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 ¶¶ÒõÂÃÐÐÉä 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. Vignesh Kasinath, Kasinath Lab at ¶¶ÒõÂÃÐÐÉä Boulder is a co-senior author and first author, Jiarui Song, is a Jane Coffin Childs postdoctoral fellow in the Cech Lab at ¶¶ÒõÂÃÐÐÉä Boulder.
This research was published on . And other co-authors include Anne Gooding, Wayne Hemphill and Liqi Yao of ¶¶ÒõÂÃÐÐÉä Boulder and Brittney Love, Anne Robertson, Leonard Zon and Trista North of Harvard Medical School.