'; ?> geneimprint : Hot off the Press http://www.geneimprint.com/site/hot-off-the-press Daily listing of the most recent articles in epigenetics and imprinting, collected from the PubMed database. en-us Thu, 22 Jun 2017 17:32:15 PDT Thu, 22 Jun 2017 17:32:15 PDT jirtle@radonc.duke.edu james001@jirtle.com Epigenomics: dissecting hybridization and polyploidization. Jackson SA
Genome Biol (Jun 2017)

Epigenetic profiling in diploid, allopolyploid, and domesticated cotton shows that despite most DNA methylation being conserved and stably inherited, alterations likely due to hybridization and domestication affect gene expression.]]> Tue, 20 Jun 2017 00:00:00 PDT Haploidy in Humans: An Evolutionary and Developmental Perspective. Sagi I, Benvenisty N
Dev Cell (Jun 2017)

Although haploidy has not been observed in vertebrates, its natural occurrence in various eukaryotic species that had diverged from diploid ancestors suggests that there is an innate capacity for an organism to regain haploidy and that haploidy may confer evolutionary benefits. Haploid embryonic stem cells have been experimentally generated from mouse, rat, monkey, and humans. Haploidy results in major differences in cell size and gene expression levels while also affecting parental imprinting, X chromosome inactivation, and mitochondrial metabolism genes. We discuss here haploidy in evolution and the barriers to haploidy, in particular in the human context.]]> Tue, 20 Jun 2017 00:00:00 PDT Detection of Imprinting Effects for Quantitative Traits on X Chromosome Using Nuclear Families with Multiple Daughters. Yu K, Zhou JY, Fung WK
Ann Hum Genet (Jul 2017)

Genomic imprinting is an epigenetic phenomenon in which the expression of an allele copy depends on its parental origin. This mechanism has been found to play an important role in many complex diseases. Statistical tests for imprinting effects have been developed for more than 15 years, but they are only suitable for autosomes. It was not until recently that the parental-asymmetry test on the X chromosome (XPAT) was proposed to test for imprinting effects. However, this test can only be used for qualitative traits. Therefore, in this article, we propose a class of PAT-type tests to test for imprinting for quantitative traits on the X chromosome in the presence of association, namely, Q-XPAT(c), Q-1-XPAT(c) and Q-C-XPAT(c), where c is a constant. These methods can accommodate complete and incomplete nuclear families with an arbitrary number of daughters. Extensive simulation studies demonstrate that the proposed tests control the size well under the null hypothesis of no imprinting effects and are powerful under various family structures. Moreover, by setting the inbreeding coefficient in females to be nonzero and using the assortative mating pattern in simulations, the proposed tests are shown to be valid under Hardy-Weinberg disequilibrium.]]> Fri, 16 Jun 2017 00:00:00 PDT Quantitative Analysis of the DNA Methylation Sensitivity of Transcription Factor Complexes. Kribelbauer JF, Laptenko O, Chen S, Martini GD, Freed-Pastor WA, Prives C, Mann RS, Bussemaker HJ
Cell Rep (Jun 2017)

Although DNA modifications play an important role in gene regulation, the underlying mechanisms remain elusive. We developed EpiSELEX-seq to probe the sensitivity of transcription factor binding to DNA modification in vitro using massively parallel sequencing. Feature-based modeling quantifies the effect of cytosine methylation ((5)mC) on binding free energy in a position-specific manner. Application to the human bZIP proteins ATF4 and C/EBPβ and three different Pbx-Hox complexes shows that (5)mCpG can both increase and decrease affinity, depending on where the modification occurs within the protein-DNA interface. The TF paralogs tested vary in their methylation sensitivity, for which we provide a structural rationale. We show that (5)mCpG can also enhance in vitro p53 binding and provide evidence for increased in vivo p53 occupancy at methylated binding sites, correlating with primed enhancer histone marks. Our results establish a powerful strategy for dissecting the epigenomic modulation of protein-DNA interactions and their role in gene regulation.]]> Wed, 14 Jun 2017 00:00:00 PDT Strand-specific CpG hemimethylation, a novel epigenetic modification functional for genomic imprinting. Patiño-Parrado I, Gómez-Jiménez Ã, López-Sánchez N, Frade JM
Nucleic Acids Res (Jun 2017)

