Chromatin remodelers are multidomain machines that reposition nucleosomes along genomic DNA using a helicase-like ATPase motor. Yet how the remodeler ATPase is regulated to achieve particular remodeling outcomes has been unclear. I will discuss our recent biochemical work describing the domain architecture for the Chd1 remodeler on the nucleosome. In contrast with what has been described for other remodelers, this domain organization suggests an inhibitory mechanism for sensing DNA flanking the nucleosome. I will present a model for how domain-domain communication allows Chd1 to slide nucleosomes away from bound transcription factors and generate evenly spaced nucleosome arrays.

Asymmetric cell division, where daughter cells inherit unequal amounts of specific factors, is critical for development and cell fate specification. Asymmetric cell division occurs in polarized cells as a result of positioning the centrosomes along the polarity axis. Using an individual-based stochastic model of microtubule dynamics and experiments in the early C. elegans embryo, we explore potential sources of cortical force generation and demonstrate the need for both cortical and centrosomal asymmetries for recapitulating the in vivo dynamics and proper positioning of the centrosomes.