Researchers have found a new evidence that helps to explain how stress influence our very DNA without any change to the underlying sequence of As, Gs, Ts and Cs.
"There has been a big discussion about whether the stress effect can be transmitted to the next generation without DNA sequence change," said Shunsuke Ishii of RIKEN Tsukuba Institute.
Advertisement"Many people were doubtful about such phenomena because the mechanism was unknown. Our finding has now demonstrated that such phenomena really can occur," added Ishii.
Our genes encode proteins, but whether and how those genetic instructions are ultimately read and expressed depends on how those genes are chemically modified and "packaged" into a more complex structure known as chromatin. Some portions of the genome are more tightly wound into what's known as heterochromatin. Heterochromatin is maintained from one generation to the next and typically doesn't contain active genes, Ishii explained.
Ishii and his colleagues now confirm that ATF-2 (activation transcription factor-2) which they discovered in yeast over 20 years ago, is required for heterochromatin assembly in multicellular organisms. When fruitflies are exposed to stressful conditions, the ATF-2 is modified and disrupts heterochromatin, releasing genes from their usual silenced state. Importantly, these changes in genomic structure are passed on from one generation to the next.
The researchers expect that this finding in flies has relevance for humans, noting that we also carry the ATF-2 gene. Those epigenetic changes may influence basic cellular functions as well as metabolism, behaviour and disease.
According to Ishii, the take-home message is this: "I hope that people understand that various stresses can change gene expression without DNA sequence change."
He also said that the youngest among us - developing embryos and infants - may be especially sensitive to that kind of stress-induced epigenetic change and "we should be more careful about stresses on them."
The study has been published in Cell.