Biology subjects

Yang, X.

Publications and source records attributed to Yang, X..

At least 793 records · Page 44Linked to original sources

bioRxiv2020

Identification of Lysine Isobutyrylation as A New Histone Modification Mark

Short-chain acylation of lysine residues in eukaryotic proteins are recognized as essential posttranslational chemical modifications (PTMs) that regulate cellular processes from transcription, cell cycle, metabolism, to signal transduction. Lysine butyrylation was initially discovered as a normal straight chain butyrylation (Knbu). Here we report its structural isomer, branched chain butyrylation, i.e. lysine isobutyrylation (Kibu), existing as a new PTM on nuclear histones. Uniquely, isobutyryl-CoA is derived from valine catabolism and branched chain fatty acid oxidation which is distinct from the metabolism of n-butyryl-CoA. Several histone acetyltransferases were found to possess lysine isobutyryltransferase activity, especially p300 and HAT1. We resolved the X-ray crystal structures of HAT1 in complex with isobutyryl-CoA that gleaned an atomic level insight into HAT-catalyzed isobutyrylation. RNA-Seq profiling revealed that isobutyrate greatly affected the expression of genes associated with many pivotal biological pathways. Our findings identify Kibu as a novel chemical modification mark in histones and suggest its extensive role in regulating epigenetics and cellular physiology.

biochemistry↗

bioRxiv2020

SARS-CoV-2 infects human pluripotent stem cell-derived cardiomyocytes, impairing electrical and mechanical function

Global health has been threatened by the COVID-19 pandemic, caused by the novel severe acute respiratory syndrome coronavirus (SARS-CoV-2)1. Although considered primarily a respiratory infection, many COVID-19 patients also suffer severe cardiovascular disease2-4. Improving patient care critically relies on understanding if cardiovascular pathology is caused directly by viral infection of cardiac cells or indirectly via systemic inflammation and/or coagulation abnormalities3,5-9. Here we examine the cardiac tropism of SARS-CoV-2 using human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) and three-dimensional engineered heart tissues (3D-EHTs). We observe that hPSC-CMs express the viral receptor ACE2 and other viral processing factors, and that SARS-CoV-2 readily infects and replicates within hPSC-CMs, resulting in rapid cell death. Moreover, infected hPSC-CMs show a progressive impairment in both electrophysiological and contractile properties. Thus, COVID-19-related cardiac symptoms likely result from a direct cardiotoxic effect of SARS-CoV-2. Long-term cardiac complications might be possible sequelae in patients who recover from this illness.

pathology↗

bioRxiv2020

Orthosteric-allosteric dual inhibitors of PfHT1 as selective anti-malarial agents

Artemisinin-resistant malaria parasites have emerged and been spreading, posing a significant public health challenge. Anti-malarial drugs with novel mechanisms of action are therefore urgently needed. In this report, we exploit a "selective starvation" strategy by selectively inhibiting Plasmodium falciparum hexose transporter 1 (PfHT1), the sole hexose transporter in Plasmodium falciparum, over human glucose transporter 1 (hGLUT1), providing an alternative approach to fight against multidrug-resistant malaria parasites. Comparison of the crystal structures of human GLUT3 and PfHT1 bound to C3361, a PfHT1-specific moderate inhibitor, revealed an inhibitor binding-induced pocket that presented a promising druggable site. We thereby designed small-molecules to simultaneously block the orthosteric and allosteric pockets of PfHT1. Through extensive structure-activity relationship (SAR) studies, the TH-PF series was identified to selectively inhibit PfHT1 over GLUT1 and potent against multiple strains of the blood-stage P. falciparum. Our findings shed light on the next-generation chemotherapeutics with a paradigm-shifting structure-based design strategy to simultaneously targeting the orthosteric and allosteric sites of a transporter. Significance statementBlocking sugar uptake in P. falciparum by selectively inhibiting the hexose transporter PfHT1 kills the blood-stage parasites without affecting the host cells, indicating PfHT1 as a promising therapeutic target. Here, we report the development of novel small-molecule inhibitors that are selectively potent to the malaria parasites over human cell lines by simultaneously targeting the orthosteric and the allosteric binding sites of PfHT1. Our findings established the basis for the rational design of next-generation anti-malarial drugs.

