SMC Complexes in DNA Damage Response and Genome Stability
Summary
Structural maintenance of chromosomes (SMC) complexes—cohesin, condensin and SMC5/6—are central to the organisation and safeguarding of genomic material. Beyond their canonical roles in chromosome cohesion and condensation, SMC5/6 is specialised in responding to DNA damage by stabilising stalled replication forks, modulating recombination intermediates and promoting repair. Recent work has elucidated how SMC5/6 engages directly with single‐stranded DNA through distinctive hinge interfaces, recruits ubiquitin- and SUMO-dependent factors and coordinates with transcriptional complexes to facilitate accurate repair of double-strand breaks. Defects in SMC5/6 function give rise to genomic instability, developmental disorders and cancer-associated phenotypes, underscoring its global significance. The interplay between SMC complexes and post-translational modifications ensures swift cellular responses to genotoxic stress and maintains genome integrity across eukaryotic species.
Research from Nature Portfolio
Recent structural analyses have delineated unique hinge interfaces within the SMC5/6 complex that govern its assembly and DNA-binding specificity. Two specialised features—the molecular ‘latch’ and functional ‘hub’—stabilise a toroidal structure selectively engaging single-stranded DNA. Mutations in these regions diminish complex integrity, compromise DNA association and sensitize cells to genotoxic stress, revealing how SMC5/6 directly recognises and processes damaged DNA to uphold chromosomal stability.
SMC Complexes in DNA Damage Response and Genome Stability publication trend
The graph below shows the total number of articles in smc complexes in dna damage response and genome stability across all publications each year (not limited to Nature Index journals).
Technical terms
SMC complex: Multiprotein assemblies (cohesin, condensin, SMC5/6) that form ring-shaped structures to organise chromosomes and facilitate repair.
Homologous recombination: An error-free DNA repair pathway that uses a homologous sequence as a template to accurately restore double-strand breaks.
SUMOylation: Covalent attachment of small ubiquitin-like modifier (SUMO) proteins to target lysines, regulating protein interactions during DNA damage response.
Replication fork: The Y-shaped junction where parental DNA strands separate and new strands are synthesised, vulnerable to stalling under stress.
References
- Specialized interfaces of Smc5/6 control hinge stability and DNA association. Nature Communications (2017).
- The SMC5/6 complex recruits the PAF1 complex to facilitate DNA double‐strand break repair in Arabidopsis. The EMBO Journal (2023).
- RNF4 sustains Myc-driven tumorigenesis by facilitating DNA replication. Journal of Clinical Investigation (2024).
- In‐frame deletion of SMC5 related with the phenotype of primordial dwarfism, chromosomal instability and insulin resistance. Clinical and Translational Medicine (2023).
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