ArticleHuman molecular genetics2013
The SNM1B/APOLLO DNA nuclease functions in resolution of replication stress and maintenance of common fragile site stability.
Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Mapping the genetic landscape of the DNA damage response with Cas12a-based combinatorial knockout screens.bioRxiv : the preprint server for biology · 2026Article
- Inherited human Apollo deficiency causes severe bone marrow failure and developmental defects.Blood · 2022Article
- Identification of Bioactive SNM1A Inhibitors.ACS omega · 2021Article
- Topoisomerase II contributes to DNA secondary structure-mediated double-stranded breaks.Nucleic acids research · 2020Article
- Heterochromatin replication goes hand in hand with telomere protection.Nature structural & molecular biology · 2020Review
- Telomerase promotes formation of a telomere protective complex in cancer cells.Science advances · 2019Article
- Identifying Putative Susceptibility Genes and Evaluating Their Associations with Somatic Mutations in Human Cancers.American journal of human genetics · 2019Article
- Promotion of Cell Death in Cisplatin-Resistant Ovarian Cancer Cells through KDM1B-DCLRE1B Modulation.International journal of molecular sciences · 2019Article
- From Human Cytogenetics to Human Chromosomics.International journal of molecular sciences · 2019Review
- Fragile sites in cancer: more than meets the eye.Nature reviews. Cancer · 2017Review
- SNM1B/Apollo in the DNA damage response and telomere maintenance.Oncotarget · 2017Review
- Review
- Article
- DNA secondary structure at chromosomal fragile sites in human disease.Current genomics · 2015Article
- Updating the mechanisms of common fragile site instability: how to reconcile the different views?Cellular and molecular life sciences : CMLS · 2014Review
- Are common fragile sites merely structural domains or highly organized "functional" units susceptible to oncogenic stress?Cellular and molecular life sciences : CMLS · 2014Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
SNM1B/Apollo is a DNA nuclease that has important functions in telomere maintenance and repair of DNA interstrand crosslinks (ICLs) within the Fanconi anemia (FA) pathway. SNM1B is required for efficient localization of key repair proteins, such as the FA protein, FANCD2, to sites of ICL damage and functions epistatically to FANCD2 in cellular survival to ICLs and homology-directed repair. The FA pathway is also activated in response to replication fork stalling. Here, we sought to determine the importance of SNM1B in cellular responses to stalled forks in the absence of a blocking lesion, such as ICLs. We found that depletion of SNM1B results in hypersensitivity to aphidicolin, a DNA polymerase inhibitor that causes replication stress. We observed that the SNM1B nuclease is required for efficient localization of the DNA repair proteins, FANCD2 and BRCA1, to subnuclear foci upon aphidicolin treatment, thereby indicating SNM1B facilitates direct repair of stalled forks. Consistent with a role for SNM1B subsequent to recognition of the lesion, we found that SNM1B is dispensable for upstream events, including activation of ATR-dependent signaling and localization of RPA, γH2AX and the MRE11/RAD50/NBS1 complex to aphidicolin-induced foci. We determined that a major consequence of SNM1B depletion is a marked increase in spontaneous and aphidicolin-induced chromosomal gaps and breaks, including breakage at common fragile sites. Thus, this study provides evidence that SNM1B functions in resolving replication stress and preventing accumulation of genomic damage.
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