pharmacology and toxicology↗

bioRxiv2020

Fertility-LightGBM: A fertility-related protein prediction model by multi-information fusion and light gradient boosting machine

The identification of fertility-related proteins plays an essential part in understanding the embryogenesis of germ cell development. Since the traditional experimental methods are expensive and time-consuming to identify fertility-related proteins, the purposes of predicting protein functions from amino acid sequences appeared. In this paper, we propose a fertility-related protein prediction model. Firstly, the model combines protein physicochemical property information, evolutionary information and sequence information to construct the initial feature space ALL. Then, the least absolute shrinkage and selection operator (LASSO) is used to remove redundant features. Finally, light gradient boosting machine (LightGBM) is used as a classifier to predict. The 5-fold cross-validation accuracy of the training dataset is 88.5%, and the independent accuracy of the training dataset is 91.5%. The results show that our model is more competitive for the prediction of fertility-related proteins, which is helpful for the study of fertility diseases and related drug targets.

bioinformatics↗

bioRxiv2020

Probing acetylated-α-synuclein monomer-aggregate complexes by NMR elucidates mechanism of fibril seeding

Amyloid fibril formation of -synuclein (S) is associated with multiple neurodegenerative diseases, including Parkinsons Disease (PD). Growing evidence suggests that progression of PD is linked to cell-to-cell propagation of S fibrils, which leads to seeding of endogenous intrinsically disordered monomer via templated elongation and secondary nucleation. A molecular understanding of the seeding mechanism and driving interactions is crucial to inhibit progression of amyloid formation. Here, using relaxation-based solution NMR experiments designed to probe large complexes, we probe weak interactions of intrinsically disordered acetylated-S (Ac-S) monomers with seeding-competent Ac-S fibrils and seeding-incompetent off-pathway oligomers to identify Ac-S monomer residues at the binding interface. Under conditions that favor fibril elongation, we determine that the first 11 N-terminal residues on the monomer form a common binding site for both fibrils and off-pathway oligomers. Additionally, the presence of off-pathway oligomers within a fibril seeding environment suppresses seeded amyloid formation, as observed through thioflavin-T fluorescence experiments. This highlights that off-pathway S oligomers can act as an auto-inhibitor against S fibril elongation. Based on these data taken together with previous results, we propose a model in which Ac-S monomer recruitment to the fibril is driven by interactions between the intrinsically disordered monomer N-terminus and the intrinsically disordered flanking regions (IDR) on the fibril surface. We suggest that this monomer recruitment may play a role in the elongation of amyloid fibrils and highlight the potential of the IDRs of the fibril as important therapeutic targets against seeded amyloid formation. SignificanceCell-to-cell spreading of S fibrils leads to amyloid seeding of endogenous monomer. Detailed atomic-level mechanistic understanding of the fibril seeding process of S is essential for design of therapeutic approaches against Parkinsons disease. In light of its complexity, this process remains ill-defined at the molecular level. Using relaxation-based solution NMR experiments, we mapped a common N-terminal binding interface of the Ac-S intrinsically disordered monomer with Ac-S fibrils and off-pathway oligomers to elucidate critical monomer-aggregate interactions during seeded aggregation and in equilibrium with mature aggregates. From this work, we propose a new paradigm, in which Ac-S monomer recruitment to the fibril is driven by interactions between the intrinsically disordered monomer N-terminus and the flanking IDRs on the fibril surface.

biophysics↗

bioRxiv2020

SARS-Cov-2-, HIV-1-, Ebola-neutralizing and anti-PD1 clones are predisposed

Antibody repertoire refers to the totality of the superbly diversified antibodies within an individual to cope with the vast array of possible pathogens. Despite this extreme diversity, antibodies of the same clonotype, namely public clones, have been discovered among individuals. Although some public clones could be explained by antibody convergence, public clones in naive repertoire or virus-neutralizing clones from not infected people were also discovered. All these findings indicated that public clones might not occur by random and they might exert essential functions. However, the frequencies and functions of public clones in a population have never been studied. Here, we integrated 2,449 Rep-seq datasets from 767 donors and discovered 5.07 million public clones - ~10% of the repertoire are public in population. We found 38 therapeutic clones out of 3,390 annotated public clones including anti-PD1 clones in healthy people. Moreover, we also revealed clones neutralizing SARS-CoV-2, Ebola, and HIV-1 viruses in healthy individuals. Our result demonstrated that these clones are predisposed in the human antibody repertoire and may exert critical functions during particular immunological stimuli and consequently benefit the donors. We also implemented RAPID - a Rep-seq Analysis Platform with Integrated Databases, which may serve as a useful tool for others in the field.

