Structural Basis for Polθ-Helicase DNA Binding and Microhomology-Mediated End-Joining.
Fumiaki ItoZiyuan LiLeonid MinakhinHtet A KhantRichard T PomerantzXiaojiang S ChenPublished in: bioRxiv : the preprint server for biology (2024)
DNA double-strand breaks (DSBs) present a critical threat to genomic integrity, often precipitating genomic instability and oncogenesis. Repair of DSBs predominantly occurs through homologous recombination (HR) and non-homologous end joining (NHEJ). In HR-deficient cells, DNA polymerase theta (Polθ) becomes critical for DSB repair via microhomology-mediated end joining (MMEJ), also termed theta-mediated end joining (TMEJ). Thus, Polθ is synthetically lethal with BRCA1/2 and other HR factors, underscoring its potential as a therapeutic target in HR-deficient cancers. However, the molecular mechanisms governing Polθ-mediated MMEJ remain poorly understood. Here we present a series of cryo-electron microscopy structures of the Polθ helicase domain (Polθ-hel) in complex with DNA containing 3'-overhang. The structures reveal the sequential conformations adopted by Polθ-hel during the critical phases of DNA binding, microhomology searching, and microhomology annealing. The stepwise conformational changes within the Polθ-hel subdomains and its functional dimeric state are pivotal for aligning the 3'-overhangs, facilitating the microhomology search and subsequent annealing necessary for DSB repair via MMEJ. Our findings illustrate the essential molecular switches within Polθ-hel that orchestrate the MMEJ process in DSB repair, laying the groundwork for the development of targeted therapies against the Polθ-hel.
Keyphrases
- dna binding
- dna repair
- single molecule
- dna damage
- circulating tumor
- structural basis
- transcription factor
- electron microscopy
- cell free
- working memory
- induced apoptosis
- transcranial magnetic stimulation
- gene expression
- molecular dynamics
- young adults
- oxidative stress
- cell death
- single cell
- heat stress
- nucleic acid
- breast cancer risk