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==One of the epigenetic responses to stress is to turn on genes that will increase mutations and turn off genes that repair mutations.

Is the turning on of the genes random, or by design? Are the increased mutations intiated by random, or by design? Is the turning off genes random, or by design?

==In this case the epigenetic program is maximizing the chance of error prone replication to come across a solution to the stress, much the way error prone PCR is used in directed evolution to derive novel proteins with beneficial properties.

Would you say that they are both directed, or just PCR?

==Now if mutations were not essential to the ability of living systems to adapt to stress, why would the epigenetic program increase mutation rates and downregulate repair when the cell was under stress?

Maybe it tries to adapt by matching its code to the feedback of the new environment. Maybe it knows what it’s looking for once it has found it, and thus must downregulate repair so this strategy does not defeat itself. Who knows. Epigenetics is still a new field. All I’m trying to point out to you is that the more they find out, the less random adaptation becomes.

The turning on and off of epigenetic markers is subject to mutation and natural selection so it is just as random/designed as anything else in life. One of the most famous epigenetic markers to be subjected to mutation and selection in human populations is the one that would turn off the lactase gene after weaning in mammals.

Directed evolution is an experimental method whereby Scientists use error prone PCR to generate novel proteins and test them for the desired properties. This is analogous to the epigenetic stress response whereby genes that promote mutation are up regulated and genes that repair mutation are down regulated.

Indeed it is trying to adapt by CHANGING its code. Selection is what makes it “know” once it has arrived at solution.

Epigenetics is not a magic code word that makes the random go away.