Dissection of Polycomb complexes reveals canonical PRC1-independent 3D chromatin interactions

Polycomb-mediated 3D chromatin interactions persist even when canonical Polycomb repressive complex 1 (cPRC1) is depleted, contradicting existing models that place cPRC1 at the center of this process. Using Polycomb subunit degrons combined with Region Capture Micro-C, ChIP-seq, nascent transcriptomics, and live-cell imaging, the authors show that within cPRC1, polyhomeotic proteins are the main contributors to interactions, and that the residual interactions do not depend on any single variant PRC1 or PRC2 complex. The work raises the possibility of a more general, cPRC1-independent mechanism for Polycomb-mediated interactions.