It is certainly hard to understand how early life events are leading to later disease. Here is an incredible nutrigenomics story done in agouti mice:
We find that the somatic epigenetic state of Avy is affected by in utero methyl donor supplementation only when the allele is paternally contributed. Exposure to methyl donor supplementation during midgestation shifts Avy phenotypes not only in the mice exposed as fetuses, but in their offspring. This finding indicates that methyl donors can change the epigenetic state of the Avy allele in the germ line, and that the altered state is retained through the epigenetic resetting that takes place in gametogenesis and embryogenesis. Thus a mother’s diet may have an enduring influence on succeeding generations.
Nature genetics as an advance online publication about comparative genome sequencing of E. coli where 13 de novo mutations in 5 strains were monitored over 44 d (or ~660 generations). It is a great study – not only because the author list includes one of my previous coauthors – but for giving a first insight about development of a mutation and fixing its allele frequency. Unfortunately, there is no flowchart and the methods are somewhat vague, what has been sequenced (or resequenced) in which strain at what time . In other words who are the winners? Did they manage that by their own strength or with a little help of some friends? Why rises the allele frequency always to 100% and what about some discrepancy of allele frequency and fitness? We will hopefully see more of these studies, yea, yea.