scholarly journals Impacts of Macronutrients on Gene Expression: Recent Evidence to Understand Productive and Reproductive Performance of Livestock

Author(s):  
Md. Mahmodul Hasan Sohel ◽  
Yusuf Konca ◽  
Mehmet Ulas Cinar

In order to identify the effects of nutrients on gene expression and to assess the interactions between genes and nutrition by means of various cutting-edge technologies, the interdisciplinary branch ‘Nutrigenomics’ was created. Therefore, nutrigenomics corresponds to the use of knowledge and techniques of nutrition, genomics, transcriptomics, proteomics, epigenomics, and metabolomics to seek and explain the cross-talk between nutrition and genes in molecular level. Macronutrients are important dietary signals that control metabolic programming of cells and have important roles in maintaining cellular homeostasis by influencing specific gene expression. Recent advancements in molecular genetics studies, for instance, use of next-generation sequencing, microarray and qPCR array to investigate the expression of transcripts, genes, and miRNAs, has a crucial impact on understanding and quantitative measurement of the impact of dietary macronutrients on gene function. This review will shade a light on the interactions and mechanisms how the dietary source of macronutrients changes the expression of specific mRNA and miRNA. Furthermore, it will highlight the exciting recent findings in relation to animal performance characteristics which eventually help us to identify a dietary target to improve animal production.

Catalysts ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 62
Author(s):  
Won-Yong Jeon ◽  
Seyoung Mun ◽  
Wei Beng Ng ◽  
Keunsoo Kang ◽  
Kyudong Han ◽  
...  

Enzymatic biofuel cells (EBFCs) have excellent potential as components in bioelectronic devices, especially as active biointerfaces to regulate stem cell behavior for regenerative medicine applications. However, it remains unclear to what extent EBFC-generated electrical stimulation can regulate the functional behavior of human adipose-derived mesenchymal stem cells (hAD-MSCs) at the morphological and gene expression levels. Herein, we investigated the effect of EBFC-generated electrical stimulation on hAD-MSC cell morphology and gene expression using next-generation RNA sequencing. We tested three different electrical currents, 127 ± 9, 248 ± 15, and 598 ± 75 nA/cm2, in mesenchymal stem cells. We performed transcriptome profiling to analyze the impact of EBFC-derived electrical current on gene expression using next generation sequencing (NGS). We also observed changes in cytoskeleton arrangement and analyzed gene expression that depends on the electrical stimulation. The electrical stimulation of EBFC changes cell morphology through cytoskeleton re-arrangement. In particular, the results of whole transcriptome NGS showed that specific gene clusters were up- or down-regulated depending on the magnitude of applied electrical current of EBFC. In conclusion, this study demonstrates that EBFC-generated electrical stimulation can influence the morphological and gene expression properties of stem cells; such capabilities can be useful for regenerative medicine applications such as bioelectronic devices.


1979 ◽  
Vol 27 (10) ◽  
pp. 1363-1364 ◽  
Author(s):  
W A Anderson ◽  
C Burnett

Estrogen is an essential requirement for the postpubertal trophic development and maintenance of the differentiated state of the oviduct, uterus, cervix, vagina and mammary glands of mammals. Estrogen, apparently functioning through its specific cytoplasmic receptor protein via a multistep interaction pathway induces gene expression of specific biochemical events leading to growth and differentiation of target tissues (Jensen et al., Proc Natl Acad Sci, 59:632, 1968; Gorski et al., Recent Prog Horm Res 24:45, 1968). One biochemical expression of the estrogen gene is the synthesis of specific mRNA transcripts for certain specific marker proteins, including ovalbumin, lysozyme and ovomucoid in the chick oviduct (O'Malley and McGuire, Proc Natl Acad Sci 60:1527, 1968; Palmiter and Schimke, J Biol Chem 248:1502, 1973), tubulin in the mammalian oviduct (Brenner and Anderson, Handbook of Physiology 7(2):123, 1973; Brenner et al., Endocrinology 95:1094, 1974) and peroxidase (EC 1,11.1.7) in the rodent uterus (Brockelmann and Fawcett, Biol Reprod 1:59, 1969; Churg and Anderson, J Cell Biol 62:449, 1974; Anderson et al., J Cell Biol 64:668, 1975).


2020 ◽  
Author(s):  
Michelle D. Catalina ◽  
Prathyusha Bachali ◽  
Anthony E. Yeo ◽  
Nicholas S. Geraci ◽  
Michelle A. Petri ◽  
...  

