Search

Cattle and other ruminants produce large quantities of methane (~110 million metric tonnes per annum), which is a potent greenhouse gas affecting global climate change. Methane (CH4) is a natural by-product of gastro-enteric microbial fermentation of feedstuffs in the rumen and contributes to 6% of total CH4 emissions from anthropogenic-related sources. The extent to which the host genome and rumen microbiome influence CH4 emission is not yet well known. This study confirms individual variation in CH4 production was influenced by individual host (cow) genotype, as well as the host’s rumen microbiome composition. Abundance of a small proportion of bacteria and archaea taxa were influenced to a limited extent by the host’s genotype and certain taxa were associated with CH4 emissions. However, the cumulative effect of all bacteria and archaea on CH4 production was 13%, the host genetics (heritability) was 21% and the two are largely independent. This study demonstrates variation in CH4 emission is likely not modulated through cow genetic effects on the rumen microbiome. Therefore, the rumen microbiome and cow genome could be targeted independently, by breeding low methane-emitting cows and in parallel, by investigating possible strategies that target changes in the rumen microbiome to reduce CH4 emissions in the cattle industry., Author summary Methane is a potent greenhouse gas and ruminant livestock contribute a substantial amount of total methane from human activities. Variation between cows’ methane production has been found partly due to their genetics (heritable), making genetic selection a promising strategy for breeding low methane emitting cows. We hypothesized that the total methane production by a cow is affected by rumen microbes which are directly responsible for production of methane, as well as the cows’ own genetics and their interaction. We sampled the rumen contents of 750 dairy cows and found the relative abundance of some bacteria and archaea to be heritable and associated with methane production, but the majority of variation in relative abundance of rumen bacteria and archaea is due to non-genetic factors. We compared the amount of variation in methane production associated with host genetics as well as rumen bacteria and archaea and found the host genetics to explain 21% and rumen microbes 13%. Importantly, the two were largely independent of each other, so breeding for low methane emitting cows is unlikely to result in unfavorable changes in the rumen microbiome. However, further functional annotation of rumen microbiota is needed to confirm this. Strategies that target each source of variation can be conducted in parallel to optimize reduction in methane production from dairy cows.

The human gastrointestinal (GI) tract is the habitat for hundreds of microbial species, of which many cannot be cultivated readily, presumably because of the dependencies between species 1. Studies of microbial co-occurrence in the gut have indicated community substructures that may reflect functional and metabolic interactions between cohabiting species 2,3. To move beyond species co-occurrence networks, we systematically identified transcriptional interactions between pairs of coexisting gut microbes using metagenomics and microarray-based metatranscriptomics data from 233 stool samples from Europeans. In 102 significantly interacting species pairs, the transcriptional changes led to a reduced expression of orthologous functions between the coexisting species. Specific species-species transcriptional interactions were enriched for functions important for H 2 and CO 2 homeostasis, butyrate biosynthesis, ATP-binding cassette (ABC) transporters, flagella assembly and bacterial chemotaxis, as well as for the metabolism of carbohydrates, amino acids and cofactors. The analysis gives the first insight into the microbial community-wide transcriptional interactions, and suggests that the regulation of gene expression plays an important role in species adaptation to coexistence and that niche segregation takes place at the transcriptional level.