Imprinted genes are regulated by allele-specific differentially DNA-methylated regions (DMRs). Epigenetic methylation of the CpGs constituting these DMRs is established in the germline, resulting in a 5-methylcytosine-specific pattern that is tightly maintained in somatic tissues. Here, we show a novel epigenetic mark, characterized by strand-specific hemimethylation of contiguous CpG sites affecting the germline DMR of the murine Peg3, but not Snrpn, imprinted domain. This modification is enriched in tetraploid cortical neurons, a cell type where evidence for a small proportion of formylmethylated CpG sites within the Peg3-controlling DMR is also provided. Single nucleotide polymorphism (SNP)-based transcriptional analysis indicated that these epigenetic modifications participate in the maintainance of the monoallelic expression pattern of the Peg3 imprinted gene. Our results unexpectedly demonstrate that the methylation pattern observed in DMRs controlling defined imprinting regions can be modified in somatic cells, resulting in a novel epigenetic modification that gives rise to strand-specific hemimethylated domains functional for genomic imprinting. We anticipate the existence of a novel molecular mechanism regulating the transition from fully methylated CpGs to strand-specific hemimethylated CpGs.]]> Mon, 12 Jun 2017 00:00:00 PDT Reprogramming of the Tumor in the Hypoxic Niche: The Emerging Concept and Associated Therapeutic Strategies. Qiu GZ, Jin MZ, Dai JX, Sun W, Feng JH, Jin WL
Trends Pharmacol Sci (Jun 2017)

Hypoxia exerts a profound impact on diverse aspects of cancer biology. Increasing evidence has revealed novel functions of hypoxia in cancer cell epigenomics, epitranscriptomics, metabolism, and intercellular communication, all hotspots of cancer research. Several drugs have been developed to target intratumoral hypoxia and have entered clinical trials to treat refractory tumors. However, direct targeting of hypoxia signaling still has limitations in the clinic with regard to cancer progression and resistance to therapy. Comprehensive understanding of the molecular mechanisms by which hypoxia reshapes tumors and their microenvironment, as well as how tumor cells adapt to and thrive in hypoxic conditions, will therefore continue to be a focus of cancer research and will provide new directions for hypoxic tumor treatment.]]> Mon, 12 Jun 2017 00:00:00 PDT EpiCompare: An online tool to define and explore genomic regions with tissue or cell type-specific epigenomic features. He Y, Wang T
Bioinformatics (Jun 2017)

The Human Reference Epigenome Map, generated by the Roadmap Epigenomics Consortium, contains thousands of genome-wide epigenomic datasets that describe epigenomes of a variety of different human tissue and cell types. This map has allowed investigators to obtain a much deeper and more comprehensive view of our regulatory genome, for example defining regulatory elements including all promoters and enhancers for a given tissue or cell type. An outstanding task is to combine and compare different epigenomes in order to identify regions with epigenomic features specific to certain types of tissues or cells, for example, lineage-specific regulatory elements. Currently available tools do not directly address this question. This need motivated us to develop a tool that allows investigators to easily identify regions with epigenetic features unique to specific epigenomes that they choose, making detection of common regulatory elements and/or cell type-specific regulatory elements an interactive and dynamic experience.]]> Mon, 12 Jun 2017 00:00:00 PDT Colorectal Cancer Screening: Recommendations for Physicians and Patients From the U.S. Multi-Society Task Force on Colorectal Cancer. Rex DK, Boland CR, Dominitz JA, Giardiello FM, Johnson DA, Kaltenbach T, Levin TR, Lieberman D, Robertson DJ
Gastroenterology (Jun 2017)

