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Studies in mammals have shown that “ memories ” of various environmental effects – such as diet, weight and stress – are passed from fathers to offspring, although these states are not encoded in the sequences. DNA carried by semen. Now we have a new explanation of how this is possible.
History has a lot to do with epigenetics. Molecules that attach to DNA can act as on-off switches that control which sections of DNA are used – but so far we don’t know which of these molecules can carry the parameters marked by the experiments of life of a father, to be incorporated into an embryo via the sperm.
“The great advancement of this study is that it identified a non-DNA-based way by which sperm remember a father’s environment (diet) and pass this information on to the embryo,” he said. said McGill University epigeneticist Sarah Kimmins.
Using mice, epigeneticist Ariane Lismer and her colleagues were able to demonstrate that the effects of a low-folate diet could be transmitted by altering histone molecules in semen. Simply put, histones are really basic proteins that DNA wraps around for tangle-free storage.
In mammals, when male bodies build sperm, they shed most of the histone coils, to allow for tighter wrapping.
But there is still a small percentage left (1% in mice and 15% in humans), providing a scaffold for DNA in regions specific to sperm creation and function, metabolism and development of the sperm. ’embryo – to allow cellular mechanisms to use these DNA instructions.
The chemical modification of these histones – the most common form being methylation – is what allows or prevents the “reading” of DNA so that it can be transcribed into protein products. Poor nutrition can cause these histones to change their methylation status.
That’s why we hear about the importance of folate to women during pregnancy: A mother’s folate helps stabilize DNA methylation in her young.
By feeding male mice a low-folate diet from the time they were weaned, the researchers were able to track histone changes in the male’s sperm and resulting embryos. And indeed, changes in sperm histones were also present in the developing embryo.
“No one has been able to track how these inherited environmental signatures are passed from sperm to the embryo before,” Lismer said.
The team also found that these effects could be cumulative and lead to an increased severity of birth defects.
Interestingly, the birth defects seen in mice, including birth underdevelopment and spinal abnormalities, are well documented in folate-deficient human populations.
Researchers hope that expanding our knowledge of the mechanisms of inheritance will reveal new ways to treat and prevent such conditions. But there is still a long way to go before that date.
“Our next steps will be to determine if these induced harmful changes in semen proteins (histones) can be repaired. We have exciting new work that suggests this is indeed the case,” Kimmins said.
This research was published in Development cell.
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