We finally know how sperm ‘remember’ and transmit non-DNA-coded traits to embryos

Mammalian studies have shown that ‘memories’ of various environmental effects, such as diet, weight, and stress, are passed down from parent to child, despite the fact that these states are not encoded in the DNA sequences carried by them. sperm. Now, we have a new explanation of how it is possible.

The story has a lot to do with epigenetics. Molecules that adhere to DNA can act as on-off switches that control which sections of DNA are used, but until now we have not known which of these molecules can carry the configuration marked by a parent’s life experiences, to be incorporated into an embryo through sperm.

“The breakthrough of this study is that it has identified a non-DNA-based means by which sperm cells remember the environment (diet) of the father and transmit that information to the embryo,” said McGill University epigenetist Sarah Kimmins.

Using mice, epigenetics Ariane Lismer and her colleagues were able to show that the effects of a folate-deficient diet could be transmitted by altering the histone molecules in sperm. Simply put, histones are really basic proteins that DNA wraps around for tangle-free storage.

In mammals, when male bodies produce sperm, they shed most of the histone spools to allow for tighter packing.

But there is still a small percentage left (1 percent in mice and 15 percent in humans), which provides a scaffold for DNA in specific regions for sperm creation and function, metabolism, and embryonic development, to allow them to Cellular mechanisms make use of these DNA instructions.

The chemical modification of these histones – the most common form is methylation – is what allows or prevents DNA from being “read” so that it can be transcribed into protein products. A poor diet can cause these histones to change their methylation status.

That’s why we hear about the importance of folate to women during pregnancy: Folate from the mother helps stabilize DNA methylation in her young.

By feeding male mice a folate-deficient diet from the time they were weaned, the researchers were able to track changes in the histones in the male’s sperm and in the resulting embryos. And in fact, changes in sperm histones were also present in the developing embryo.

“No one has been able to track how those heritable environmental signatures are passed from sperm to embryo before,” Lismer said.

The team also found that these effects could be cumulative and lead to an increase in the severity of birth defects.

Interestingly, the birth defects observed in mice, including underdevelopment at birth and abnormalities of the spine, are well documented in folate-deficient human populations.

The researchers hope that expanding our understanding of inheritance mechanisms will reveal new ways to treat and prevent such conditions. But there is much more to resolve before then.

“Our next steps will be to determine whether these damaging induced changes in sperm 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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