Genomic imprinting results in the differential expression of genes, depending on which allele is inherited from the mother and which from the father. The effects of such differential gene expression are reflected in phenotypic differences between the reciprocal heterozygotes (Aa vs. aA). Although many imprinted genes have been identified and play a key role in development, little is known about the contribution of imprinting to quantitative variation in trait expression. Here, we examine this problem by mapping imprinting effects on adult body composition traits in the F(3) generation of an intercross between the Large (LG/J) and Small (SM/J) inbred mouse strains. We identified eight pleiotropic imprinted quantitative trait loci (iQTL) located throughout the genome. Most iQTL are in novel locations that have not previously been associated with imprinting effects, but those on chromosomes 7, 12, and centromeric 18 lie in regions previously identified as containing imprinted genes. Our results show that the effects of genomic imprinting are relatively small, with reciprocal heterozygotes differing by approximately 0.25 standard deviation units and the effects at each locus accounting for 1% to 4% of the phenotypic variance. We detected a variety of imprinting patterns, with paternal expression being the most common. These results indicate that genomic imprinting has small, but detectable, effects on the normal variation of complex traits in adults and is likely to be more common than usually thought.
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http://dx.doi.org/10.1073/pnas.0706562105 | DOI Listing |
Gene
January 2025
Faculty of Biotechnology, Ho Chi Minh City Open University, Ho Chi Minh City 700000 Viet Nam.
Cells preserve and convey certain gene expression patterns to their progeny through the mechanism called epigenetic memory. Epigenetic memory, encoded by epigenetic markers and components, determines germline inheritance, genomic imprinting, and X chromosome inactivation. First discovered long non coding RNAs were implicated in genomic imprinting and X-inactivation and these two phenomena clearly demonstrate the role of lncRNAs in epigenetic memory regulation.
View Article and Find Full Text PDFOpen Biol
January 2025
Department of Epigenetics, Medical Research Institute (MRI), Tokyo Medical and Dental University (TMDU), Tokyo 113-8510, Japan.
Retrotransposon Gag-like (RTL) 8A, 8B and 8C are eutherian-specific genes derived from a certain retrovirus. They cluster as a triplet of genes on the X chromosome, but their function remains unknown. Here, we demonstrate that and play important roles in the brain: their double knockout (DKO) mice not only exhibit reduced social responses and increased apathy-like behaviour, but also become obese from young adulthood, similar to patients with late Prader-Willi syndrome (PWS), a neurodevelopmental genomic imprinting disorder.
View Article and Find Full Text PDFMol Plant
January 2025
State Key Laboratory of Wheat Improvement, School of Advanced Agricultural Sciences, Peking University, Beijing 100871, China; Beijing Life Science Academy, Beijing 102299, China. Electronic address:
It has been hypothesized that DNA damage has the potential to induce DNA hypermethylation, contributing to carcinogenesis in mammals. However, there is no sufficient evidence to support that DNA damage can cause genome-wide DNA hypermethylation. Here, we demonstrated that DNA single-strand breaks with 3'-blocked ends (DNA 3'-blocks) can not only reinforce DNA methylation at normally methylated loci but also can induce DNA methylation at normally nonmethylated loci in plants.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Federal Research Centre «Fundamentals of Biotechnology», Russian Academy of Sciences, Moscow, Russia, 119071.
Background: TRIM28 plays a crucial role in maintaining genomic stability and establishing imprinting, facilitated by the diversity of KRAB zinc finger proteins. The SUMOylation of TRIM28 is essential for its function and is enhanced in the presence of the KRAB domain. Previously, we demonstrated that Kaiso, another factor capable of interacting with TRIM28, can promote its SUMOylation.
View Article and Find Full Text PDFNeuron
January 2025
Department of Neurogenetics, Max Planck Institute for Multidisciplinary Sciences, Göttingen, Germany. Electronic address:
In Alzheimer's disease (AD) research, the 5xFAD mouse model is commonly used as a heterozygote crossed with other genetic models to study AD pathology. We investigated whether the parental origin of the 5xFAD transgene affects plaque deposition. Using quantitative light-sheet microscopy, we found that paternal inheritance of the transgene led to a 2-fold higher plaque burden compared with maternal inheritance, a finding consistent across multiple 5xFAD colonies.
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