immunology↗

bioRxiv2020

Pancreatic α and β cells are globally phase-locked

The Ca2+ modulated pulsatile secretion of glucagon and insulin by pancreatic and {beta} cells plays a key role in glucose homeostasis. However, how and {beta} cells coordinate via paracrine interaction to produce various Ca2+ oscillation patterns is still elusive. Using a microfluidic device and transgenic mice in which and {beta} cells were labeled with different colors, we were able to record islet Ca2+ signals at single cell level for long times. Upon glucose stimulation, we observed heterogeneous Ca2+ oscillation patterns intrinsic to each islet. After a transient period, the oscillations of and {beta} cells were globally phase-locked, i.e., the two types of cells in an islet each oscillate synchronously but with a phase shift between the two. While the activation of cells displayed a fixed time delay of ~20 s to that of {beta} cells, {beta} cells activated with a tunable delay after the cells. As a result, the tunable phase shift between and {beta} cells set the islet oscillation period and pattern. Furthermore, we demonstrated that the phase shift can be modulated by glucagon. A mathematical model of islet Ca2+ oscillation taking into consideration of the paracrine interaction was constructed, which quantitatively agreed with the experimental data. Our study highlights the importance of cell-cell interaction to generate stable but tunable islet oscillation patterns.

systems biology↗

bioRxiv2020

Bone Marrow Stromal Cells in a Mouse Model of Implant Osseointegration

Metal implants are commonly used in orthopaedic surgery. The mechanical stability and longevity of implants depend on adequate bone deposition along the implant surface. The cellular and molecular mechanisms underlying peri-implant bone formation (i.e. osseointegration) are incompletely understood. Herein, our goal was to determine the specific bone marrow stromal cell populations that contribute to bone formation around metal implants. To do this, we utilized a mouse tibial implant model that is clinically representative of human joint replacement procedures. Using a lineage-tracing approach with the Acta2.creERT2 and Tmem100.creERT2 transgenic alleles, we found that Pdgfra- and Ly6a/Sca1-expressing stromal cells (PS cells) multiply and differentiate in the peri-implant environment to give rise to osteocytes in newly formed bone tissue. Single cell RNA-seq analysis indicated that PS cells are quiescent in uninjured bone tissue; however, they express markers of proliferation and osteogenic differentiation shortly after implantation surgery. Our findings indicate that PS cells are mobilized to repair bone tissue and facilitate implant osseointegration following surgery. Biologic therapies targeting PS cells might improve osseointegration in patients undergoing orthopaedic procedures.

cell biology↗

bioRxiv2020

SARS-CoV-2 manipulates the SR-B1-mediated HDL uptake pathway for its entry

The recently emerged pathogenic severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread rapidly, leading to a global COVID-19 pandemic. Binding of the viral spike protein (SARS-2-S) to cell surface receptor angiotensin-converting enzyme 2 (ACE2) mediates host cell infection. In the present study, we demonstrate that in addition to ACE2, the S1 subunit of SARS-2-S binds to HDL and that SARS-CoV-2 hijacks the SR-B1-mediated HDL uptake pathway to facilitate its entry. SR-B1 facilitates SARS-CoV-2 entry into permissive cells by augmenting virus attachment. MAb (monoclonal antibody)-mediated blocking of SARS-2-S-HDL binding and SR-B1 antagonists strongly inhibit HDL-enhanced SARS-CoV-2 infection. Notably, SR-B1 is co-expressed with ACE2 in human pulmonary and extrapulmonary tissues. These findings revealed a novel mechanism for SARS-CoV-2 entry and could provide a new target to treat SARS-CoV-2 infection.

microbiology↗

bioRxiv2020

Non-epigenetic mechanisms enable short memories of the environment for cell cycle commitment

