19
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Nutritional Influence on Epigenetic Marks and Effect on Livestock Production

      review-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Nutrition represents one of the greatest environmental determinants of an individual’s health. While nutrient quantity and quality impart direct effects, the interaction of nutrition with genetic and epigenetic modifications is often overlooked despite being shown to influence biological variation in mammals. Dissecting complex traits, such as those that are diet or nutrition related, to determine the genetic and epigenetic contributions toward a phenotype can be a formidable process. Epigenetic modifications add another layer of complexity as they do not change the DNA sequence itself but can affect transcription and are important mediators of gene expression and ensuing phenotypic variation. Altered carbohydrate metabolism and rates of fat and protein deposition resulting from diet-induced hypo- or hyper-methylation highlight the capability of nutritional epigenetics to influence livestock commodity quality and quantity. This interaction can yield either products tailored to consumer preference, such as marbling in meat cuts, or potentially increasing productivity and yield both in terms of carcass yield and/or offspring performance. Understanding how these and other desirable phenotypes result from epigenetic mechanisms will facilitate their inducible potential in livestock systems. Here, we discuss the establishment of the epigenome, examples of nutritional mediated alterations of epigenetics and epigenetic effects on livestock production.

          Related collections

          Most cited references52

          • Record: found
          • Abstract: found
          • Article: not found

          High density DNA methylation array with single CpG site resolution.

          We have developed a new generation of genome-wide DNA methylation BeadChip which allows high-throughput methylation profiling of the human genome. The new high density BeadChip can assay over 480K CpG sites and analyze twelve samples in parallel. The innovative content includes coverage of 99% of RefSeq genes with multiple probes per gene, 96% of CpG islands from the UCSC database, CpG island shores and additional content selected from whole-genome bisulfite sequencing data and input from DNA methylation experts. The well-characterized Infinium® Assay is used for analysis of CpG methylation using bisulfite-converted genomic DNA. We applied this technology to analyze DNA methylation in normal and tumor DNA samples and compared results with whole-genome bisulfite sequencing (WGBS) data obtained for the same samples. Highly comparable DNA methylation profiles were generated by the array and sequencing methods (average R2 of 0.95). The ability to determine genome-wide methylation patterns will rapidly advance methylation research. Copyright © 2011 Elsevier Inc. All rights reserved.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Genome-wide erasure of DNA methylation in mouse primordial germ cells is affected by AID deficiency.

            Epigenetic reprogramming including demethylation of DNA occurs in mammalian primordial germ cells (PGCs) and in early embryos, and is important for the erasure of imprints and epimutations, and the return to pluripotency. The extent of this reprogramming and its molecular mechanisms are poorly understood. We previously showed that the cytidine deaminases AID and APOBEC1 can deaminate 5-methylcytosine in vitro and in Escherichia coli, and in the mouse are expressed in tissues in which demethylation occurs. Here we profiled DNA methylation throughout the genome by unbiased bisulphite next generation sequencing in wild-type and AID-deficient mouse PGCs at embryonic day (E)13.5. Wild-type PGCs revealed marked genome-wide erasure of methylation to a level below that of methylation deficient (Np95(-/-), also called Uhrf1(-/-)) embryonic stem cells, with female PGCs being less methylated than male ones. By contrast, AID-deficient PGCs were up to three times more methylated than wild-type ones; this substantial difference occurred throughout the genome, with introns, intergenic regions and transposons being relatively more methylated than exons. Relative hypermethylation in AID-deficient PGCs was confirmed by analysis of individual loci in the genome. Our results reveal that erasure of DNA methylation in the germ line is a global process, hence limiting the potential for transgenerational epigenetic inheritance. AID deficiency interferes with genome-wide erasure of DNA methylation patterns, indicating that AID has a critical function in epigenetic reprogramming and potentially in restricting the inheritance of epimutations in mammals.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              DNA methylation, insulin resistance, and blood pressure in offspring determined by maternal periconceptional B vitamin and methionine status.

              A complex combination of adult health-related disorders can originate from developmental events that occur in utero. The periconceptional period may also be programmable. We report on the effects of restricting the supply of specific B vitamins (i.e., B(12) and folate) and methionine, within normal physiological ranges, from the periconceptional diet of mature female sheep. We hypothesized this would lead to epigenetic modifications to DNA methylation in the preovulatory oocyte and/or preimplantation embryo, with long-term health implications for offspring. DNA methylation is a key epigenetic contributor to maintenance of gene silencing that relies on a dietary supply of methyl groups. We observed no effects on pregnancy establishment or birth weight, but this modest early dietary intervention led to adult offspring that were both heavier and fatter, elicited altered immune responses to antigenic challenge, were insulin-resistant, and had elevated blood pressure-effects that were most obvious in males. The altered methylation status of 4% of 1,400 CpG islands examined by restriction landmark genome scanning in the fetal liver revealed compelling evidence of a widespread epigenetic mechanism associated with this nutritionally programmed effect. Intriguingly, more than half of the affected loci were specific to males. The data provide the first evidence that clinically relevant reductions in specific dietary inputs to the methionine/folate cycles during the periconceptional period can lead to widespread epigenetic alterations to DNA methylation in offspring, and modify adult health-related phenotypes.
                Bookmark

                Author and article information

                Contributors
                Journal
                Front Genet
                Front Genet
                Front. Genet.
                Frontiers in Genetics
                Frontiers Media S.A.
                1664-8021
                24 October 2016
                2016
                : 7
                : 182
                Affiliations
                [1] 1Department of Animal and Veterinary Science, University of Idaho, Moscow ID, USA
                [2] 2Department of Animal and Veterinary Sciences, University of Vermont, Burlington VT, USA
                Author notes

                Edited by: Sami Dridi, University of Arkansas, USA

                Reviewed by: Seong W. Kang, University of Arkansas, USA; Kaixiong Ye, Cornell University, USA

                *Correspondence: Brenda M. Murdoch, bmurdoch@ 123456uidaho.edu Stephanie McKay, stephanie.mckay@ 123456uvm.edu

                This article was submitted to Nutrigenomics, a section of the journal Frontiers in Genetics

                Article
                10.3389/fgene.2016.00182
                5075561
                2ff9987e-4047-4a1e-af6b-ad81d23233b3
                Copyright © 2016 Murdoch, Murdoch, Greenwood and McKay.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                : 29 April 2016
                : 27 September 2016
                Page count
                Figures: 1, Tables: 1, Equations: 0, References: 78, Pages: 10, Words: 0
                Funding
                Funded by: U.S. Department of Agriculture 10.13039/100000199
                Award ID: Multi-state Hatch grant UI-NC1184
                Funded by: U.S. Department of Agriculture 10.13039/100000199
                Award ID: Multi-state Hatch grant VT-H02017MS
                Funded by: U.S. Department of Agriculture 10.13039/100000199
                Award ID: Multi-state Hatch grant UI-BGD566
                Funded by: U.S. Department of Agriculture 10.13039/100000199
                Award ID: OREI grant no. 2015-51300-24158
                Categories
                Genetics
                Review

                Genetics
                epigenetics,livestock,nutrients,nutritional epigenetics,methylation
                Genetics
                epigenetics, livestock, nutrients, nutritional epigenetics, methylation

                Comments

                Comment on this article