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East Lansing, MI, United States

Zhang X.,University of Georgia | Misztal I.,Wageningen University | Heidaritabar M.,Wageningen University | Bastiaansen J.W.M.,Wageningen University | And 9 more authors.
Livestock Science | Year: 2015

The objective of this study is to investigate if selection on similar traits in different populations progress from selection on similar genes. With the aid of high-density genome wide single-nucleotide polymorphism (SNP) genotyping, it is possible to directly assess changes in allelic frequencies and regions under selection and address the question. We compared the allele frequencies before and after two generations of selection on an index containing body weight at 6. wk, ultrasound measurement of breast meat, and leg score in two commercial chicken breeds with different selection histories: M breed was primarily selected for rapid growth and commonly used as a broiler breeder sire line; F breed was primarily used as dual-purposed dam line selected for both egg production and growth. Selection was performed on both lines with the same selection intensity and method (Genomic Best Linear Unbiased Prediction, GBLUP, using the single-step approach, ssGBLUP). Results: After quality control, 52,742 and 52,639 SNPs in M breed and F breed were kept in 4922 and 4904 animals, respectively. The average allele frequency change for both breeds on the autosomes was 0.049. Threshold value for detecting selected regions, where allele frequency changes exceeded expectations under drift were 0.140 and 0.136 for breeds M and F, respectively. According to the criterion used in this study, there were 25 and 17 selection regions detected on breeds M and F, respectively, without any overlap of regions between the breeds. Average heterozygosity change in F breed was greater compared to M breed (0.008 vs. 0.002, P<0.01). Also, there was no overlapping of selected regions with high heterozygosity change between breeds M and F. Conclusions: The results indicate that in newly selected populations, even using the same criteria and selection methods, the historical selection goals and breed development determine the loci that most impact selection progress. These results are consistent with quantitative genetic theory that contribution of loci to selection progress depends on initial allele frequency. Therefore it should not be assumed that the same loci will be under selection in different populations even if similar selection goals and methods are used. © 2014 Elsevier B.V. Source


Luo J.,University of Maryland University College | Mitra A.,University of Maryland University College | Tian F.,University of Maryland University College | Chang S.,Avian Disease and Oncology Laboratory | And 7 more authors.
PLoS ONE | Year: 2012

Marek's disease (MD) is a lymphoproliferative disease in chicken induced by Marek's disease virus (MDV). Although studies have focused on the genetic differences between the resistant and susceptible chicken, less is known about the role of epigenetic factors in MD. In this study, genome-wide histone modifications in the non-MHC-associated resistant and susceptible chicken lines were examined. We found that tri-methylation at histone H3 Lys4 (H3K4me3) enrichment is positively correlated with the expression of protein coding genes as well as microRNA (miRNA) genes, whereas tri-methylation at histone H3 Lys27 (H3K27me3) exhibits a negative correlation. By identifying line-specific histone modifications in MDV infection, we found unique H3K4me3 islands in the resistant chicken activated genes, which are related to immune response and cell adhesion. Interestingly, we also found some miRNAs from unique H3K27me3 patterns in the susceptible chickens that targeted genes involved in 5-hydroxytryptamine (5-HT)-receptor and adrenergic receptor pathways. In conclusion, dynamic line-specific histone modifications in response to MDV infection suggested that intrinsic epigenetic mechanisms may play a role in MD-resistance and -susceptibility. © 2012 Luo et al. Source


Crooijmans R.P.M.A.,Wageningen University | Fife M.S.,The Pirbright Institute | Fitzgerald T.W.,Wellcome Trust Sanger Institute | Strickland S.,University of Delaware | And 5 more authors.
BMC Genomics | Year: 2013

Background: Detecting genetic variation is a critical step in elucidating the molecular mechanisms underlying phenotypic diversity. Until recently, such detection has mostly focused on single nucleotide polymorphisms (SNPs) because of the ease in screening complete genomes. Another type of variant, copy number variation (CNV), is emerging as a significant contributor to phenotypic variation in many species. Here we describe a genome-wide CNV study using array comparative genomic hybridization (aCGH) in a wide variety of chicken breeds.Results: We identified 3,154 CNVs, grouped into 1,556 CNV regions (CNVRs). Thirty percent of the CNVs were detected in at least 2 individuals. The average size of the CNVs detected was 46.3 kb with the largest CNV, located on GGAZ, being 4.3 Mb. Approximately 75% of the CNVs are copy number losses relatively to the Red Jungle Fowl reference genome. The genome coverage of CNVRs in this study is 60 Mb, which represents almost 5.4% of the chicken genome. In particular large gene families such as the keratin gene family and the MHC show extensive CNV.Conclusions: A relative large group of the CNVs are line-specific, several of which were previously shown to be related to the causative mutation for a number of phenotypic variants. The chance that inter-specific CNVs fall into CNVRs detected in chicken is related to the evolutionary distance between the species. Our results provide a valuable resource for the study of genetic and phenotypic variation in this phenotypically diverse species. © 2013 Crooijmans et al.; licensee BioMed Central Ltd. Source


Lee L.F.,Avian Disease and Oncology Laboratory | Kreager K.,Dallas Center | Heidari M.,Avian Disease and Oncology Laboratory | Zhang H.,Avian Disease and Oncology Laboratory | And 3 more authors.
Avian Diseases | Year: 2013

We have previously shown that deletion of the meq gene from the genome of Cosmid-cloned rMd5 strain of Marek's disease virus (MDV-1) resulted in loss of transformation and oncogenic capacity of the virus. The rMd5ΔMeq (Meq null) virus has been shown to be an excellent vaccine in maternal antibody positive (MAb+) chickens challenged with a very virulent plus (vv+) strain of MDV, 648A. The only drawback was that it retained its ability to induce bursa and thymus atrophy (BTA) like that of the parental rMd5 in maternal antibody negative (MAb-) chickens. We recently reported that the attenuated Meq null virus did not induce BTA at the 40th cell culture passage onward. Its protective ability against challenge with vv+ MDV, strain 686 was similar to the original virus at the 19th passage in MAb- chickens. In this study, we compared the same series of attenuated meq null viruses in commercial chickens. In commercial chickens with MAb, the attenuated viruses quickly lost protection with increasing cell culture attenuation. These data suggest that although attenuation of these meq null viruses eliminated BTA, it had no influence on their protective efficacy in MAb- chickens. However, in commercial chickens (MAb+), the best protection was provided by the original 19th passage; the attenuated 40th passage was as good as one of the currently commercial CVI988/Rispens vaccine, and it did not induce BTA. Therefore, protection against virulent MDV challenge and induction of lymphoid organ atrophy are simultaneously attenuated by serial passage in vitro. © American Association of Avian Pathologists. Source

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