This document updates the colorectal cancer (CRC) screening recommendations of the U.S. Multi-Society Task Force of Colorectal Cancer (MSTF), which represents the American College of Gastroenterology, the American Gastroenterological Association, and The American Society for Gastrointestinal Endoscopy. CRC screening tests are ranked in 3 tiers based on performance features, costs, and practical considerations. The first-tier tests are colonoscopy every 10 years and annual fecal immunochemical test (FIT). Colonoscopy and FIT are recommended as the cornerstones of screening regardless of how screening is offered. Thus, in a sequential approach based on colonoscopy offered first, FIT should be offered to patients who decline colonoscopy. Colonoscopy and FIT are recommended as tests of choice when multiple options are presented as alternatives. A risk-stratified approach is also appropriate, with FIT screening in populations with an estimated low prevalence of advanced neoplasia and colonoscopy screening in high prevalence populations. The second-tier tests include CT colonography every 5 years, the FIT-fecal DNA test every 3 years, and flexible sigmoidoscopy every 5 to 10 years. These tests are appropriate screening tests, but each has disadvantages relative to the tier 1 tests. Because of limited evidence and current obstacles to use, capsule colonoscopy every 5 years is a third-tier test. We suggest that the Septin9 serum assay (Epigenomics, Seattle, Wash) not be used for screening. Screening should begin at age 50 years in average-risk persons, except in African Americans in whom limited evidence supports screening at 45 years. CRC incidence is rising in persons under age 50, and thorough diagnostic evaluation of young persons with suspected colorectal bleeding is recommended. Discontinuation of screening should be considered when persons up to date with screening, who have prior negative screening (particularly colonoscopy), reach age 75 or have <10 years of life expectancy. Persons without prior screening should be considered for screening up to age 85, depending on age and comorbidities. Persons with a family history of CRC or a documented advanced adenoma in a first-degree relative age <60 years or 2 first-degree relatives with these findings at any age are recommended to undergo screening by colonoscopy every 5 years, beginning 10 years before the age at diagnosis of the youngest affected relative or age 40, whichever is earlier. Persons with a single first-degree relative diagnosed at ≥60 years with CRC or an advanced adenoma can be offered average-risk screening options beginning at age 40 years.]]> Sat, 10 Jun 2017 00:00:00 PDT Beta cell heterogeneity: an evolving concept. Avrahami D, Klochendler A, Dor Y, Glaser B
Diabetologia (Jun 2017)

Beta cells are primarily defined by their ability to produce insulin and secrete it in response to appropriate stimuli. It has been known for some time, however, that beta cells are not functionally identical to each other and that the rates of insulin synthesis and release differ from cell to cell, although the functional significance of this variability remains unclear. Recent studies have used heterogeneous gene expression to isolate and evaluate different subpopulations of beta cells and to demonstrate alterations in these subpopulations in diabetes. In the last few years, novel technologies have emerged that permit the detailed evaluation of the proteome (e.g. time-of-flight mass spectroscopy, [CyTOF]) and transcriptome (e.g. massively parallel RNA sequencing) at the single-cell level, and tools for single beta cell metabolomics and epigenomics are quickly maturing. The first wave of single beta cell proteome and transcriptome studies were published in 2016, giving a glimpse into the power, but also the limitations, of these approaches. Despite this progress, it remains unclear if the observed heterogeneity of beta cells represents stable, distinct beta cell types or, alternatively, highly dynamic beta cell states. Here we provide a concise overview of recent developments in the emerging field of beta cell heterogeneity and the implications for our understanding of beta cell biology and pathology.]]> Fri, 09 Jun 2017 00:00:00 PDT NaviSE: superenhancer navigator integrating epigenomics signal algebra. Ascensión AM, Arrospide-Elgarresta M, Izeta A, Araúzo-Bravo MJ
BMC Bioinformatics (Jun 2017)

Superenhancers are crucial structural genomic elements determining cell fate, and they are also involved in the determination of several diseases, such as cancer or neurodegeneration. Although there are pipelines which use independent pieces of software to predict the presence of superenhancers from genome-wide chromatin marks or DNA-interaction protein binding sites, there is not yet an integrated software tool that processes automatically algebra combinations of raw data sequencing into a comprehensive final annotated report of predicted superenhancers.]]> Wed, 07 Jun 2017 00:00:00 PDT Uncovering the transcriptomic and epigenomic landscape of nicotinic receptor genes in non-neuronal tissues. Zhang B, Madden P, Gu J, Xing X, Sankar S, Flynn J, Kroll K, Wang T
BMC Genomics (Jun 2017)

Nicotinic acetylcholine receptors (nAChRs) play an important role in cellular physiology and human nicotine dependence, and are closely associated with many human diseases including cancer. For example, previous studies suggest that nAChRs can re-wire gene regulatory networks in lung cancer cell lines. However, the tissue specificity of nAChRs genes and their regulation remain unexplored.]]> Tue, 06 Jun 2017 00:00:00 PDT Looking Back: Epigenomics.
Cell Stem Cell (Jun 2017)

Our understanding of how changes in epigenomics facilitate reprogramming and lineage specification has grown extensively over the last decade. For our tenth anniversary, we asked authors who cited a selection of our most popular papers in this area about how these studies influenced their work and the field.]]> Fri, 02 Jun 2017 00:00:00 PDT Colorectal Cancer Screening: Recommendations for Physicians and Patients from the U.S. Multi-Society Task Force on Colorectal Cancer. Rex DK, Boland CR, Dominitz JA, Giardiello FM, Johnson DA, Kaltenbach T, Levin TR, Lieberman D, Robertson DJ
Am J Gastroenterol (Jun 2017)

