Summary
Histone variants fine-tune the regulation of transcription, replication, DNA damage repair, and cell division relies on distinct chromatin states. The histone H3 variant CENP-A/CENH3 seeds the kinetochore, creating the physical interface between centromeric chromatin and mitotic spindles. How kinetochore proteins modify CENP-A nucleosome dynamics and how these dynamics affect centromere chromatin states is poorly understood. Using interdisciplinary analyses, we report that CENP-A nucleosomes are intrinsically elastic, but CENP-C binding suppresses this innate elasticity. Shifting the balance between elastic and rigid CENP-A states in vivo results in the suppression of centromeric chromatin plasticity, so that centromeric chromatin becomes less permissive to RNA polymerase 2, thereby diminishing new CENP-A loading. These data suggest a link between innate structural properties possessed by histone variant nucleosomes, and adaptability of chromatin states in vivo, which in turn dictate the transcriptional plasticity of the underlying locus.