Humans are inextricably linked to each other and our natural world, and microorganisms lie at the nexus of those interactions. Microorganisms form genetically flexible, taxonomically diverse, and biochemically rich communities, i.e., microbiomes that are integral to the health and development of macroorganisms, societies, and ecosystems.

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Microbial communities inhabit spatial architectures that divide a global environment into isolated or semi-isolated local environments, which leads to the partitioning of a microbial community into a collection of local communities. Despite its ubiquity and great interest in related processes, how and to what extent spatial partitioning affects the structures and dynamics of microbial communities is poorly understood. Using modeling and quantitative experiments with simple and complex microbial communities, we demonstrate that spatial partitioning modulates the community dynamics by altering the local interaction types and global interaction strength. Partitioning promotes the persistence of populations with negative interactions but suppresses those with positive interactions. For a community consisting of populations with both positive and negative interactions, an intermediate level of partitioning maximizes the overall diversity of the community. Our results reveal a general mechanism underlying the maintenance of microbial diversity and have implications for natural and engineered communities.

Many ecosystems retain an ecological memory of past conditions that affects responses to future stimuli. However, it remains unknown what mechanisms and dynamics may govern such a memory in microbial communities. Here, in both a human dietary intervention cohort and an artificial gut, we show that the human gut microbiome encodes a memory of past carbohydrate exposures. Changes in the relative abundance of primary degraders were sufficient to enhance metabolism, and these changes were mediated by transcriptional changes within hours of initial exposure. We further found that ecological memory of one carbohydrate species impacted metabolism of others. These findings demonstrate that the human gut microbiome's .

Many ecosystems retain an ecological memory of past conditions that affects responses to future stimuli. However, it remains unknown what mechanisms and dynamics may govern such a memory in microbial communities. Here, in both a human dietary intervention cohort and an artificial gut, we show that the human gut microbiome encodes a memory of past carbohydrate exposures. Changes in the relative abundance of primary degraders were sufficient to enhance metabolism, and these changes were mediated by transcriptional changes within hours of initial exposure. We further found that ecological memory of one carbohydrate species impacted metabolism of others. These findings demonstrate that the human gut microbiome's metabolic potential reflects dietary exposures over preceding days and changes within hours of exposure to a novel nutrient.

Akkermansia muciniphila, a prominent member of the gastrointestinal tract (GI) microbiota, uses mucins as a sole source of carbon and nitrogen. A. muciniphila is considered a next-generation probiotic because its abundance in humans positively correlates with protection from metabolic syndrome and obesity. However, A. muciniphila is intractable to genetic analysis and thus the molecular mechanisms underlying the metabolism of mucin, its colonization of the GI tract, and its impact on host physiology are poorly understood. Here, we developed and applied transposon mutagenesis to identify A. muciniphila factors important for the use of mucin and determined that mucin degradation products accumulate in internal compartments through a process that requires pili and a periplasmic protein complex. We further determined that the degradation of mucin and related proteoglycans is important for colonization of the GI by A. muciniphila but only in the context of competing microbes. In germ free mice, mucin use by A. muciniphila repressed the expression of host genes required for mevalonate and cholesterol biosynthesis in the colon, providing a molecular link between A. muciniphila metabolism of mucins, the regulation of lipid homeostasis and potential probiotic activities.

The infant gut microbiome is a crucial factor in health and development. In preterm infants, altered gut microbiome composition and function have been linked to serious neonatal complications such as necrotizing enterocolitis and sepsis, which can lead to long-term disability. Although many studies have described links between microbiome composition and disease risk, there is a need for biomarkers to identify infants at risk of these complications in practice. In this study, we obtained stool samples from preterm infant participants longitudinally during the first postnatal months, and measured pH and redox, as well as SCFA content and microbiome composition by 16S rRNA gene amplicon sequencing. These outcomes were compared to clinical data to better understand the role of pH and redox in infant gut microbiome development and overall health, and to assess the potential utility of pH and redox as biomarkers. We found that infants born earlier or exposed to antibiotics exhibited increased fecal pH, and that redox potential increased with postnatal age. These differences may be linked to changes in SCFA content, which was correlated with pH and increased with age. Microbiome composition was also related to birth weight, age, pH, and redox. Our findings suggest that pH and redox may serve as biomarkers of metabolic state in the preterm infant gut.