We define cellular pliancy as the ability of a cell to adapt and respond to stress, injury or disease. Cells with low pliancy have a lower ability to respond to stress, and as a result are more prone to death. Cells with high pliancy are much more adaptable, able to survive stressful conditions, and even be prone to re-enter the cell cycle, potentially creating a permissive state for cancer initiation. We have proposed that the purposeful organization of the genome in the nucleus contributes to cell type specific pliancy. The neural retina proves to be an ideal model to study this trait, as it contains several different cell types from one common progenitor, that span the spectrum of pliancy behavior[1]. Since the model of cellular pliancy hypothesizes that the adaptability of a cell depends on its ability to access responsive genes in times of stress, the way that specific gene organization affects cellular function needs to be fully understood. general that the structure of the nucleus a

Deconstructing the Nucleus to Elucidate Cellular Pliancy in the Retina

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Deconstructing the Nucleus to Elucidate Cellular Pliancy in the Retina