Premium
Prenatal stress and transgenerational epigenetic programming via the paternal lineage
Author(s) -
Morgan Christopher Paul,
Bale Tracy L
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.307.4
Subject(s) - transgenerational epigenetics , epigenetics , lineage (genetic) , prenatal stress , biology , genetics , pregnancy , gene , offspring
Sex‐biased neurodevelopmental disorders, including autism and schizophrenia, have been associated with fetal antecedents such as maternal stress. The mechanisms through which stress programs offspring outcomes are not well understood, though they likely involve complex interactions between maternal environment, placental changes, embryo sex, and epigenetics. We have recently identified early gestation as a period sensitive to sex‐specific programming effects of stress. Male offspring showed increased stress sensitivity as adults in behavioral and physiological measures. These males also had reduced testosterone levels, smaller testes, and shorter anogenital distances, suggesting a disruption in normal perinatal masculinization. Further, we have recently found that this stress‐sensitive dysmasculinized phenotype can be transmitted along the paternal lineage from prenatal stress exposed males to second‐generation male offspring. Analysis by RT‐PCR array in postnatal day 1 (PN1) brains showed a feminized pattern of gene expression in these second‐generation male brains. This mode of transmission implicates epigenetic programming of the germline in the persistence of the phenotype, an effect that could be mediated by miRNAs. These results provide insight into mechanisms contributing to sex biased vulnerability to prenatal stress during early pregnancy and the heritability of such outcomes. Grant Funding Source : NIH MH073030