Cells continuously survey their environment in order to make fundamental decisions, including whether to divide, migrate, or differentiate. However, a fascinating phenomenon in biology is that cells often possess memory--they temporally integrate both past and present signals to make a reliable decision. Cellular memory manifests across different biological systems over different timescales, and a variety of underlying molecular mechanisms have been proposed. Here we investigate a non-epigenetic molecular mechanism underpinning how a single yeast cell can remember its recent environmental history to decide whether to enter the cell cycle. This "memories" is encoded by the phosphorylation level of the cell cycle inhibitor Whi5. G1 cyclin Cln3 senses environmental nutrient levels and promotes cell-cycle entry by phosphorylating and thus inactivating Whi5. We developed an optogenetic system whereby the nuclear localization of Cln3 can be rapidly and reversibly controlled by light. By monitoring cellular response to different temporal profiles of Cln3, we found that cell cycle entry requires the time duration of nuclear Cln3, supporting the model of "cellular memories". Moreover, instead of the memory could last for the entire G1 phase as previously observed in glucose, we found Whi5 re-activates rapidly, with a similar half-time [~] 12 min, in a variety of nutrient and stress conditions. Our results suggest yeast cell can shortly remember its recent environmental cues to decide whether to enter the cell cycle.

molecular biology↗

bioRxiv2020

DeepPSC (protein structure camera): computer vision-based reconstruction of proteins backbone structure from alpha carbon trace as a case study

Deep learning has been increasingly used in protein tertiary structure prediction, a major goal in life science. However, all the algorithms developed so far mostly use protein sequences as input, whereas the vast amount of protein tertiary structure information available in the Protein Data Bank (PDB) database remains largely unused, because of the inherent complexity of 3D data computation. In this study, we propose Protein Structure Camera (PSC) as an approach to convert protein structures into images. As a case study, we developed a deep learning method incorporating PSC (DeepPSC) to reconstruct protein backbone structures from alpha carbon traces. DeepPSC outperformed all the methods currently available for this task. This PSC approach provides a useful tool for protein structure representation, and for the application of deep learning in protein structure prediction and protein engineering.

bioinformatics↗

bioRxiv2020

Human Embryonic Stem Cell-derived Lung Organoids: a Model for SARS-CoV-2 Infection and Drug Test

The coronavirus disease 2019 (COVID-19) pandemic is caused by infection with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which is spread primary via respiratory droplets and infects the lungs. Currently widely used cell lines and animals are unable to accurately mimic human physiological conditions because of the abnormal status of cell lines (transformed or cancer cells) and species differences between animals and humans. Organoids are stem cell-derived self-organized three-dimensional culture in vitro and model the physiological conditions of natural organs. Here we demonstrated that SARS-CoV-2 infected and extensively replicated in human embryonic stem cells (hESCs)-derived lung organoids, including airway and alveolar organoids. Ciliated cells, alveolar type 2 (AT2) cells and rare club cells were virus target cells. Electron microscopy captured typical replication, assembly and release ultrastructures and revealed the presence of viruses within lamellar bodies in AT2 cells. Virus infection induced more severe cell death in alveolar organoids than in airway organoids. Additionally, RNA-seq revealed early cell response to SARS-CoV-2 infection and an unexpected downregulation of ACE2 mRNA. Further, compared to the transmembrane protease, serine 2 (TMPRSS2) inhibitor camostat, the nucleotide analog prodrug Remdesivir potently inhibited SARS-CoV-2 replication in lung organoids. Therefore, human lung organoids can serve as a pathophysiological model for SARS-CoV-2 infection and drug discovery.

microbiology↗

bioRxiv2020

A Comprehensive Classification of Coronaviruses and Inferred Cross-Host Transmissions

In this work, we present a unified and robust classification scheme for coronaviruses based on concatenated protein clusters. This subsequently allowed us to infer the apparent "horizontal gene transfer" events via reconciliation with the corresponding gene trees, which we argue can serve as a marker for cross-host transmissions. The cases of SARS-CoV, MERS-CoV, and SARS-CoV-2 are discussed. Our study provides a possible technical route to understand how coronaviruses evolve and are transmitted to humans.

bioinformatics↗

bioRxiv2020

Somatic mosaicism in the mature brain reveals clonal cellular distributions during cortical development

