Studies have shown that “memories” of various environmental influences, such as diet and weight, are passed on from parents to children even though these states are not encoded in the DNA sequence.
The molecules that attach themselves to DNA can act like the on-off switches, which control which sections of DNA are used – but so far we didn’t know which of these molecules could carry the settings that characterize paternal life experiences, to be incorporated into the fetus by animals. Seminal.
“The great achievement in this study is that it identified a non-DNA-based method through which sperm can remember the paternal environment (diet) and transmit this information to the fetus,” said Sarah Chemins, a geneticist at McGill University.
Using mice, epigenetic geneticist Ariane Lesmer and colleagues were able to demonstrate that the effects of a diet deficient in folic acid could be transmitted by altering the histone molecules in sperm. Put simply, histones are really essential proteins that DNA wraps around to store without tangles.
And in mammals, when the bodies of males build sperm, they throw off most of the histone reels, to allow for a tighter packing.
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But there is still a small percentage (1% in mice and 15% in humans), providing a scaffolding for DNA in areas of sperm formation and function, metabolism, and embryo development – to allow cellular mechanisms to take advantage of these DNA instructions.
The chemical modification of these histones allows, or prevents the “reading” of the DNA so that it can be copied into protein products.
This is why we hear about the importance of folic acid for women during pregnancy: The mother’s folic acid helps stabilize the DNA methylation in her young.
By feeding the male mice a diet deficient in folic acid since the time of weaning, the researchers were able to track changes in the histones of the male sperm and in the resulting embryos. Indeed, sperm histone alterations were also present in the developing fetus.
“Nobody has been able to track how these heritable environmental signatures were transmitted from sperm to the fetus before,” Lesmer said.
The team also discovered that these effects could be cumulative and lead to an increase in the severity of birth defects.
Interestingly, the birth defects seen in mice, including retardation at birth and spinal deformities, were well documented in human groups with folate deficiency.
The researchers hope that expanding our knowledge of the mechanisms of genetics will reveal new ways to treat and prevent such conditions.
This research was published in Developmental Cell.
Source: ScienceAlert
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