The effect of epigenetic marks across generations has helped bring epigenetics to the public eye like never before. The health implications are enormous and so is the contribution to basic science, particularly evolution.
However, one important distinction is whether it is a true form of molecular inheritance, known as transgenerational epigenetic inheritance, or the shared effect of a exposure known as a transgenerational epigenetic effect or an intergenerational effect (depending on who you ask).
This is because when a parent (F0) is exposed to an environmental factor, they are exposing not only themselves, but also the germ cells that go on to form the next generation (F1). And if it’s a pregnant mother (F0), not only is she exposing herself and the embryo (F1), but also the precursor germ cells that go on to form the next generation (F2). So in order to distinguish between the two, experiments must go into at least the F2, F3, or even further depending on the parental situation.
Taking A Bite of Transgenerational Epigenetics
Interestingly, the same type of exposure is capable of creating both profiles, and the discrimination really seems to come down to experimental design (and the difficulty in following humans for that long) and the genes of interest (in animal models).
Lets take diet for example. We’ve seen that diet can most certainly cause some sort of transgenerational epigenetic response, as made famous in humans by the dutch hunger winter. In some cases parental diet produces only the temporary transgenerational (intergenerational) effect and in others it appears to be true transgenerational epigenetic inheritance.
Paternal Diet Affects Intergenerational Obesity in Fruit Flies
While most studies have focused on tracing the inheritance from mom, dad’s contribution has recently risen to the spotlight as well. And on that note, J. Andrew Pospisilik and team from the Max Planck Institute of Immunobiology and Epigenetics have made an observation about the sensitive developmental windows of epigenetic reprogramming. By using “a Drosophila model of paternal-diet-induced intergenerational metabolic reprogramming (IGMR)” the team found:
- It takes only two days of a bad diet to cause obesity in offspring.
- Paternal sugar disrupts the chromatin domains in mature sperm and offspring embryos.
- There is a H3K9/K27me3-dependent reprogramming of metabolic genes during two distinct developmental windows: germline and zygotic.
- While their system deals with variegation in flies, they also found evidence of a similar system that regulates metabolism variation in mice and humans, thus showing the usefulness of their model as a proxy for the effect of paternal sugar on offspring obesity.
Go and take a bite out of diet and development in Cell, January 2015