Since Gregor Mendel’s famous experiments crossing literally tens of thousands of pea plants in the late 1800s, we have known that genes are passed from one parents to the children. Since the Hershey-Chase experiments in 1952, where they radioactively marked both DNA and proteins in a generation of viruses to figure out which material was being transferred to the second generation of viruses, we have known that DNA was the carrier of genetic information. It tends to be forgotten that prior to that point, most believed proteins (and not DNA, which was called the “stupid molecule/tetranucleotide,” and considered too simple to carry genetic information) were the key.
It wasn’t until this century, the 21st, that we began to realize that even the same DNA sequence can give rise to different characteristics: even to the point of the two individuals looking and acting totally different despite having identical DNA sequences.
What you experience has been known, for several years, to affect your personal development. In the same way that the foods you eat affect your gut biome (or the bacterial symbionts which help you digest your food), what you experience affects how your life advances. These changes, outside of the DNA sequence, are refered to as “epigenetic,” and mediate processes like learning, allergies, and personality development.
Up until 2013 we believed that these changes solely represented a way for an organism to dynamically react to its environment, but that these changes disappeared between generations (with the only conserved epigenetic signals existing in “imprinting regions“) when dealing with mammals. This was slightly turned on its head in 2013, when Dias and Ressler discovered that traumatic sensitization to a smell (acetophenone) by its combination with shocks, led to increased sensitivity towards this evolutionarily unimportant smell in at least 2 following generations even when these individuals had personally never experience it before.
Researchers were stumped at first, wondering how conditioning in regard to a novel stimuli (new experience) could be transferred between generations: it certainly wasn’t encoded in their DNA sequence. But the methylation (and acetylation) pattern, primarily responsible for epigenetic gene regulation, is not directly passed on between generations (except for imprinting genes) in mammals. In 2014, the puzzel appears to be partially solved by research done at ETH Zurich.
A team led by Gapp and Sarkies, at ETH Zurich, investigated the role of micro RNAs in transgenerational mediation of heightened stress response (as with the rats and the acetophenone). They found that the number and types of micro-RNA were changed in the sperm, brain, and blood, and affected transcription (so the phenotype) of following . Since the fetal development takes place in the woman, who would have altered serum levels, and is triggered by the man (through his sperm) this could effectively lead to the phenotypic changes in the offspring and their gene expression.
To understand this completely, it is important to explain that initial cell differentiation, or the development of a “stem” cell into a specific type of tissue, is regulated both by the modification of histones but also transcription factors, signal molecules, and RNA interference. These results indicate that RNAi (RNA interference) may play a larger role in passing on experience to the next generation, than was previously considered. The roles it plays in passing experience between generations is likely far greater than just mediating reactions to trauma