Neuromag November 2017 | Page 21

Since epigenetics can influence every aspect of our biology by acting on our genes, learning the rules that govern where epigenetic markers are placed or how these precise markers are maintained could help us begin to an- swer some very long-standing ques- tions in biology. Questions like why disease susceptibility increases with old age, why some people live to much older ages than others, or even po- tentially accelerate the adaptability of species to environmental change. Curiously, the pattern of epigenetic markers on the genomes of identical twins can differ, despite their identical genetic make-up. These differences become more pronounced with age, suggesting that the older identical twins get the less identical they are. This phenomenon called epivariation (surprise, surprise) can be driven by many factors such as random varia- tion, mutation in the DNA sequence onto which epigenetic markers are placed or, most excitingly, environ- mental stimuli. Now why is that excit- ing I hear you ask? Well, genetic variation by mutation is a slow process that relies on the suc- cess of subsequent generations in the wild, something which is not likely considering that genetic mutation oc- curs in random locations on the ge- nome and is therefore indifferent to the environmental pressures placed on an organism. Epivariation therefore offers a far faster way for an organ- ism to adapt to changes in its environ- ment and potentially pass these im- mediate benefits onto their offspring. Transgenerational epigenetic inherit- ance, as it is known, excites the living shit out of me and epigeneticists alike as it suggests that the decisions we make about the environment in which we live can have some influence over the genetics of our descendants; not the DNA sequences they inherit but how they are used, thus blending na- ture and nurture into one. the electric shock and then freeze in place when the smell arrives, just clas- sical Pavlovian conditioning. Well they next allowed the conditioned mice (F0) to rest for two weeks, then mate with unconditioned mice. The offspring (F1) were then exposed to acetophe- none but without any foot shock. They found that the offspring observed similar freezing behaviour to their par- ents, and significantly greater than the different control groups. Proving that it was odor specific, not a learned be- haviour from the mice’s parents and that it required sexual transmission via gametes. This behaviour was even transferable to the next generation (F2), even though neither F1 nor F2 were ever exposed to the odor prior to testing. In 2014 an epigenetics study entitled “Parental olfactory experience influ- ences behaviour and neural structure in subsequent generations” [3] found that by providing an odor stimuli to mice (acetophenone, kind of like or- ange blossom I’m told) and then shortly afterwards giving them a mild electric shock they could cause the mice to freeze in response to the odor alone. Nothing surprising, right? The mice learn to associate the smell with Spooky huh? Inheritance of a behav- ioural trait across 2 generations that needs only gametes to occur. Looking deeper into the possible cause of this phenomenon the researchers checked the methylation state of the gene which produces the specific smell-re- ceptor for acetophenone. They found that the gene had significantly lower methylation than controls, indicat- ing dis-inhibition of expression of this gene, and therefore greater sensitivity In twins, epigenetic markers decrease in similarity over time (Yellow = similar; red and green = dissimilar) [1]. Lower twin picture [2]. November 2017 | NEUROMAG | 21