Nucleic acid testing is important for infectious-disease diagnosis, but combining high sensitivity with accessible testing remains challenging. Here we show a chip-based visual detection strategy for one or two viral RNA targets that involves only sample loading, without further instrumentation or manual actuation. Target-activated CRISPR-Cas13a alters the wettability of a molecular barrier, causing liquid to cross a preset threshold and generate a dam-break drainage signal. The chip detects a single target at 10 aM within 2 min and two targets at 100 aM within 5 min, with costs of $0.20 and $0.30 per test, respectively. We further establish a practical clinical-sample workflow combining room-temperature lysis with RNase inhibition and validate the platform across 40 nasal-swab samples tested for SARS-CoV-2, influenza A virus and influenza B virus, with results concordant with RT–PCR. This threshold-based fluidic strategy provides a route towards rapid, low-cost and instrument-free molecular testing outside centralized laboratories. Nucleic acid testing is central to infectious-disease diagnosis, and methods which combine high sensitivity with operational simplicity and ease of interpretation are particularly desirable. Here the authors present their CRISPR-based ‘dam-break drainage’ chip, where a positive result is clearly visualised via the release of test liquid from a sample reservoir.

Phosphorus (P) availability is closely associated with algal bloom types, yet filamentous attached algae frequently proliferate in clear waters or low-P systems. To examine associations between algal dominance and microbial P-cycling potential, sediment–periphyton assemblages from a low-P artificial water-diversion canal were incubated for 120 days under three water matrices representing oligotrophic, lake-like, and eutrophic conditions. Algal dominance was assessed by microscopy and metagenomic relative abundance profiling, together with sediment P fractions, bacterial communities, and P-cycling genes. Filamentous attached algae remained dominant under low-P treatments, accompanied by depletion of sediment P, especially redox-sensitive BD-P, and higher relative abundances of genes associated with P scavenging and organic P utilization, including aphA and glpQ. In contrast, eutrophic treatments were associated with planktonic algae accounting for more than 70% of the algal community at the bloom stage and with distinct bacterial assemblages and P-cycling gene profiles. Candidate phosphate-solubilizing taxa, including Ideonella, Runella, Sphingopyxis, and Gemmatimonas, were statistically associated with community variation. These results suggest that the level of P in the water, microbial P-cycling potential, and sediment P dynamics may jointly contribute to algal niche differentiation at the water–sediment interface, providing a framework for understanding filamentous algal proliferation in low-P aquatic systems.

Mycorrhizal fungi play crucial roles in enhancing plant adaptation to heavy metal (HM)stress by interacting with host plants and other root microbiota, yet the molecular mechanisms underlying these interactions remain unclear. To elucidate how ectomycorrhizal fungi (EMF) mediate molecular dialogue between root-associated fungi and host plants under HM stress, we employed root metatranscriptomic analyses on a Pinus-Suillus system across a gradient of soil HM contamination. Our findings revealed that HM contamination significantly reduced both the richness and transcriptional activity of root-associated fungi, shown by the number and expression levels of detected genes. S. hirtellus inoculation effectively restored fungal community composition and enhanced functional potential under HM stress, particularly benefiting EMF taxa (Rhizopogon and Suillus) and dark septate endophytes (Phialocephala and Hyaloscypha). Additionally, S. hirtellus inoculation reconstructed the relationships between root-associated fungi and P. taeda towards more targeted and specialized symbiotic partnerships to primarily reactivate pathways involved in metal exclusion and detoxification, core metabolic activities, and nutrient exchange, ultimately mitigating HM toxicity and promoting plant growth. Collectively, our study provides mechanistic insights into how EMF improve plant fitness by reshaping plant-fungal coordination under HM stress, advancing our understanding of mutualistic strategies that support forest ecosystem sustainability in contaminated environments.

Soils are among the most diverse but least understood environments on the planet. Just below our feet, secluded from our sight, we find complex communities of bacteria, fungi, protists and animals. These communities organize themselves in both time and space, from fast to slow growers, from decomposers to predators, from early colonizers to late arrivers. Despite a growing understanding of community dynamics, the lives of organisms within the soil often remain poorly understood: how do organisms grow, propagate, and disperse within their particle-packed environments? In this essay, I reflect on the microbial life cycles found in soils. Starting from a single gram of soil collected on our campus, I explore the conceptual building blocks underlying life cycle biology, how life cycles emerge within their environment and how they are coupled between species. Microbes express widely diverse life cycle motifs with many unique life stages promoting growth and/or propagation. These life stages have a major impact on community ecology; they determine the fate of microbes within soils and affect how, when, and where microbes interact. A life cycle perspective is thus essential for deepening our understanding of the community dynamics that unfold underfoot.

E. coli is a prototroph and can synthesize all twenty proteinogenic amino acids when required to grow in minimal medium. There are approximately sixty protein-coding genes individually essential for amino acid synthesis. This is a large mutational target for the accumulation of detrimental mutations. E. coli can rewire biosynthetic pathways in response to mutational damage, but the limits of this capacity are poorly understood. Here, to address evolutionary robustness, we asked whether and how the phenotypes of irreversible mutations causing auxotrophy could be suppressed or bypassed in the absence of horizontal gene transfer (HGT). Spontaneous suppressors could be selected for only ten of fifty-nine mutants tested (detection limit ∼7x10-11). Mechanisms of suppression included: regional amplifications; mutations increasing gene or operon expression; mutations relaxing enzyme specificity; and mutations causing biochemical pathway diversions. Overall, the data show that spontaneous suppression of auxotrophy caused by an irreversible mutation is an evolutionary survival mechanism relevant only to a minority of the genes essential for amino acid synthesis. As a consequence, the essential genetic foundations for amino acid prototrophy are expected to be degraded over time by mutations (Muller’s ratchet) and metabolic rewiring alone will be insufficient to counteract this effect. This implies that maintaining phenotypes, including prototrophy in E. coli, and potentially other bacterial species, is likely to be reliant on HGT of housekeeping genes to counteract the effects of inevitable mutational inactivation. Accordingly, chromosomal HGT in bacteria may be critical for survival across diverse environmental niches.

Human artificial chromosomes (HACs) are engineered, chromosome-scale DNA molecules that replicate and segregate autonomously in mammalian cells, offering a unique platform for large, stable, nonintegrating genetic delivery. The first generation of HACs emerged prior to synthetic genomics efforts, and their development has aided understanding of chromosome structure and centromere function. In parallel, microbial synthetic genomics demonstrated that entire viral, bacterial, and yeast chromosomes can be designed, synthesized, assembled, and functionally validated, establishing core principles for genome-scale engineering. Recent advances in large DNA assembly, long-read sequencing, and epigenetic centromere specification now position HACs within this broader synthetic genomics framework. We review and integrate lessons from microbial systems with advances in mammalian chromosome biology and discuss how HACs are becoming increasingly precise and customizable platforms. Current efforts promise to expand their potential for gene and cell therapy, functional genomics, humanized models, and the rational construction of synthetic mammalian genomes.