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Journal Article

Nucleosome Remodeling by Fun30(SMARCAD1) in the DNA Damage Response

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Bantele,  Susanne C. S.
Pfander, Boris / DNA Replication and Genome Integrity, Max Planck Institute of Biochemistry, Max Planck Society;

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Pfander,  Boris
Pfander, Boris / DNA Replication and Genome Integrity, Max Planck Institute of Biochemistry, Max Planck Society;

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Citation

Bantele, S. C. S., & Pfander, B. (2019). Nucleosome Remodeling by Fun30(SMARCAD1) in the DNA Damage Response. FRONTIERS IN MOLECULAR BIOSCIENCES, 6: UNSP 78. doi:10.3389/fmolb.2019.00078.


Cite as: https://hdl.handle.net/21.11116/0000-0005-5281-C
Abstract
Many cellular pathways are dedicated to maintain the integrity of the genome. In eukaryotes, the underlying DNA transactions occur in the context of chromatin. Cells utilize chromatin and its dynamic nature to regulate those genome integrity pathways. Accordingly, chromatin becomes restructured and modified around DNA damage sites. Here, we review the current knowledge of a chromatin remodeler Fun30(SMARCAD1) which plays a key role in genome maintenance. Fun30(SMARCAD1) promotes DNA end resection and the repair of DNA double-stranded breaks (DSBs). Notably, however, Fun30(SMARCAD1) plays additional roles in maintaining heterochromatin and promoting transcription. Overall, Fun30(SMARCAD1) is involved in distinct processes and the specific roles of Fun30(SMARCAD1) at DSBs, replication forks and sites of transcription appear discordant at first view. Nonetheless, a picture emerges in which commonalities within these context-dependent roles of Fun30(SMARCAD1) exist, which may help to gain a more global understanding of chromatin alterations induced by Fun30(SMARCAD1).