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Genomic imprinting-the non-equivalence of maternal and paternal genomes-is a critical process that has evolved independently in many plant and mammalian species. According to kinship theory, imprinting is the inevitable consequence of conflictive selective forces acting on differentially expressed parental alleles. Yet, how these epigenetic differences evolve in the first place is poorly understood. Here we report the identification and molecular dissection of a parent-of-origin effect on gene expression that might help to clarify this fundamental question. Toxin-antidote elements (TAs) are selfish elements that spread in populations by poisoning non-carrier individuals. In reciprocal crosses between two Caenorhabditis tropicalis wild isolates, we found that the slow-1/grow-1 TA is specifically inactive when paternally inherited. This parent-of-origin effect stems from transcriptional repression of the slow-1 toxin by the PIWI-interacting RNA (piRNA) host defence pathway. The repression requires PIWI Argonaute and SET-32 histone methyltransferase activities and is transgenerationally inherited via small RNAs. Remarkably, when slow-1/grow-1 is maternally inherited, slow-1 repression is halted by a translation-independent role of its maternal mRNA. That is, slow-1 transcripts loaded into eggs-but not SLOW-1 protein-are necessary and sufficient to counteract piRNA-mediated repression. Our findings show that parent-of-origin effects can evolve by co-option of the piRNA pathway and hinder the spread of selfish genes that require sex for their propagation.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10990930 | PMC |
http://dx.doi.org/10.1038/s41586-024-07155-z | DOI Listing |
BMC Genomics
December 2024
Agricultural Research and Development Program, Central State University, Wilberforce, USA.
BMC Med
December 2024
School of Biomedical Sciences, Biomedical Sciences Research Institute, Ulster University, Coleraine, Northern Ireland, BT52 1SA, UK.
Background: The human ZFP57 gene is a major regulator of imprinted genes, maintaining DNA methylation marks that distinguish parent-of-origin-specific alleles. DNA methylation of the gene itself has shown sensitivity to environmental stimuli, particularly folate status. However, the role of DNA methylation in ZFP57's own regulation has not been fully investigated.
View Article and Find Full Text PDFArch Oral Biol
November 2024
Cell and Molecular Biology Facility, Jubilee Centre for Medical Research, Jubilee Mission Medical College and Research Institute, Thrissur, Kerala 680005, India. Electronic address:
Horm Res Paediatr
November 2024
Division of Endocrinology and Diabetes, Stead Family Department of Pediatrics, University of Iowa, Iowa City, Iowa, USA.
Introduction: The cause of increased diabetes mellitus (DM) risk in individuals with Turner syndrome (TS) is poorly understood. Parent-of-origin effects related to whether the maternal or paternal X chromosome (Xchr) remains intact have been found for several TS phenotypes, including hypercholesterolemia. Therefore, Xchr parent-of-origin may impact DM risk in TS.
View Article and Find Full Text PDFBiol Psychiatry Glob Open Sci
November 2024
Centralized Sequencing Program, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland.
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