Salk Institute

Emerson Lab
Emerson Lab



Our genome is a patchwork of neighborhoods that couldn't be more different: Some areas are hustling and bustling with gene activity, while others are sparsely populated and in perpetual lock-down. But once in a while the wrong gene ends up in a quiet zone, often with disastrous results.

In the cell's nucleus, DNA molecules are wrapped around histone proteins and coiled into a structure called heterocromatin. This highly condense packaging allows the long DNA molecules to fit neatly into the nucleus. In areas of gene activity, the tightly packed heterochromatin is unfurled just enough to make the DNA accessible to regulatory proteins. In many different types of cancers, however, the gene for the tumor suppressor p16 gets buried deep inside heterochromatin. Why the particular stretch of DNA that houses p16 is flagged with chemical marks and wound up so tightly that it becomes accessible had, until recently, remained a mystery.

For a long time scientists have been trying to understand how tumor suppressor genes get silenced in cancer. Understanding one of the key molecular events that leads to their inactivation might allow them to exploit this mechanism to develop novel therapies.

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