AI Summary
A molecular machine called PRC2 plays a crucial role in determining cell development and can cause cancer if mutated. New research has shown how ribonucleic acid (RNA) helps PRC2 switch genes on and off. This knowledge could lead to new treatments for hard-to-treat cancers. The study used cryo-electron microscopy to photograph PRC2 in action.
Deep inside our cells-;each one complete with an identical set of genes-;a molecular machine known as PRC2 plays a critical role in determining which cells become heart cells, versus brain or muscle or skin cells.
When the machine is missing or broken, normal fetal development can’t occur. If it’s mutated, cells can grow uncontrollably, and cancer can arise-;a fact that has made PRC2 a source of keen interest for drug developers.
New research by scientists at CU Boulder and Harvard Medical School offers an unprecedented look at how PRC2, or polycomb repressive complex 2, does its job and, specifically, how ribonucleic acid (RNA) helps it switch genes on and off.
The findings, published Sept. 22 in the journal Science, shed new light on how development occurs and could pave the way for novel therapeutics for hard-to-treat cancers, including blood, pancreatic and colon cancer, leukemia and pediatric tumors.
We know PRC2 is extremely important for development and for maintaining the identity of cells, and we know that RNA regulates it. But mechanistically, we didn’t know how.”
Vignesh Kasinath, co-senior author, assistant professor of biochemistry at CU Boulder
For the study, Kasinath’s lab collaborated with Nobel Laureate Thomas Cech and colleagues at the BioFrontiers Institute to photograph PRC2 in action, using state-of-the-art “cryo-electron microscopy.” The technique involves freezing samples to extremely cold temperatures to preserve their native structure and then hitting them with an electron beam at speeds nearly the speed of light to create ultra-high-resolution 3D images.
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