Studies in mammals have shown that “memories” of various environmental effects, such as diet, weight, and stress, are passed from parents to offspring, although these states are not encoded in DNA sequences. which transport sperm. We now have a new explanation of how this is possible.
History 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 did not know which of these molecules can carry the parameters marked by the life experiences of a parent to incorporate them into an embryo using sperm.
“The breakthrough in this study is that it has identified a non-DNA-based medium by which sperm remember the parent’s environment (diet) and transmit this information to the embryo,” said the epigenetist of the McGill University, Sarah Kimmins.
Using mice, epigenetist Ariane Lismer and colleagues were able to show that the effects of a folate-deficient diet could be transmitted by altering histone molecules in sperm. Simply put, histones are really basic proteins that DNA rolls up to store without mess.
In mammals, when male bodies build sperm, they throw away most of the histone coils to allow for tighter packaging.
But there is still a small percentage (1% in mice and 15% in humans), which provides scaffolds for DNA in specific regions for sperm creation and function, metabolism and embryonic development, to allow 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 the “reading” of DNA 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 for women during pregnancy: a mother’s folate helps stabilize DNA methylation in her offspring.
By feeding male mice on a folate-deficient diet from the time they were weaned, the researchers were able to track changes in male sperm histones and 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 these inheritable environmental signatures are transmitted from sperm to the embryo,” Lismer said.
The team also found that these effects could be cumulative and lead to an increase in the severity of birth defects.
Interestingly, congenital defects observed in mice, including underdevelopment at birth and spinal abnormalities, are well documented in folate-deficient human populations.
Researchers hope that expanding our knowledge of inheritance mechanisms will reveal new ways to treat and prevent these conditions. But there is much more to work on sooner.
“Our next steps will be to determine if these harmful changes induced in sperm proteins (histones) can be repaired. We have exciting new work that suggests this is the case,” Kimmins said.
This research was published in Developmental cell.