Elizabeth Finn

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We study how the DNA in a nucleus organizes itself in order to understand how cells make decisions.

The chromosomes that make up the human genome, if put together and stretched end to end, would be about three meters long. All of that DNA has to fold and wrap and coil itself to fit into each cell’s nucleus without any tangles, which could be disastrous when a cell divides. But this folding process isn’t as simple as finding a way of packing everything neatly into the smallest possible space because where genes wind up within the nucleus can change their activity. A genome that’s organized “wrong” is a hallmark of cancer.

Previously, I used fluorescence imaging to map how chromosomes folded in thousands of different cells. I found that not just every cell, but in fact every chromosome, folded itself a little bit differently. This means there are a lot of “right” ways to fold a genome. But I also saw some interesting patterns: some folded shapes were more common in some cell types, and some regions within the cell were more variable. My work led me to hypothesize that variability itself might be a feature of how the genome works, rather than unfortunate noise hiding true signals.

My lab expands on this hypothesis in two ways: first, we’re examining how cell-to-cell variability in genome organization changes during development and disease. Second, we’re working to understand how variability in genome organization is controlled by the cell.

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