The structure of the human neocortex underlies species-specific features and is a reflection of intricate developmental programs. Here we analyzed neocortical cellular lineages through a comprehensive assessment of brain somatic mosaicism--which acts as a neutral recorder of lineage history. We employed deep whole genome and variant sequencing in a single postmortem neurotypical human brain across 25 anatomic regions and three distinct modalities: bulk geographies, sorted cell types, and single nuclei. We identified 259 mosaic variants, revealing remarkable differences in localization, clonal abundance, cell type specificity, and clade distribution. We identified a set of hierarchical cellular diffusion barriers, whereby the left-right axis separation of the neocortex occurs prior to anterior-posterior and dorsal-ventral axis separation. We also found that stochastic distribution is a driver of clonal dispersion, and that rules regarding cellular lineages and anatomical boundaries are often ignored. Our data provides a comprehensive analysis of brain somatic mosaicism across the human cerebral cortex, deconvolving clonal distributions and migration patterns in the human embryo. One Sentence SummaryComprehensive evaluation of brain somatic mosaicism in the adult human identifies rules governing cellular distribution during embryogenesis.

genomics↗

bioRxiv2020

JQ-1 ameliorates schistosomiasis liver fibrosis by suppressing JAK2 and STAT3 activation

Schistosomiasis is a serious parasitic infection caused by Schistosoma. The parasite deposits eggs in the host liver, causing inflammation that activates hepatic stellate cells (HSCs), which leads to liver fibrosis. Currently, there is no effective therapy for liver fibrosis; thus, treatments are urgently needed. Therefore, in the present study, mice infected with Schistosoma japonicum were treated with JQ-1, a small-molecule bromodomain inhibitor with reliable anti-tumor and anti-inflammatory activities. The fibrotic area of the liver measured by computer-assisted morphometric analysis and the expression levels of the cytoskeletal protein alpha smooth muscle actin (-SMA) and of collagen assessed by quantitative PCR and immunohistochemistry were significantly decreased in the liver following JQ-1 treatment compared with vehicle-treated controls. Total RNA was extracted from the liver of JQ-1-treated Schistosoma-infected mice for RNA-sequencing analysis. Gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses indicated that JQ-1 affected biological processes and the expression of cellular components known to play key roles in HSC transdifferentiation into myofibroblasts. In vitro treatment with JQ-1 of JS-1 cells, a mouse HSC line, indicated that JQ-1 significantly inhibited JS-1 proliferation but had no effect on JS-1 activity, senescence, or apoptosis. Western blot results showed that JQ-1 inhibited the expression of phosphorylated JAK2 and phosphorylated STAT3 without altering expression levels of these non-phosphorylated proteins. Taken together, these findings suggested that JQ-1 treatment ameliorated S. japonicum egg-induced liver fibrosis, at least in part, by suppressing HSC activation and proliferation through the inhibition of JAK2/STAT3 signaling. These results lay a foundation for the development of novel approaches to treat and control liver fibrosis caused by S. japonicum. Author summaryWhen a host is infected with Schistosoma, a common parasite that affects more than a million people and hundreds of thousands of livestock, the parasite deposits eggs in the liver of the host. The eggs lead to liver inflammation, which activates stellate cells in the liver. These stellate cells generate most of the excessive extracellular matrix that replaces healthy liver parenchyma with fibrous tissue, causing liver fibrosis. Schistosoma japonicum causes the most severe liver damage of all the schistosome parasites. Therefore, inhibiting the activation of the liver stellate cells and removing the activated stellate cells are key strategies for treating liver fibrosis caused by this parasite. JQ-1 is a potent inhibitor of the BET family of bromodomain proteins and is structurally similar to inhibitors being tested in clinical trials for various types of cancers. Here we found that administering JQ-1 to mice infected with S. japonicum decreased the degree of liver fibrosis. JQ-1 inhibited the activation and proliferation of liver stellate cells by blocking the phosphorylation and thus the activation of JAK2 and STAT3 to achieve its therapeutic effects. Thus, this study provides insights into the development of new therapeutic strategies for Schistosoma-induced liver fibrosis.