This document updates the colorectal cancer (CRC) screening recommendations of the U.S. Multi-Society Task Force of Colorectal Cancer (MSTF), which represents the American College of Gastroenterology, the American Gastroenterological Association, and The American Society for Gastrointestinal Endoscopy. CRC screening tests are ranked in 3 tiers based on performance features, costs, and practical considerations. The first-tier tests are colonoscopy every 10 years and annual fecal immunochemical test (FIT). Colonoscopy and FIT are recommended as the cornerstones of screening regardless of how screening is offered. Thus, in a sequential approach based on colonoscopy offered first, FIT should be offered to patients who decline colonoscopy. Colonoscopy and FIT are recommended as tests of choice when multiple options are presented as alternatives. A risk-stratified approach is also appropriate, with FIT screening in populations with an estimated low prevalence of advanced neoplasia and colonoscopy screening in high prevalence populations. The second-tier tests include CT colonography every 5 years, the FIT-fecal DNA test every 3 years, and flexible sigmoidoscopy every 5 to 10 years. These tests are appropriate screening tests, but each has disadvantages relative to the tier 1 tests. Because of limited evidence and current obstacles to use, capsule colonoscopy every 5 years is a third-tier test. We suggest that the Septin9 serum assay (Epigenomics, Seattle, Wash) not be used for screening. Screening should begin at age 50 years in average-risk persons, except in African Americans in whom limited evidence supports screening at 45 years. CRC incidence is rising in persons under age 50, and thorough diagnostic evaluation of young persons with suspected colorectal bleeding is recommended. Discontinuation of screening should be considered when persons up to date with screening, who have prior negative screening (particularly colonoscopy), reach age 75 or have <10 years of life expectancy. Persons without prior screening should be considered for screening up to age 85, depending on age and comorbidities. Persons with a family history of CRC or a documented advanced adenoma in a first-degree relative age <60 years or 2 first-degree relatives with these findings at any age are recommended to undergo screening by colonoscopy every 5 years, beginning 10 years before the age at diagnosis of the youngest affected relative or age 40, whichever is earlier. Persons with a single first-degree relative diagnosed at ≥60 years with CRC or an advanced adenoma can be offered average-risk screening options beginning at age 40 years.Am J Gastroenterol advance online publication, 6 June 2017; doi:10.1038/ajg.2017.174.]]> Tue, 30 May 2017 00:00:00 PDT Williams syndrome deletions and duplications: Genetic windows to understanding anxiety, sociality, autism, and schizophrenia. Crespi BJ, Procyshyn TL
Neurosci Biobehav Rev (Aug 2017)

We describe and evaluate an integrative hypothesis for helping to explain the major neurocognitive features of individuals with Williams syndrome region deletions and duplications. First, we demonstrate how the cognitive differences between Williams syndrome individuals, individuals with duplications of this region, and healthy individuals parallel the differences between individuals subject to effects of increased or decreased oxytocin. Second, we synthesize evidence showing that variation in expression of the gene GTF2I (General Transcription Factor II-I) underlies the primary social phenotypes of Williams syndrome and that common genetic variation in GTF2I mediates oxytocin reactivity, and its correlates, in healthy populations. Third, we describe findings relevant to the hypothesis that the GTF2I gene is subject to parent of origin effects whose behavioral expression fits with predictions from the kinship theory of genomic imprinting. Fourth, we describe how Williams syndrome can be considered, in part, as an autistic syndrome of Lorna Wing's 'active-but-odd' autism subtype, in contrast to associations of duplications with both schizophrenia and autism.]]> Sat, 13 May 2017 00:00:00 PDT Omics analysis of human bone to identify genes and molecular networks regulating skeletal remodeling in health and disease. Reppe S, Datta HK, Gautvik KM
Bone (Aug 2017)

