Piwi-interacting RNAs (piRNAs) are small non-coding RNAs that associate with PIWI proteins for transposon silencing via DNA methylation and are highly expressed and extensively studied in the germline. Mature germline piRNAs typically consist of 24-32 nucleotides, with a strong preference for a 5' uridine signature, an adenosine signature at position 10, and a 2'-O-methylation signature at the 3' end. piRNA presence in somatic tissues, however, is not well characterized and requires further systematic evaluation. In the current study, we identified piRNAs and associated machinery from mouse somatic tissues representing the three germ layers. piRNA specificity was improved by combining small RNA size selection, sodium periodate treatment enrichment for piRNA over other small RNA, and small RNA next-generation sequencing. We identify PIWIL1, PIWIL2, and PIWIL4 expression in brain, liver, kidney, and heart. Of note, somatic piRNAs are shorter in length and tissue-specific, with increased occurrence of unique piRNAs in hippocampus and liver, compared to the germline. Hippocampus contains 5,494 piRNA-like peaks, the highest expression among all tested somatic tissues, followed by cortex (1,963), kidney (580), and liver (406). The study identifies 26 piRNA sequence species and 40 piRNA locations exclusive to all examined somatic tissues. Although piRNA expression has long been considered exclusive to the germline, our results support that piRNAs are expressed in several somatic tissues that may influence piRNA functions in the soma. Once confirmed, the PIWI/piRNA system may serve as a potential tool for future research in epigenome editing to improve human health by manipulating DNA methylation.
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http://dx.doi.org/10.1080/15592294.2019.1600389 | DOI Listing |
PLoS Genet
January 2025
Mater Research Institute-University of Queensland, Translational Research Institute, Woolloongabba, Brisbane, Australia.
Adaptation to existence outside the womb is a key event in the life of a mammal. The absence of macrophages in rats with a homozygous mutation in the colony-stimulating factor 1 receptor (Csf1r) gene (Csf1rko) severely compromises pre-weaning somatic growth and maturation of organ function. Transfer of wild-type bone marrow cells (BMT) at weaning rescues tissue macrophage populations permitting normal development and long-term survival.
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View Article and Find Full Text PDFMod Pathol
January 2025
Department of Pathology, Boston Children's Hospital, Boston, MA, 02115 USA. Electronic address:
Soft tissue tumors with smooth muscle differentiation are rare in pediatric patients. Despite often showing morphologic features sufficient for classification as "leiomyosarcoma" in adults (e.g.
View Article and Find Full Text PDFCell Biosci
January 2025
School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong S.A.R., China.
Background: Pathogenic or null mutations in WRN helicase is a cause of premature aging disease Werner syndrome (WS). WRN is known to protect somatic cells including adult stem cells from premature senescence. Loss of WRN in mesenchymal stem cells (MSCs) not only drives the cells to premature senescence but also significantly impairs the function of the stem cells in tissue repair or regeneration.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Neuropediatrics, Charité-Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität Berlin, and Berlin Institute of Health, 13353 Berlin, Germany.
Epilepsy affects 50 million people worldwide and is drug-resistant in approximately one-third of cases. Even when a structural lesion is identified as the epileptogenic focus, understanding the underlying genetic causes is crucial to guide both counseling and treatment decisions. Both somatic and germline DNA variants may contribute to the lesion itself and/or influence the severity of symptoms.
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