Higher-order chromatin packing serves as a structural barrier to the recognition and repair of genomic lesions. The initiation and outcome of the repair response is dictated by a highly coordinated yet complex interplay between chromatin modifying enzymes and their cognate readers, damage induced chemical modifications, nucleosome density, transcriptional state, and cell cycle-dependent availability of DNA repair machinery. The physical and chemical properties of the DNA lesions themselves further regulate the nature of ensuing chromatin responses. Here we review recent discoveries across these various contexts, where chromatin regulates the homology-guided double-strand break repair mechanism, homologous recombination, and also highlight the key knowledge gaps vital to generate a holistic understanding of this process and its contributions to genome integrity.

高阶染色质堆积是识别和修复基因组损伤的结构障碍。修复反应的启动和结果取决于染色质修饰酶与其同源阅读器之间高度协调但复杂的相互作用、损伤诱导的化学修饰、核小体密度、转录状态和 DNA 修复机制的细胞周期依赖性可用性。DNA 损伤本身的物理和化学特性进一步调节随后染色质反应的性质。在这里，我们回顾了最近在这些不同背景下的发现，其中染色质调节同源引导的双链断裂修复机制、同源重组、