Rahia Mashoodh

Bio: Rahia Mashoodh is an academic researcher from University of Cambridge. The author has contributed to research in topics: Offspring & Biology. The author has an hindex of 11, co-authored 19 publications receiving 977 citations. Previous affiliations of Rahia Mashoodh include Columbia University & Dalhousie University.

Paternal social enrichment effects on maternal behavior and offspring growth

Abstract: Paternal environmental experiences are significant predictors of developmental outcomes in offspring and can occur even in the absence of paternal care. Although there has been a recent focus on the role of environmentally induced changes in the male germline in producing these effects, the potential mediating role of mothers has not been investigated. A role for mothers in the transmission of paternal effects has been well acknowledged in behavioral ecology, which predicts that females will dynamically adjust their reproductive investment in response to the qualities of their mate. In the present study, we show that a lifetime of socially enriched compared with impoverished housing conditions shifts anxiety-like behavior and gene expression of male mice. Females that mate with enriched-reared males exhibit increased levels of pup nursing and licking toward their offspring, which are associated with changes in gene expression within the maternal hypothalamus. Significantly, these changes in maternal behavior are correlated with the general levels of anxiety exhibited by their male mates. Further, we show that paternal environmental enrichment results in increased growth of their offspring. These results suggest that maternal–paternal interactions at mating may guide offspring development, with significant implications for the transgenerational transmission of paternal environmental experiences.

Maternal modulation of paternal effects on offspring development.

Abstract: The paternal transmission of environmentally induced phenotypes across generations has been reported to occur following a number of qualitatively different exposures and appear to be driven, at least in part, by epigenetic factors that are inherited via the sperm. However, previous studies of paternal germline transmission have not addressed the role of mothers in the propagation of paternal effects to offspring. We hypothesized that paternal exposure to nutritional restriction would impact male mate quality and subsequent maternal reproductive investment with consequences for the transmission of paternal germline effects. In the current report, using embryo transfer in mice, we demonstrate that sperm factors in adult food restricted males can influence growth rate, hypothalamic gene expression and behaviour in female offspring. However, under natural mating conditions females mated with food restricted males show increased pre- and postnatal care, and phenotypic outcomes observed during embryo transfer conditions are absent or reversed. We demonstrate that these compensatory changes in maternal investment are associated with a reduced mate preference for food restricted males and elevated gene expression within the maternal hypothalamus. Therefore, paternal experience can influence offspring development via germline inheritance, but mothers can serve as a modulating factor in determining the impact of paternal influences on offspring development.

Genes in Context Gene–Environment Interplay and the Origins of Individual Differences in Behavior

Abstract: Interactions between genes and the environment are a critical feature of development. Insights into the dynamic interplay between these factors have come from laboratory studies exploring experience-dependent changes in gene function, which illustrate the importance of environmental factors in determining activity of the genome. These studies have implications for our understanding of the origins of individual differences in behavior and may provide new ways of thinking about the transmission of traits across generations. Here we will highlight how these new findings illustrate the importance of putting genes in context.

Paternal Stress Exposure Alters Sperm MicroRNA Content and Reprograms Offspring HPA Stress Axis Regulation

Abstract: Neuropsychiatric disease frequently presents with an underlying hyporeactivity or hyperreactivity of the HPA stress axis, suggesting an exceptional vulnerability of this circuitry to external perturbations Parental lifetime exposures to environmental challenges are associated with increased offspring neuropsychiatric disease risk, and likely contribute to stress dysregulation While maternal influences have been extensively examined, much less is known regarding the specific role of paternal factors To investigate the potential mechanisms by which paternal stress may contribute to offspring hypothalamic-pituitary-adrenal (HPA) axis dysregulation, we exposed mice to 6 weeks of chronic stress before breeding As epidemiological studies support variation in paternal germ cell susceptibility to reprogramming across the lifespan, male stress exposure occurred either throughout puberty or in adulthood Remarkably, offspring of sires from both paternal stress groups displayed significantly reduced HPA stress axis responsivity Gene set enrichment analyses in offspring stress regulating brain regions, the paraventricular nucleus (PVN) and the bed nucleus of stria terminalis, revealed global pattern changes in transcription suggestive of epigenetic reprogramming and consistent with altered offspring stress responsivity, including increased expression of glucocorticoid-responsive genes in the PVN In examining potential epigenetic mechanisms of germ cell transmission, we found robust changes in sperm microRNA (miR) content, where nine specific miRs were significantly increased in both paternal stress groups Overall, these results demonstrate that paternal experience across the lifespan can induce germ cell epigenetic reprogramming and impact offspring HPA stress axis regulation, and may therefore offer novel insight into factors influencing neuropsychiatric disease risk