The message from this chapter is that the field of epigenetic studies of hu- man disease has painted itself into a corner through excessive purism. By requiring a model of cellular reprogramming, we have ignored the potential role of cell subtype proportion changes. By requiring mechanisms indepen- dent of DNA sequence variation to mediate effects, we have failed to grasp the opportunity to reveal genetic contributions to phenotypes, while our colleagues in the world of functional variant studies have made excellent progress. By downplaying the role of TFs, we are blinded to the contribution of cell signaling in cellular responses to extrinsic perturbations. In Chapter 5 we tried on for size the new term “cellular genomics” to describe an alter- native way of doing these studies for those uncomfortable still calling this new, more inclusive approach epigenetics. Whatever it is called, it represents a way of merging epigenetics with the work performed by our GWAS and functional variant research colleagues.
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