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Toffano, A.

Publications and source records attributed to Toffano, A..

2 recordsLinked to original sources

Micro-scale spatial metagenomics: revealing high-resolution spatial biogeography of gut microbiomes

Spatial organisation is a fundamental yet poorly resolved aspect of gut microbial ecology. Conventional shotgun metagenomics provides rich functional information but relies on homogenised, macro-scale samples that obscure the micron-scale distributions critical for understanding microbial community dynamics. Here, we introduce Micro-Scale Spatial Metagenomics (MSSM), a new methodological framework that couples laser micro-dissection of tissue sections, ultra-low-input library preparation, and genome-resolved bioinformatics to reconstruct microbial communities from intestinal microsamples measuring as little as [~]500 {micro}m{superscript 2} ({approx}100 bacterial cells). We describe a fully optimised laboratory and computational pipeline that enables quantitative, strain-resolved, and functionally informed spatial profiling directly from intact gut tissue. Using chicken intestinal samples, we validated MSSM through combinatorial single-cell fluorescence in situ hybridisation (FISH) imaging and comparisons with macro-scale metagenomics, demonstrating its robustness and accuracy. MSSM captured fine-scale heterogeneity in taxonomic and functional composition across intestinal cryosections, hinting at spatially structured assemblages and segregation of metabolic capacities. Strain-level analyses uncovered coexisting Lawsonibacter lineages exhibiting distinct spatial distributions and host-specific occurrence patterns, while SNP-level microdiversity analyses showed that genetically coherent clonal populations cluster at spatial scales below [~]200 {micro}m. By enabling shotgun metagenomics at micron resolution, MSSM closes a longstanding methodological gap and provides a scalable platform for studying microbial ecosystems in situ. This approach unlocks a previously inaccessible view of microbial biogeography, offering new opportunities to investigate host-microbe and microbe-microbe interactions, and the spatial principles governing gut ecosystems. Significance statementUnderstanding how microbial communities are organised in space is essential to explaining their ecological and functional roles, yet microbiome research still relies overwhelmingly on bulk, spatially averaged measurements. We introduce micro-scale spatial metagenomics (MSSM), the first method that brings shotgun metagenomics to the microscale, enabling direct measurement of functional and taxonomic variation across regions containing as few as [~]100 cells. Unlike existing spatial approaches, MSSM reconstructs complete genomes and resolves strain-level diversity within intact tissue, allowing researchers to map metabolic potential, microdiversity, and community structure in situ. By coupling high-resolution sequencing with spatial context, MSSM reveals a previously inaccessible layer of microbial organisation, transforming how host-associated ecosystems can be studied.

microbiology↗

The balance between ATR and DDK activities controls TopBP1-mediated locking of dormant origins at the pre-IC stage

Replication stress, a major hallmark of cancers, and ensuing genome instability source from impaired progression of replication forks. The first line of defense against fork slowing is compensation, a long-described process that elicits firing of otherwise dormant origins. It remains unclear whether compensation requires activation of the DNA replication checkpoint or passively results from lengthening of the window of time during which dormant origins can fire when fork progression slows, or both. Using molecular DNA combing we show here that a linear relationship ties inter-origin distances to fork speeds, independently of the checkpoint status. We called this line "stressline" and further show that its slope enables precise quantification of the compensation efficiency. Comparison of the slopes in different genetic backgrounds reveals that compensation requires ATR, not CHK1, while TopBP1 and CDC7/DBF4 repress dormant origin activation. These results strongly suggest that TopBP1 locks dormant origins at the pre-IC stage and that ATR and DDK oppose to control the conversion of dormant pre-ICs into functional salvage origins. Both passive and active processes thus contribute to compensation. Moreover, Repli-seq and OK-seq analyses confirm the activating role of ATR and permit development of ATRAP-seq, a new procedure allowing mapping of early constitutive origins.

genetics↗