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The gut microbiome harbors a ‘silent reservoir’ of antibiotic resistance (AR) genes that is thought to contribute to the emergence of multidrug-resistant pathogens through horizontal gene transfer (HGT). To counteract the spread of AR, it is paramount to know which organisms harbor mobile AR genes and which organisms engage in HGT. Despite methods that characterize the overall abundance of AR genes in the gut, technological limitations of short-read sequencing have precluded linking bacterial taxa to specific mobile genetic elements (MGEs) encoding AR genes. Here, we apply Hi-C, a high-throughput, culture-independent method, to surveil the bacterial carriage of MGEs. We compare two healthy individuals with seven neutropenic patients undergoing hematopoietic stem cell transplantation, who receive multiple courses of antibiotics, and are acutely vulnerable to the threat of multidrug-resistant infections. We find distinct networks of HGT across individuals, though AR and mobile genes are associated with more diverse taxa within the neutropenic patients than the healthy subjects. Our data further suggest that HGT occurs frequently over a several-week period in both cohorts. Whereas most efforts to understand the spread of AR genes have focused on pathogenic species, our findings shed light on the role of the human gut microbiome in this process., Linking antibiotic resistance (AR) in the gut microbiome with their bacterial hosts remains challenging. Here, the authors apply bacterial Hi-C to map mobile genetic elements in metagenomes, and illustrate that genes are present in more diverse taxa in neutropenic patients than healthy subjects.

Ocean temperatures will increase significantly over the next 100 years due to global climate change1. As temperatures increase beyond current ranges, it is unclear how adaptation will impact the distribution and ecological role of marine microorganisms2. To address this major unknown, we imposed a stressful high-temperature regime for 500 generations on a strain from the abundant marine Roseobacter clade. High-temperature-adapted isolates significantly improved their fitness but also increased biofilm formation at the air-liquid interface. Furthermore, this altered lifestyle was coupled with genomic changes linked to biofilm formation in individual isolates, and was also dominant in evolved populations. We hypothesize that the increasing biofilm formation was driven by lower oxygen availability at elevated temperature, and we observe a relative fitness increase at lower oxygen. The response is uniquely different from that of Escherichia coli adapted to high temperature3 (only 3% of mutated genes were shared in both studies). Thus, future increased temperatures could have a direct effect on organismal physiology and an indirect effect via a decrease in ocean oxygen solubility, leading to an alteration in microbial lifestyle.

Microorganisms exhibit shifts in elemental stoichiometry in response to short-term temperature increases due to varying growth rate, biochemical reactions, and protein degradation. Yet, it is unknown how an organism’s elemental stoichiometry will respond to temperature change on evolutionary timescales. Here we ask how cellular elemental stoichiometry and physiology change in Escherichia coli that have adapted to high temperature over 2,000 generations compared to their low temperature adapted ancestor. Cell lines evolved to a temperature of 42.2°C via two, negatively epistatic adaptive pathways leading to mutations in either the RNA polymerase complex or the termination factor rho. Compared to the ancestor, high temperature adapted cell lines overall had 14% higher N:P ratios, but did not differ significantly in C:N or C:P. However, cell lines with mutations in the rho gene had 13% lower C:N and 34% higher N:P. Furthermore, the two adaptive strategies of the rho and RNA polymerase mutations varied significantly from one another, cell lines with the rho mutation had lower C:N, higher N:P and higher protein content compared to cell lines with the RNA polymerase mutation. Thus, specific adaptive pathways modulate the effect of temperature on the cellular elemental stoichiometry and may explain why the elemental composition of specific lineages is differentially affected by temperature changes.