pharmacology and toxicology↗

bioRxiv2020

Single-cell Long Non-coding RNA Landscape of T Cells in Human Cancer Immunity

The development of new therapeutic targets for cancer immunotherapies and the development of new biomarkers require deep understanding of T cells. To date, the complete landscape and systematic characterization of long noncoding RNAs (lncRNAs) in T cells in cancer immunity are lacking. Here, by systematically analyzing full-length single-cell RNA sequencing (scRNA-seq) data of more than 20,000 T cell libraries across three cancer types, we provide the first comprehensive catalog and the functional repertoires of lncRNAs in human T cells. Specifically, we developed a custom pipeline for de novo transcriptome assembly obtaining 9,433 novel lncRNA genes that increased the number of current human lncRNA catalog by 16% and nearly doubled the number of lncRNAs expressed in T cells. We found that a portion of expressed genes in single T cells were lncRNAs which have been overlooked by the majority of previous studies. Based on metacell maps constructed by MetaCell algorithm that partition scRNA-seq datasets into disjointed and homogenous groups of cells (metacells), 154 signature lncRNAs associated with effector, exhausted, and regulatory T cell states are identified, 84 of which are functionally annotated based on co-expression network, indicating that lncRNAs might broadly participate in regulation of T cell functions. Our findings provide a new point of view and resource for investigating the mechanisms of T cell regulation in cancer immunity as well as for novel cancer-immune biomarker development and cancer immunotherapies.

bioinformatics↗

bioRxiv2020

Association of gut microbiota with cerebral cortex and cerebrovascular abnormality in human mild traumatic brain injury

Key roles of the gut-brain axis in brain injury development have been suggested in various mouse models; however, little is known about its functional significance in human mild traumatic brain injury (TBI). Here, we decipher this axis by profiling the gut microbiota in 98 acute mild TBI patients and 62 matched controls, and subgroup of them also measured circulating mediators and applied neuroimaging. Mild TBI patients had increased -diversity and different overall microbial compositions compared with controls. 25-microbial genus classifiers distinguish patients from controls with an area under the receiver operating characteristic curve (AUC) of 0.889, while adding serum mediators and neuroimaging features further improved performance even in a small sample size (AUC = 0.969). Numerous correlations existed between gut bacteria, aberrant cortical thickness and cerebrovascular injury. Co-occurrence network analysis revealed two unique gut-brain axes in patients: 1) altered intestinal Lachnospiraceae_NK4A136_group and Eubacterium_ruminantium_group-increased serum GDNF-subcallosal hypertrophy and cerebrovascular injury; 2) decreased intestinal Eubacterium_xylanophilum_group-upregulated IL-6-thinned anterior insula. Our findings provide a new integrated mechanistic understanding and diagnostic model of mild TBI.

microbiology↗

bioRxiv2020

Red seaweed (Asparagopsis taxiformis) supplementation reduces enteric methane by over 80 percent in beef steers

The red macroalgae (seaweed) Asparagopsis spp. has shown to reduce ruminant enteric methane (CH4) production up to 99% in vitro. The objective of this study was to determine the effect of Asparagopsis taxiformis on CH4 production (g/day per animal), CH4 yield (g CH4/kg dry matter intake (DMI)), average daily gain (ADG), feed conversion efficiency (FCE), and carcass and meat quality in growing beef steers. Twenty-one Angus-Hereford beef steers were randomly allocated to one of three treatment groups: 0% (Control), 0.25% (Low Dose; LD), and 0.5% (High Dose; HD) A. taxiformis inclusion based on organic matter intake. Steers were fed 3 diets: high, medium, and low forage total mixed ration (TMR) representing typical life-stage diets of growing beef steers. The LD and HD treatments over 147 days reduced enteric CH4 yield 45 and 68%, respectively; however, there was an interaction between TMR type and the magnitude of CH4 yield reduction. Supplementing the low forage TMR reduced CH4 yield 69.8% (P <0.001) for LD and 80% (P <0.001) for HD treatment. Hydrogen (H2) yield (g H2/DMI) increased significantly (P<0.001) 336 and 590% compared to Control for the LD and HD treatments, respectively. No differences were found in carbon dioxide (CO2) yield (g CO2/DMI), ADG, carcass quality, strip loin proximate analysis and shear force, or consumer taste preferences. DMI tended (P = 0.08) to decrease 8% in steers in LD treatment but significantly (P = 0.002) reduced 14% in steers in HD treatment. Conversely, FCE tended to increase 7% in steers in LD treatment (P = 0.06) and increased 14% in steers in HD (P < 0.01) treatment compared to Control. The persistent reduction of CH4 by A. taxiformis supplementation suggests that this is a viable feed additive to significantly decrease the carbon footprint of ruminant livestock and potentially increase production efficiency.

systems biology↗