The skeleton is a metabolically active organ throughout life where specific bone cell activity and paracrine/endocrine factors regulate its morphogenesis and remodeling. In recent years, an increasing number of reports have used multi-omics technologies to characterize subsets of bone biological molecular networks. The skeleton is affected by primary and secondary disease, lifestyle and many drugs. Therefore, to obtain relevant and reliable data from well characterized patient and control cohorts are vital. Here we provide a brief overview of omics studies performed on human bone, of which our own studies performed on trans-iliacal bone biopsies from postmenopausal women with osteoporosis (OP) and healthy controls are among the first and largest. Most other studies have been performed on smaller groups of patients, undergoing hip replacement for osteoarthritis (OA) or fracture, and without healthy controls. The major findings emerging from the combined studies are: 1. Unstressed and stressed bone show profoundly different gene expression reflecting differences in bone turnover and remodeling and 2. Omics analyses comparing healthy/OP and control/OA cohorts reveal characteristic changes in transcriptomics, epigenomics (DNA methylation), proteomics and metabolomics. These studies, together with genome-wide association studies, in vitro observations and transgenic animal models have identified a number of genes and gene products that act via Wnt and other signaling systems and are highly associated to bone density and fracture. Future challenge is to understand the functional interactions between bone-related molecular networks and their significance in OP and OA pathogenesis, and also how the genomic architecture is affected in health and disease.]]> Fri, 28 Apr 2017 00:00:00 PDT Early detection of gastric cancer using global, genome-wide and IRF4, ELMO1, CLIP4 and MSC DNA methylation in endoscopic biopsies. Pirini F, Noazin S, Jahuira-Arias MH, Rodriguez-Torres S, Friess L, Michailidi C, Cok J, Combe J, Vargas G, Prado W, Soudry E, Pérez J, Yudin T, Mancinelli A, Unger H, Ili-Gangas C, Brebi-Mieville P, Berg DE, Hayashi M, Sidransky D, Gilman RH, Guerrero-Preston R
Oncotarget (Jun 2017)

Clinically useful molecular tools to triage gastric cancer patients are not currently available. We aimed to develop a molecular tool to predict gastric cancer risk in endoscopy-driven biopsies obtained from high-risk gastric cancer clinics in low resource settings.We discovered and validated a DNA methylation biomarker panel in endoscopic samples obtained from 362 patients seen between 2004 and 2009 in three high-risk gastric cancer clinics in Lima, Perú, and validated it in 306 samples from the Cancer Genome Atlas project ("TCGA"). Global, epigenome wide and gene-specific DNA methylation analyses were used in a Phase I Biomarker Development Trial to identify a continuous biomarker panel that combines a Global DNA Methylation Index (GDMI) and promoter DNA methylation levels of IRF4, ELMO1, CLIP4 and MSC.We observed an inverse association between the GDMI and histological progression to gastric cancer, when comparing gastritis patients without metaplasia (mean = 5.74, 95% CI, 4.97-6.50), gastritis patients with metaplasia (mean = 4.81, 95% CI, 3.77-5.84), and gastric cancer cases (mean = 3.38, 95% CI, 2.82-3.94), respectively (p < 0.0001). Promoter methylation of IRF4 (p < 0.0001), ELMO1 (p < 0.0001), CLIP4 (p < 0.0001), and MSC (p < 0.0001), is also associated with increasing severity from gastritis with no metaplasia to gastritis with metaplasia and gastric cancer.Our findings suggest that IRF4, ELMO1, CLIP4 and MSC promoter methylation coupled with a GDMI>4 are useful molecular tools for gastric cancer risk stratification in endoscopic biopsies.]]> Tue, 18 Apr 2017 00:00:00 PDT Neurodevelopmental consequences in offspring of mothers with preeclampsia during pregnancy: underlying biological mechanism via imprinting genes. Nomura Y, John RM, Janssen AB, Davey C, Finik J, Buthmann J, Glover V, Lambertini L
Arch Gynecol Obstet (Jun 2017)

Preeclampsia is known to be a leading cause of mortality and morbidity among mothers and their infants. Approximately 3-8% of all pregnancies in the US are complicated by preeclampsia and another 5-7% by hypertensive symptoms. However, less is known about its long-term influence on infant neurobehavioral development. The current review attempts to demonstrate new evidence for imprinting gene dysregulation caused by hypertension, which may explain the link between maternal preeclampsia and neurocognitive dysregulation in offspring.]]> Thu, 06 Apr 2017 00:00:00 PDT Early detection of pancreatic cancer: Where are we now and where are we going? Zhou B, Xu JW, Cheng YG, Gao JY, Hu SY, Wang L, Zhan HX
Int J Cancer (Jul 2017)