AbstractGene expression signatures can stratify patients with heterogeneous diseases, such as Systemic Lupus Erythematosus (SLE), yet understanding the contributions of ancestral background to this heterogeneity is not well elucidated. We hypothesized that ancestry would significantly influence gene expression signatures and measured 34 gene modules in 1566 SLE patients of african (AA), european (EA) or native american (NAA) ancestry to determine the impact of ancestry on gene expression. Healthy subject ancestry-specific gene expression provided the transcriptomic background upon which the SLE patient signatures were built. Although standard therapy affected every gene signature, and significantly increased myeloid cell signatures, logistic regression analysis determined that ancestral background significantly changed 23/34 gene signatures. Additionally, the strongest association to gene expression changes was autoantibodies and this also had etiology in ancestry; the AA predisposition to have both RNP and dsDNA autoantibodies compared to EA predisposition to have only antidsDNA. A machine learning approach was used to determine a gene signature characteristic to distinguish AA SLE and was most influenced by genes characteristic of the perturbed B cell axis in AA SLE patients.


2021 ◽  
Author(s):  
Deborah Weighill ◽  
Marouen Ben Guebila ◽  
Kimberly Glass ◽  
John Quackenbush ◽  
John Platig

AbstractThe majority of disease-associated genetic variants are thought to have regulatory effects, including the disruption of transcription factor (TF) binding and the alteration of downstream gene expression. Identifying how a person’s genotype affects their individual gene regulatory network has the potential to provide important insights into disease etiology and to enable improved genotype-specific disease risk assessments and treatments. However, the impact of genetic variants is generally not considered when constructing gene regulatory networks. To address this unmet need, we developed EGRET (Estimating the Genetic Regulatory Effect on TFs), which infers a genotype-specific gene regulatory network (GRN) for each individual in a study population by using message passing to integrate genotype-informed TF motif predictions - derived from individual genotype data, the predicted effects of variants on TF binding and gene expression, and TF motif predictions - with TF protein-protein interactions and gene expression. Comparing EGRET networks for two blood-derived cell lines identified genotype-associated cell-line specific regulatory differences which were subsequently validated using allele-specific expression, chromatin accessibility QTLs, and differential TF binding from ChIP-seq. In addition, EGRET GRNs for three cell types across 119 individuals captured regulatory differences associated with disease in a cell-type-specific manner. Our analyses demonstrate that EGRET networks can capture the impact of genetic variants on complex phenotypes, supporting a novel fine-scale stratification of individuals based on their genetic background. EGRET is available through the Network Zoo R package (netZooR v0.9; netzoo.github.io).


2018 ◽  
Author(s):  
Oswaldo A. Lozoya ◽  
Tianyuan Wang ◽  
Dagoberto Grenet ◽  
Taylor C. Wolfgang ◽  
Mack Sobhany ◽  
...  

AbstractThe impact of mitochondria in epigenetics is emerging but our understanding of this relationship and its impact on gene expression remain incomplete. We previously showed that acute mitochondrial DNA (mtDNA) loss leads to histone hypoacetylation. It remains to be defined if these changes are maintained when mitochondrial dysfunction is chronic and, importantly, if they are sufficient to alter gene expression. To fill these gaps, we here studied both a progressive and a chronic model of mtDNA depletion using biochemical, pharmacological, genomics and genetic assays. We show that histones are hypoacetylated in both models. We link these effects to decreased histone acetyltransferase (HAT) activity independent of changes in ATP citrate lyase function, which can be reversibly modulated by altering specifically the mitochondrial pool of acetyl-CoA. Also, we determined that these changes regulate locus-specific gene expression and physiological outcomes, including the production of prostaglandins. These results may be relevant to the pathophysiology of mtDNA depletion syndromes and to understanding the effects of environmental agents, such as AZT or antibiotics, that lead to physical or functional mtDNA loss.


2021 ◽  
Author(s):  
Meng-Ying Lin ◽  
Urte Schlueter ◽  
Benjamin Stich ◽  
Andreas P.M. Weber

Altered transcript abundances and cell specific gene expression patterns that are caused by regulatory divergence play an important role in the evolution of C4 photosynthesis. How these altered gene expression patterns are achieved and whether they are driven by cis- or trans-regulatory changes is mostly unknown. To address this question, we investigated the regulatory divergence between C3 and C3-C4 intermediates, using allele specific gene expression (ASE) analyses of Moricandia arvensis (C3-C4), M. moricandioides (C3) and their interspecific F1 hybrids. ASE analysis on SNP-level showed similar relative proportions of regulatory effects among hybrids: 36% and 6% of SNPs were controlled by cis-only and trans-only changes, respectively. GO terms associated with metabolic processes and the positioning of chloroplast in cells were abundant in transcripts with cis-SNPs shared by all studied hybrids. Transcripts with cis-specificity expressed bias toward the allele from the C3-C4 intermediate genotype. Additionally, ASE evaluated on transcript-level indicated that ~27% of transcripts show signals of ASE in Moricandia hybrids. Promoter-GUS assays on selected genes revealed altered spatial gene expression patterns, which likely result from regulatory divergence in their promoter regions. Assessing ASE in Moricandia interspecific hybrids contributes to the understanding of early evolutionary steps towards C4 photosynthesis and highlights the impact and importance of altered transcriptional regulations in this process.


