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- W2953679327 abstract "Alternative lengthening of telomeres (ALT) is a telomerase-independent telomere maintenance mechanism that occurs in a subset of cancers. One of the hallmarks of ALT cancer is the excessively clustered telomeres in promyelocytic leukemia (PML) bodies, represented as large bright telomere foci. Here, we present a model system that generates telomere clustering in nuclear polySUMO (small ubiquitin-like modification)/polySIM (SUMO-interacting motif) condensates, analogous to PML bodies, and thus artificially engineered ALT-associated PML body (APB)-like condensates in vivo. We observed that the ALT-like phenotypes (i.e., a small fraction of heterogeneous telomere lengths and formation of C circles) are rapidly induced by introducing the APB-like condensates together with BLM through its helicase domain, accompanied by ssDNA generation and RPA accumulation at telomeres. Moreover, these events lead to mitotic DNA synthesis (MiDAS) at telomeres mediated by RAD52 through its highly conserved N-terminal domain. We propose that the clustering of large amounts of telomeres in human cancers promotes ALT that is mediated by MiDAS, analogous to Saccharomyces cerevisiae type II ALT survivors." @default.
- W2953679327 created "2019-07-12" @default.
- W2953679327 creator A5018167935 @default.
- W2953679327 creator A5029412437 @default.
- W2953679327 date "2019-06-06" @default.
- W2953679327 modified "2023-10-16" @default.
- W2953679327 title "Clustered telomeres in phase-separated nuclear condensates engage mitotic DNA synthesis through BLM and RAD52" @default.
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- W2953679327 doi "https://doi.org/10.1101/gad.324905.119" @default.
- W2953679327 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6601508" @default.
- W2953679327 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31171703" @default.
- W2953679327 hasPublicationYear "2019" @default.
- W2953679327 type Work @default.