Pancreatic cancer (PC) is one of the most lethal malignancies. Recent studies indicate that patients with incidentally diagnosed PC have better prognosis than those with symptoms and that there is a sufficient window for early detection. However, effective early diagnosis remains difficult and depends mainly on imaging modalities and the development of screening methodologies with highly sensitive and specific biomarkers. This review summarizes recent advances in effective screening for early diagnosis of PC using imaging modalities and novel molecular biomarkers discovered from various "omics" studies including genomics, epigenomics, non-coding RNA, metabonomics, liquid biopsy (CTC, ctDNA and exosomes) and microbiomes, and their use in body fluids (feces, urine and saliva). Although many biomarkers for early detection of PC have been discovered through various methods, larger scale and rigorous validation is required before their application in the clinic. In addition, more effective and specific biomarkers of PC are urgently needed.]]> Mon, 27 Feb 2017 00:00:00 PST Three intronic lncRNAs with monoallelic expression derived from the MEG8 gene in cattle. Yang W, Li D, Wang G, Zhang C, Zhang M, Zhang W, Li S
Anim Genet (Jun 2017)

The field of long noncoding RNA (lncRNA) research has been rapidly advancing in recent years. Antisense lncRNAs, intergenetic lncRNAs and enhancer lncRNAs can regulate genomic imprinting, which leads to parent-origin-specific monoalletic expression of genes. However, the function of intronic ncRNAs in genomic imprinting remains unclear. Previously, we obtained the cDNA sequence of cattle MEG8 gene, which is located in the DLK1-DIO3 imprinted clusters of cattle chromosome 21. In this study, we undertook a systematic search for transcripts mapping to the MEG8 intronic region and identified three novel lncRNAs, named MEG8 intronic RNA 1 (MEG8-IT1), MEG8 intronic RNA 2 (MEG8-IT2) and MEG8 intronic RNA 3 (MEG8-IT3) according to the GENCODE annotated bibliography. We characterized the expression pattern of these lncRNAs using RT-PCR in adult cattle tissues, and they were expressed in all tested eight tissues, similar to the expression pattern of MEG8. The allele-specific expression of three novel lncRNAs was assessed using a polymorphism-based sequencing approach. Three single nucleotide polymorphism sites were identified in these three lncRNAs. We found that the three lncRNAs showed monoallelic expression in the analyzed tissues, suggesting that they may be imprinted in cattle. These results expand the number of known monoallelically expressed lncRNAs from the DLK1-DIO3 domain and contribute to further investigation of lncRNA regulatory mechanisms and function.]]> Wed, 07 Dec 2016 00:00:00 PST A new model for parent-of-origin effect analyses applied to Brown Swiss cattle slaughterhouse data. Blunk I, Mayer M, Hamann H, Reinsch N
Animal (Jul 2017)

Genomic imprinting is a phenomenon that arises when the expression of genes depends on the parental origin of alleles. Epigenetic mechanisms may induce the full or partial suppression of maternal or paternal alleles, thereby leading to different types of imprinting. However, imprinting effects have received little consideration in animal breeding programmes, although their relevance to some agricultural important traits has been demonstrated. A recently proposed model (imprinting model) with two path-of-transmission (male and female)-specific breeding values for each animal accounts for all types of imprinting simultaneously (paternal, maternal, full and partial). Imprinting effects (or more generally: parent-of-origin effects (POE)) are determined by taking the difference between the two genetic effects in each animal. However, the computation of their prediction error variance (PEV) is laborious; thus, we propose a new model that is equivalent to the aforementioned imprinting model, which facilitates the direct estimation of imprinting effects instead of taking the differences and the PEV is readily obtained. We applied the new model to slaughterhouse data for Brown Swiss cattle, among which imprinting has never been investigated previously. Data were available for up to 173 051 fattening bulls, where the pedigrees contained up to 428 710 animals representing the entire Brown Swiss population of Austria and Germany. The traits analysed comprised the net BW gain, fat score, EUROP class and killing out percentage. The analysis demonstrated that the net BW gain, fat score and EUROP class were influenced significantly by POE. After estimating the POE, the new model yielded estimates with reliabilities ranging between 0.4 and 0.9. On average, the imprinting variances accounted for 9.6% of the total genetic variance, where the maternal gamete was the main contributor. Moreover, our results agreed well with those obtained using linear models when the EUROP class and fat score were treated as categorical traits by applying a GLMM with a logit link function.]]> Tue, 06 Dec 2016 00:00:00 PST