Integrative assessment of classical and molecular phenotypes in MCF10A cells [ATAC-seq]
Maintenance of proper phenotypic state of mammary epithelial cells is crucial for normal function, however the molecular networks underlying control of various cellular phenotypes are not well understood. To date most studies have assessed the impact of extracellular signals on a single phenotypic response, such as proliferation, or have focused on elucidation of molecular changes associated with single perturbations. However, these approaches ignore that ligands frequently induce multiple phenotypic changes and that similar phenotypic responses can be induced by multiple ligands. As a consequence, little is known about the core molecular mechanisms that drive cells to different phenotypic states. Here we deeply profiled the phenotypic and molecular responses of MCF10A mammary epithelial cells to a diverse panel of ligands known to have a role in the normal mammary gland. These ligands elicited multiple phenotypic responses, including changes in proliferation, migration, and differentiation status. Analysis of companion RNAseq, ATACseq, and proteomic data identified distinct molecular features associated with ligand treatments and phenotypic changes. These data provide a robust resource to address questions about how environmental signals are encoded into molecular and phenotypic responses, the associations between molecular modalities, and temporal encoding of molecular and phenotypic responses.  Overall design: Chromatin accessibility profiles of MCF10A cells in 7 conditions (6 ligand treatments and 1 control), measured at 0, 24, and 48 hours post-treatment. 48 samples total.