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Copy number variation in Y chromosome multicopy genes is linked to a paternal parent-of-origin effect on CNS autoimmune disease in female offspring
Journal article   Open access   Peer reviewed

Copy number variation in Y chromosome multicopy genes is linked to a paternal parent-of-origin effect on CNS autoimmune disease in female offspring

Laure K Case, Emma H Wall, Erin E Osmanski, Julie A Dragon, Naresha Saligrama, James F Zachary, Bernardo Lemos, Elizabeth P Blankenhorn and Cory Teuscher
Genome biology, v 16(1), pp 28-28
10 Feb 2015
PMID: 25886764
url
https://doi.org/10.1186/s13059-015-0591-7View
Published, Version of Record (VoR) Open

Abstract

Spermatogenesis - genetics Humans Male MicroRNAs - metabolism Gene Expression Profiling Spermatozoa - metabolism Y Chromosome - genetics Autoimmune Diseases - genetics Lymphocyte Activation - immunology Inheritance Patterns - genetics Female Encephalomyelitis, Autoimmune, Experimental - genetics X Chromosome - genetics Genetic Linkage Animals, Newborn Genetic Predisposition to Disease Mice, Inbred C57BL CD4-Positive T-Lymphocytes - metabolism Linear Models DNA Copy Number Variations - genetics Gene Dosage Sex Characteristics Sex Ratio Phenotype Animals MicroRNAs - genetics Cytokines - biosynthesis
The prevalence of some autoimmune diseases is greater in females compared with males, although disease severity is often greater in males. The reason for this sexual dimorphism is unknown, but it may reflect negative selection of Y chromosome-bearing sperm during spermatogenesis or male fetuses early in the course of conception/pregnancy. Previously, we showed that the sexual dimorphism in experimental autoimmune encephalomyelitis (EAE) is associated with copy number variation (CNV) in Y chromosome multicopy genes. Here, we test the hypothesis that CNV in Y chromosome multicopy genes influences the paternal parent-of-origin effect on EAE susceptibility in female mice. We show that C57BL/6 J consomic strains of mice possessing an identical X chromosome and CNV in Y chromosome multicopy genes exhibit sperm head abnormalities and female-biased sex ratio. This is consistent with X-Y intragenomic conflict arising from an imbalance in CNV between homologous X:Y chromosome multicopy genes. These males also display paternal transmission of EAE to female offspring and differential loading of microRNAs within the sperm nucleus. Furthermore, in humans, families of probands with multiple sclerosis similarly exhibit a female-biased sex ratio, whereas families of probands affected with non-sexually dimorphic autoimmune diseases exhibit unbiased sex ratios. These findings provide evidence for a mechanism at the level of the male gamete that contributes to the sexual dimorphism in EAE and paternal parent-of-origin effects in female mice, raising the possibility that a similar mechanism may contribute to the sexual dimorphism in multiple sclerosis.

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Collaboration types
Domestic collaboration
Web of Science research areas
Biotechnology & Applied Microbiology
Genetics & Heredity
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