Transgenerational epigenetic programming with stress and microRNA

This 2015 Pennsylvania rodent study found:

“Sperm miRs [microRNAs, a small non-coding RNA that has a role in gene expression] function to reduce maternal mRNA [messenger RNA, a large RNA that carries codes for protein production] stores in early zygotes, ultimately reprogramming gene expression in the offspring hypothalamus and recapitulating the offspring stress dysregulation phenotype.”

The researchers caused stress-induced changes at an early stage of embryonic development with microRNA injections. The resultant adverse effects weren’t observed until the subjects were adults!

Most of the news coverage focused on it being a male’s stress, not a female’s, that affected the developing embryo. Either or both sexes can epigenetically disadvantage a fetus – okay.

Demonstrating how a damaging influence can begin immediately after conception, but the symptoms didn’t present until adulthood, was what made this study newsworthy.


Although the term “transgenerational” was used in the study’s title, abstract, and elsewhere, the study demonstrated that the epigenetic effects were intergenerational rather than transgenerational. Per the definition in A review of epigenetic transgenerational inheritance of reproductive disease, for the term to apply, the researchers needed to provide evidence in at least the next 2 male and/or 3 female generations of:

“Altered epigenetic information between generations in the absence of continued environmental exposure.”


From the press release, a coauthor of the study who also coauthored How to make a child less capable even before they are born: stress the pregnant mother-to-be stated:

“Bale suspects that when a male experiences stress it may trigger the release of miRs contained in exosomes from the epithelial cells that line the epididymis, the storage and maturation site for sperm between the testes and the vas deferens. These miRs may be incorporated into the maturing sperm and influence development at fertilization.”


This study was similar to the Treating the father’s symptoms of an inherited disease can epigenetically treat the son study in demonstrating disease epigenetics. The current study’s epigenetic mechanism was microRNA, and the other study’s was histone deacetylase (HDAC) inhibition that led to DNA methylation.

http://www.pnas.org/content/112/44/13699.full “Transgenerational epigenetic programming via sperm microRNA recapitulates effects of paternal stress”

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