bioRxiv Science⌕ Search

bioRxiv · 10.1101/383067

Changes in rumen microbiota of cows in response to dietary supplementation with nitrate, linseed and saponin alone or in combination.

Abstract

Dietary supplementation with linseed, saponins and nitrate is a promising methane mitigation strategy in ruminant production. The main objective of this work was to assess the effects of these additives on the rumen microbiota in order to understand underlying microbial mechanisms of methane abatement. Two 2 x 2 factorial design studies were conducted simultaneously, which also allowed us to make a broad-based assessment of microbial responses. Eight non-lactating cows were fed diets supplemented with linseed or saponin in order to decrease hydrogen production and nitrate to deviate hydrogen consumption; also, combinations of linseed plus nitrate or saponin plus nitrate were used to explore the interaction between dietary treatments. Amplicon sequencing of 18S and 16S rRNA genes was employed to characterise rumen microbes. Nitrate fed alone or in combination in both studies dramatically affected the composition and structure of rumen microbiota, though impacts were more evident in one of the studies. Linseed moderately modified bacterial community structure with no effect on rumen methanogens and protozoa. Indicator OTU analysis revealed that both linseed and nitrate reduced the relative abundance of hydrogen-producing Ruminococcaceae. Linseed increased the proportion of bacteria known to reduce succinate to propionate, whereas nitrate supplementation increased nitrate-reducing bacteria and decreased the metabolic activity of rumen methanogens. Saponins had no effect on the microbiota. Inconsistency found between the two studies, when nitrate was fed to the cows could be explained by changes in microbial ecosystem functioning rather than changes in microbial community structure.\n\nImportanceThis study aimed at identifying the microbial mechanisms of enteric methane mitigation when linseed, nitrate and saponins were fed to non-lactating cows alone or in a combination. Hydrogen is a limiting factor in rumen methanogenesis. We hypothesised that linseed and saponins would affect hydrogen producers and nitrate would deviate hydrogen consumption thus leading to reduced methane production in the rumen. Contrary to what was foreseen, both linseed and nitrate had a deleterious effect on hydrogen producers; linseed also redirected hydrogen consumption towards propionate production, whereas nitrate stimulated the growth of nitrate reducing and hence hydrogen-consuming bacterial taxa. Fundamental knowledge of microbial mechanism involved in rumen methanogenesis, provides novel insights for the development of new or the optimisation of existing methane mitigation strategies.

Source connections

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Popova, M., Guyader, J., Silberberg, M., Seradj, A. R., Saro, C., Bernard, A., Gerard, C., Martin, C., Morgavi, D. P.. 2018-08-02. Changes in rumen microbiota of cows in response to dietary supplementation with nitrate, linseed and saponin alone or in combination.. https://doi.org/10.1101/383067

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

SF3b inhibitors suppress proliferation of nonsmall cell lung cancer cells irrespective of EGFR mutation status

Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) are standard care for EGFR-mutant non-small cell lung cancer (NSCLC), but acquired resistance limits their durability, and alternatives that do not depend on EGFR kinase activity are needed. We asked whether inhibitors of SF3b, a core component of the U2 small nuclear ribonucleoprotein particle, act on NSCLC cells regardless of EGFR genotype. Three lung adenocarcinoma lines were treated with pladienolide B or herboxidiene at 0.01, 0.1 and 1 uM: PC9 and HCC827, both carrying an EGFR exon 19 deletion and both inhibited by gefitinib at nanomolar concentrations, and A549, which is EGFR wild type and gefitinibin sensitive. Proliferation was followed for three days by crystal violet staining, EGFR intron 2 retention was assayed by RTPCR, and EGFR protein was measured by western blotting. Both compounds produced a concentration-dependent increase in the intron 2 retained product in all three lines, and both held proliferation at or near the day 0 cell number in all three, at concentrations down to 0.01 uM. EGFR protein was lost in PC9, reduced in A549, and only partly reduced in HCC827, where a residual band persisted in lanes whose growth was fully suppressed. Since A549 is EGFR wild-type, and published knockdown data show that removing EGFR does not suppress proliferation of wild-type lines, the growth inhibition cannot be attributed to loss of EGFR alone. We read EGFR intron 2 retention as a marker of target engagement rather than as the mechanism of the growth effect. These are the results of single experiments without replicates or statistical testing and should be read as preliminary.

molecular biology↗

Shared and Specific miRNA-mRNA in Human and Murine Acute Kidney Injury

Acute kidney injury (AKI) is managed as a single clinical entity despite substantial biological heterogeneity. We established a cross-species framework to define etiology-specific molecular programs and determine how these programs relate to molecular heterogeneity and pathobiology in human AKI. We performed parallel sequencing of totalRNA (mRNA) and miRNA (kidney, whole blood) in 3 murine models (mild AKI: ischemia-reperfusion injury, IRI; cecal-ligation and puncture, CLP; endotoxemia, LPS); kidney mRNA and miRNA clearly distinguished the models, blood mRNA maintained model-specific separation, and blood miRNA was less distinct. IRI was characterized by epithelial injury/repair, and extracellular matrix remodeling (i.e., miR-125b-1-3p, Vim, Sprr2g); CLP, broader inflammatory, metabolic programs (i.e., miR-692, Pfkfb3, Cdo1); LPS, inflammatory signaling (i.e., miR-155-5p, Irf7, Gbp3). We then compared these signatures to human whole blood RNAseq. Human blood samples varied along a shared gene axis that correlated to differing degrees with all three murine models, consistent with the heterogeneous nature of clinical AKI rather than discrete assignment to a single experimental etiology. Orthologs were linked to immune processes (i.e., SIGLEC14, DAAM2, CD177, DEFA3), and the presence of tubular casts in human biopsies, reflecting that mild murine AKI models capture etiology-specific biology relevant to severe human AKI. Integration of injury etiology, severity, and time may provide a framework for developing circulating biomarkers that may resolve the biological heterogeneity of human AKI.

molecular biology↗

Distinct labeling of host and viral genomes highlights redistribution of nuclear proteins during HSV-1 infection

Herpes simplex virus type 1 (HSV-1) coordinates viral and cellular proteins during infection. While proteins associated with HSV-1 genomes have been identified, changes in proteins associated with the host genome during infection remain poorly understood. We adapted accelerated native isolation of proteins on nascent DNA (aniPOND) to label and purify cellular and viral DNA then identify associated proteins by mass spectrometry. Using this approach, we confirm observations that cellular transcription, DNA replication, and repair proteins are enriched on viral genomes after the onset of viral DNA replication. We assessed how protein interactions with cellular DNA change during infection relative to protein abundance. Targets of the viral E3 ubiquitin ligase, ICP0, are depleted from the nucleus and cellular genome during infection. Transcription regulatory factors, Pol II, and the proteasome are depleted from the host genome, while association with DNA damage response and nuclear pore proteins increases. We also provide evidence for HSV-1 disruption of ribosome biogenesis. Results demonstrate reorganization of the nucleus during infection and validate this technique to identify changes to host genome-associated factors during infection.

molecular biology↗