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MicroRNA expression analysis of livers of F1 male offspring fathered from control mice or stressed mice

ABSTRACT: Psychological stress is highly prevalent in modern society. Both epidemiologic and experimental animal studies demonstrate that chronic psychological stress exerts adverse effects on the initiation and/or progression of many diseases. Here, using a mouse model of restraint stress, we report the discovery of a novel signaling pathway linking paternal stress exposure to the reprogram of hepatic gluconeogenesis in the offspring. Offspring fathered by stressed males (Stress-F1) exhibits hyperglycemia as a result of enhanced hepatic gluconeogenesis, conpared to offspring from control fathers (Control-F1). Mechanistically, protein levels of PEPCK, a key gluconeogenic enzyme, were significantly increased, while its mRNA levels were unaffected in the stress-F1 mice, pointing to a posttranscriptional regulatory mechanism. Because MicroRNAs often play an important role in regulating gene expression at the posttranscriptional level, we investigated the expression profile of MicroRNAs in livers from Control-F1 and Stress-F1 mice.

ORGANISM(S): Merkel cell polyomavirus Cytomegalovirus Human alphaherpesvirus 2 Betapolyomavirus hominis Mus musculus Human alphaherpesvirus 1 Lymphocryptovirus JC polyomavirus Betapolyomavirus macacae Homo sapiens Human immunodeficiency virus 1 Rhadinovirus

PROVIDER: GSE73530 | GEO | 2015/09/29

SECONDARY ACCESSION(S): PRJNA297227

REPOSITORIES: GEO

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Project description:Purpose: Paternal life experiences impact offspring health via germline, and epigenetic inheritance provides a potential mechanism. However, global reprogramming during offspring embryogenesis and gametogenesis represents the largest hurdle to conceptualize it. Yet, detailed characterization of how sperm epigenetic alterations carrying “environmental memory” can evade offspring embryonic reprogramming remains elusive. Methods: we profiled the sperm DNA methylation patterns of three consecutive generations (F0, F1 and F2) in both control and stress groups by using whole-genome bisulfite sequencing (WGBS). A total of 18 sperm samples were analyzed, including three biological replicates for each generation under each treatment. In addition, small RNA sequencing was carried out on paternal sperm samples to investigate whether long-term psychological stress affected the enrichment of certain sncRNAs and to identify whether they participated in mediating the occurrence and paternal inheritance of the stress-induced DMRs Rsults: Using an optimized data analysis workflow, we obtained approximately 800 million clean reads per sample (build mm10) with strand-specific coverage ~21×, and the data covered ~96.00% of the total 21,867,837 reference CpG dinucleotides. A total of 24,427, 7,975, and 5,173 differentially methylated regions (DMRs) between control and stress groups were found in the F0, F1, and F2 generations, respectively. Inter- and transgenerational inheritance of paternal DMRs were at frequencies approximately 11.36% and 0.48%, respectively. These DMRs related to genes with functional implications for psychological stress response, and tissue inheritance of these DMRs passed paternal disorders epigenetically to offspring. More importantly, these DMRs evaded offspring embryonic reprogramming through erasure and subsequent reestablishment, but not via un-erasure way. Nonetheless, their reestablishment proportions in the primitive streak (E7.5) stage were altered. Furthermore, sncRNA-seq revealed that stress-induced tsRNA, miRNA and rsRNA dysregulation in paternal sperm might play important roles in DMRs occurrence and paternal inheritance.

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MicroRNA expression analysis of livers of F1 male offspring fathered from control mice or stressed mice

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