticide residues were detected in 70% of sites and emerged as the second strongest driver of soil biodiversity patterns after soil properties. Our analysis further revealed organism- and function-specific patterns, emphasizing complex and widespread non-target effects on soil biodiversity. Pesticides altered microbial functions, including phosphorus and nitrogen cycling, and suppressed beneficial taxa, including arbuscular mycorrhizal fungi AMF and bacterivore nematodes. Our findings highlight the need to integrate functional and taxonomic characteristics into future risk assessment methodology to safeguard soil biodiversity, a cornerstone of ecosystem functioning. A wide survey of pesticide effects on soil biodiversity across 373 sites in Europe reveals that pesticide residues occur in 70% of sites and have major effects on soil biodiversity and functional ecology.

Per- and polyfluoroalkyl substances (PFAS) are highly persistent environmental contaminants that pose a significant threat to ecosystems and human health due to their exceptional chemical stability and resistance to degradation. Conventional remediation methods—such as activated carbon adsorption, ion exchange, and advanced oxidation—primarily transfer PFAS between phases rather than achieving complete mineralization, resulting in the generation of secondary waste. Microbial bioremediation has emerged as a promising, sustainable strategy. Several bacteria, fungi, and cyanobacteria can transform or defluorinate PFAS under environmentally relevant conditions, yielding less fluorinated intermediates. Enzymatic studies have identified oxygenases and reductive dehalogenases as key catalysts in the cleavage of C–F bonds. Moreover, recent evidence indicates that the gut microbiota can adsorb and sequester PFAS, facilitating fecal elimination and reducing systemic toxicity. Advances in synthetic biology now enable the engineering of microbial systems, including probiotic strains, with enhanced PFAS uptake and degradation capabilities. However, significant challenges remain; current microbial pathways primarily act through partial transformation rather than complete mineralization, often accumulating stable fluorinated intermediates. True mineralization is constrained by low enzymatic efficiency, narrow substrate specificity, and the difficulty of translating laboratory success to complex environmental matrices. This review critically synthesizes current progress in microbial and probiotic bioremediation of PFAS, emphasizing enzymatic mechanisms, microbial pathways, and integration with conventional treatment systems. By engaging with these limitations alongside promising advances, we provide a balanced assessment of the feasibility of microbial and engineered probiotic approaches, highlighting knowledge gaps and future directions for developing safe, scalable detoxification technologies.

Ocean ecosystems are undergoing accelerating disruption from human impacts such as climate change. Warming ocean temperatures drive pathogenic outbreaks, increase harmful algal blooms and cause coral stress. These can have serious consequences for marine ecosystems, human health and the aquaculture industry, representing a critical One Health issue. Monitoring key marine species offers valuable insights, but current methods are resource-intensive, low-resolution and unsuitable for frequent deployment. Here we introduce a low-cost, field-deployable CRISPR biosensing platform for detecting marine organismal DNA and RNA. Harnessing the programmability of CRISPR diagnostics for environmental biosurveillance, we demonstrate versatility across three climate-linked indicators: Vibrio spp., Pseudo-nitzschia spp. and heat-stressed corals. Portable 3D-printed processor and incubator devices enable direct processing of filter-captured samples with temperature control. Field readiness is reinforced by lyophilized reagents, lateral flow readouts, dropper-based handling and a two-step multiplexed workflow, delivering results within 1 hour without laboratory instruments. Benchmarking with authentic pathogens and environmental seawater confirmed seawater tolerance and robust detection of 108 colony-forming units per filter of Vibrio pathogens, equivalent to 102 copies per microlitre for 1 litre of filtered sample. This decentralized platform reduces barriers to routine monitoring and can provide early warnings of ecosystem disturbances, while supporting One Health initiatives in the marine space. Human impacts on marine ecosystems are increasing the likelihood of pathogenic outbreaks, harmful algal blooms and coral stress. Here the authors develop a CRISPR biomonitoring tool that can help detect key marine species that are important to public health, the aquaculture sector and marine ecosystems.

