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Merenstein, C.

Publications and source records attributed to Merenstein, C..

2 recordsLinked to original sources

Tree microbiomes and methane emissions in upland forests

RationaleUpland forest trees emit CH , but whether emissions derive from internal microbial production or soil-derived transport remains debated. Methanogens have been detected in heartwood of several species, yet the prevalence of wood-associated methanogenesis, its metabolic basis, and its relationship to co-occurring methanotrophy are poorly understood. MethodsWe measured 1,148 stem fluxes and 276 soil fluxes, sampled internal stem gases including {delta}{superscript 1}3CH , quantified methanogens and methanotrophs via ddPCR in 564 samples, characterized communities via 16S rRNA sequencing, and upscaled fluxes. Key resultsMethanogens were detected in 97% of heartwood samples (up to 10 copies g {superscript 1}) at concentrations exceeding soil by [~]2 orders of magnitude; methane consumers were likewise near-ubiquitous across forest compartments. Wood harbored distinct microbial communities dominated by hydrogenotrophic Methanobacteriaceae, corroborated by depleted {delta}{superscript 1}3CH . Vertical flux profiles indicated soil transport only in wet microsites, with uniform emissions across height consistent with internal production across most upland species. Species-level methanogen:methanotroph ratios predicted emissions (R{superscript 2} = 0.51), indicating net flux reflects the balance between production and oxidation. Main conclusionMethane-cycling microbes are widespread in upland trees, and net methane flux reflects the species-level balance between production and consumption. Internal methanogenesis contributes widely to upland tree emissions; resolving ecosystem-scale magnitude requires improved quantification of woody surface area and vertical flux variability.

ecology↗

Interactions between the gut microbiome, dietary restriction, and aging in genetically diverse mice

The intestinal microbiome changes with age, but the causes and consequences of microbiome aging remain unclear. Furthermore, the gut microbiome has been proposed to mediate the benefit of lifespan- extending interventions such as dietary restriction, but this hypothesis warrants further exploration. Here, by analyzing 2997 metagenomes collected longitudinally from 913 deeply phenotyped, genetically diverse mice, we provide new insights into the interplay between the microbiome, aging, dietary restriction, host genetics, and a wide range of health parameters. First, we find that microbiome uniqueness increases with age across datasets and species. Moreover, age-associated changes are better explained by cumulative exposure to stochastic events (neutral theory) than by the influence of an aging host (selection theory). Second, we unexpectedly find that the majority of microbiome features are significantly heritable and that the amount of variation explained by host genetics is as large as that of aging and dietary restriction. Third, we find that the intensity of dietary restriction parallels the extent of microbiome changes and that dietary restriction does not rejuvenate the microbiome. Lastly, we find that the microbiome is significantly associated with multiple health parameters -- including body composition, immune parameters, and frailty -- but not with lifespan. In summary, this large and multifaceted study sheds light on the factors influencing the microbiome and aspects of host physiology modulated by the microbiome.

microbiology↗