ArticleInternational journal of molecular sciences2017
Characterization of Copy Number Variation's Potential Role in Marek's Disease.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Epigenetic Factor MicroRNAs Likely Mediate Vaccine Protection Efficacy against Lymphomas in Response to Tumor Virus Infection in Chickens through Target Gene Involved Signaling Pathways.Veterinary sciences · 2024Article
- Population Genomic Sequencing Delineates Global Landscape of Copy Number Variations that Drive Domestication and Breed Formation of in Chicken.Frontiers in genetics · 2022Article
- Article
- Genome-wide characterization of copy number variations in the host genome in genetic resistance to Marek's disease using next generation sequencing.BMC genetics · 2020Article
- Marek's Disease Virus Infection Induced Mitochondria Changes in Chickens.International journal of molecular sciences · 2019Article
- Detection of copy number variations in brown and white layers based on genotyping panels with different densities.Genetics, selection, evolution : GSE · 2018Article
- Genetic assessment of inbred chicken lines indicates genomic signatures of resistance to Marek's disease.Journal of animal science and biotechnology · 2018Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Marek's Disease (MD) is a highly contagious pathogenic and oncogenic disease primarily affecting chickens. Chicken Lines 63 and 72, as well as their recombinant congenic strains (RCS) with varied susceptibility to MD, are ideal models to study the complex mechanisms of genetic resistance to MD. In this study, we investigated copy number variation (CNV) in these inbred chicken lines using the Affymetrix Axiom HD 600 K SNP genotyping array. We detected 393 CNV segments across all ten chicken lines, of which 12 CNVs were specifically identified in Line 72. We then assessed genetic structure based on CNV and observed markedly different patterns. Finally, we validated two deletion events in Line 72 and correlated them with genes expression using qPCR and RNA-seq, respectively. Our combined results indicated that these two CNV deletions were likely to contribute to MD susceptibility.
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Registered trials
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