Human genetic variation influences all aspects of our biology, including the oral cavity, through which nutrients and microbes enter the body. Yet it is largely unknown which human genetic variants shape a person’s oral microbiome and potentially promote its dysbiosis. We characterized the oral microbiomes of 12,519 people by re-analysing whole-genome sequencing reads from previously sequenced saliva-derived DNA. Human genetic variation at 11 loci (10 new) associated with variation in oral microbiome composition. Several of these related to carbohydrate availability; the strongest association (P = 3.0 × 10−188) involved the common FUT2 W154X loss-of-function variant, which associated with the abundances of 58 bacterial species. Human host genetics also seemed to powerfully shape genetic variation in oral bacterial species: these 11 host genetic variants also associated with variation of gene dosages in 68 regions of bacterial genomes. Common, multi-allelic copy number variation of AMY1, which encodes salivary amylase, associated with oral microbiome composition (P = 1.5 × 10−53) and with dentures use in UK Biobank (P = 5.9 × 10−35, n = 418,039) but not with body mass index (P = 0.85), suggesting that salivary amylase abundance impacts health by influencing the oral microbiome. Two other microbiome composition-associated loci, FUT2 and PITX1, also significantly associated with dentures risk, collectively nominating numerous host–microbial interactions that contribute to tooth decay. Human genetic loci that associate with composition of the oral microbiome are identified using saliva-derived DNA, where the same host genetics also shapes oral health and genetic variation in oral bacteria.

Serial multi-omic analysis of proteome, phosphoproteome, and glycoproteome is pivotal for elucidating drug mechanisms, discovering biomarkers, and identifying therapeutic targets. However, simultaneous multi-level post-translational modifications (PTM) analysis via parallel processing is hampered by laborious, time-consuming procedures and inconsistent reproducibility. We present an integrated Multi-level PTMs-Proteomic Enrichment platform (MuPPE), enabling sequential glycoproteome, phosphoproteome, and proteome analysis from single biological samples. It combines protein aggregation capture with on-bead digestion and tandem enrichment, achieving superior reproducibility (CV 12.3% vs 17.6% conventional methods) while reducing processing time by 87.5% (4 hours vs 32 hours). MuPPE also enhances coverage, identifying more serum glycopeptides and brain phosphopeptides than other platforms. Applied to aging mouse cohorts, the platform uncovers tissue-specific PTMs remodeling and brain barrier dysfunction. For arsenic mechanisms of action, MuPPE reveals drug-induced PTMs crosstalk between glycosylation and phosphorylation-driven pathway regulation. MuPPE offers a transformative tool for advancing multi-omics insights across precision medicine and disease research. Authors develop MuPPE, which enables integrated proteome, phosphoproteome, and glycoproteome profiling from a single sample, providing deeper biological insights into aging and drug-response mechanisms.

Understanding how high species diversity is maintained in natural bacterial communities is a central question in microbial ecology. Due to the versatile heterotrophic capacities of bacteria and the rich nutrients released by deceased bacterial cells, necromass recycling plays an important role in sustaining bacterial growth. Such nutrient cycling within communities can provide additional resource niches for bacteria, but its potential effects on bacterial diversity maintenance have been neglected. Here we conducted two independent experiments and studied the assembly of 276 soil-derived bacterial communities sustained by a wide range of bacterial necromass combinations, from single-species necromass to combinations of up to nearly 1,000 species. Our results highlight the existence of a species-rich bacterial necrobiome in soil. We found that the composition of necromass-decomposing communities was determined by the various organic compounds in the different necromass combinations, and the increases in necromass-producing species constantly promoted species diversity of necromass-decomposing communities. Moreover, the average niche breadth and overlap of coexisting necromass-decomposing species in utilizing distinct single-species necromass decreased with increases in necromass diversity, supporting the hypothesis of resource partitioning in utilizing different single-species necromass. Our study provides insights into diversity maintenance in bacterial communities from a perspective of internal nutrient cycling. In this study, the authors conduct experiments involving 276 soil-derived microcosms to reveal that the ecological process of necromass recycling promotes diversity maintenance in bacterial communities. This mechanism could help explain how high microbial species diversity is maintained in natural soil communities.

Ammonia oxidation, a critical nitrogen cycle process, exhibits contradictory responses to aquatic acidification, and the underlying mechanism remains unresolved. Here, through pH manipulation experiments across diverse ecosystems and with a model ammonia-oxidizing archaea species, Nitrosopumilus maritimus strain SCM1, we discover a unifying adaptive mechanism: acidification triggers a compensatory increase in substrate affinity in ammonia-oxidizing microorganisms. This enhancement counteracts the reduction in ammonia availability, with the magnitude of increase being significantly greater in ammonia-oxidizing archaea than in ammonia-oxidizing bacteria. Consequently, in ammonia-oxidizing archaea-dominated systems, this adaptation can sustain or even stimulate oxidation rates under moderate acidification, while ammonia-oxidizing bacteria-dominated systems experience a decline. By incorporating this affinity response into models, we accurately reconcile prior disparate field observations. We thus establish the regulation of substrate affinity as a key determinant of microbial resilience, providing a framework for predicting nitrogen cycle dynamics under future acidification. This study shows that acidification increases substrate affinity in ammonia-oxidizing microbes, partly offsetting reduced ammonia availability. Stronger responses in archaea than bacteria explain contrasting ecosystem reactions.