Hainer and colleagues’ research delves into how cell fate specification and its dysregulation are mediated at the interface of transcription and chromatin dynamics—fundamental mechanisms that shape all aspects of biology, including development and disease.
Specifically, Hainer and colleagues have focused on the role of the essential chromatin remodeler, BAF, in embryonic stem (ES) cell fate. They mechanistically defined a novel role for BAF in repressing the expression of noncoding RNAs throughout the genome of ES cells, also marking the identification of the first global regulator of a specific class of noncoding RNAs termed enhancer RNAs. They further demonstrated a role for BAF in regulating pluripotency factor localization on chromatin in both ES cells and blastocysts. Importantly, the latter was due to their technological breakthrough that permitted, for the first time, determining factor localization on chromatin in single cells and early embryos. Therefore, Hainer’s research program integrates perspectives of genetics and chromatin control into the systems biology of cell-fate specification.