Studies in mammals have shown that the ‘memories’ of various environmental influences – such as diet, weight, and weight – are passed on from fathers to children, despite the fact that these states have not been coded in the DNA sequences. sperm is pregnant. Now, we have a new definition of how it is possible.
The story has a lot to do with epigenetics. Molecules that attach themselves to DNA can be away switches that control the segments of DNA that are used – but so far we do not know which of these molecules can conditions characterized by paternal life experiences of embryo introduction through sperm.
“The major drawback with this study is that it is a non-DNA-based method by which sperm remember their father’s environment (diet) and transmit that information to the embryo,” said Sarah Kimmins , epigeneticist McGill University.
Using mice, Ariane Lismer and Arigen colleagues were able to demonstrate that the effect of a folate-deficient diet could be mediated by altering histone molecules in sperm. Simply put, histones are basic proteins that DNA blows around for tangle-free storage.
In mammals, when male groups pick up sperm, they shed most of the histone spools, so they get a tighter packing.
But a small percentage remains (1 percent in mice and 15 percent in humans), providing scaffolding for DNA in areas specific to sperm formation and function, metabolism, and embryo development – to allow the cellular mechanisms use that DNA guidance.
It is a chemical modification of these histones – the most common form of methylation – that allows or prevents the DNA from being ‘read’ so that it can be transcribed into protein products. Poor diet can cause these histones to alter their methylation status.
That’s why we hear about the importance of folate for women during pregnancy: Maternal folate helps stabilize DNA methylation in childhood.
By feeding male mice a diet with folate deficiency from the time of removal, the researchers were able to monitor the changes to histones from the male sperm and in the resulting embryos. And of course, histone sperm changes were present in the developing embryo.
“No one has been able to track how these hereditary environmental names are passed from the sperm to the 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 seen in the mice, including underdevelopment at birth and spinal dysfunction, are well documented in human populations with folate deficiency.
The researchers hope that expanding our knowledge of legacy mechanisms will reveal new ways to treat and prevent these conditions. But there is much more to work out before then.
“Our next steps are to determine if these harmful changes that are suppressed in the sperm proteins (histones) can be repaired. We have exciting new work that shows that this very true, “Kimmins said.
This research was published in Cell development.