2018 ◽  
Author(s):  
Tal Cohen ◽  
Chen Mordechai ◽  
Alal Eran ◽  
Dan Mishmar

Expression quantitative trait loci (eQTLs) are instrumental in genome-wide identification of regulatory elements, yet were overlooked in the mitochondrial DNA (mtDNA). By analyzing 5079 RNA-seq samples from 23 tissues we identified association of ancient mtDNA SNPs (haplogroups T2, L2, J2 and V) and recurrent SNPs (mtDNA positions 263, 750, 1438 and 10398) with tissue-dependent mtDNA gene-expression. Since the recurrent SNPs independently occurred in different mtDNA genetic backgrounds, they constitute the best candidates to be causal eQTLs. Secondly, the discovery of mtDNA eQTLs in both coding and non-coding mtDNA regions, propose the identification of novel mtDNA regulatory elements. Third, we identified association between low m1A 947 MT-RNR2 (16S) rRNA modification levels and altered mtDNA gene-expression in twelve tissues. Such association disappeared in skin which was exposed to sun, as compared to sun-unexposed skin from the same individuals, thus supporting the impact of UV on mtDNA gene expression. Taken together, our findings reveal that both mtDNA SNPs and mt-rRNA modification affect mtDNA gene expression in a tissue-dependent manner.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. 4539-4539
Author(s):  
Anita Lavery ◽  
Leanne Stevenson ◽  
Damian McManus ◽  
Gemma E. Logan ◽  
Steven M. Walker ◽  
...  

4539 Background: The Dual Erb B Inhibition in Oesophago-gastric Cancer (DEBIOC) trial reported an acceptable safety profile for neoadjuvant Xelox +/- AZD8931 but limited efficacy. We utilized EAC patient samples from DEBIOC to evaluate the impact of neoadjuvant Xelox +/-AZD8931 on biological pathways using a unique software driven solution. Methods: 24 pre-treatment FFPE EAC biopsies and 17 matched surgical resection specimens were transcriptionally profiled using the Almac Diagnostics Xcel Array. Gene expression data was analyzed using the Almac claraT total mRNA report V3.0.0, reporting on 92 gene expression signatures and 7337 single genes associated with 10 key biologies. Paired Wilcoxon tests (5% significance level) were used to evaluate changes in claraT scores pre- and post-treatment. EGFR and Her2 expression were assessed by IHC and FISH. Results: 15 patients received Xelox+AZD8931 and 9 Xelox alone. Hierarchical clustering of biopsies identified 4 major clusters: Inflammation active, Genomic Instability active, EGFR & MAPK active, and EMT & Angiogenesis active. Comparison of signature scores pre- and post- neoadjuvant treatment demonstrated a significant reduction in scores relating to DNA damage repair (DDR) deficiency (Almac DNA Damage assay, p< 0.0001; BRCAness Profile, p= 0.0025; HRD Gene Signature, p< 0.0001; BRCA1ness Signature, p= 0.0004) and a significant increase in angiogenesis signatures (Almac Angiogenesis Assay, p= 0.0002; Angio Predictive G model, p= 0.0228; Angiogenesis Signature A, p= 0.0034) and EMT signatures (EMT Signature, p= 0.0031, EMT Enrichment Score, p= 0.0013, Pan-Can EMT Signature B, p= 0.0001). Comparing pre- and post-treatment signature scores in patients treated with Xelox +/-AZD8931 revealed a significant reduction in EGFR Sensitivity Signature ( p= 0.0088), ERBB2-specific Gene Expression Signature ( p= 0.0127) and Hallmark PI3K-AKT-MTOR Signaling ( p= 0.0195) in those treated with Xelox + AZD8931 in keeping with the mechanism of action of AZD8931. Downregulation of AKT signaling was confirmed in AZD8931 treated and resistant cell lines. Conclusions: We report the use of a novel software tool to apply 92 gene expression signatures to EAC biopsy and resection specimens from the DEBIOC trial to provide insight into mechanisms of action. Neoadjuvant treatment was associated with a reduction in DDR deficiency and an increase in angiogenesis and EMT signatures whilst a reduction in EGFR, Her2 and AKT pathways was noted with AZD8931 treatment.


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