Histone chaperone FACT regulates homologous recombination by chromatin remodeling through interaction with RNF20

Oliveira, Douglas V.N.P.; Nakamura, Kae; Ikura, Tsuyoshi; Okada, Masahiro; Kobayashi, Junya; Yanagihara, Hirokazu; Saito, Yuichiro; Tauchi, Hiroshi; Komatsu, Kenshi

doi:10.1242/jcs.135855

Cited by 51 publications

(56 citation statements)

References 51 publications

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“…The histone chaperone FACT (for 'facilitates chromatin transcription') removes cH2AX-H2B dimers from sites of damage, which is inhibited by PARylation of FACT (Heo et al, 2008). At the same time, FACT is bound to the E3 ubiquitin ligase RNF20 that mono-ubiquitylates histone H2B (Oliveira et al, 2014). Once repair is finished, nucleosomal organisation must be restored to reinstate proper chromatin structure and function (Polo, 2014).…”

Section: G2 Checkpoint Recovery -Plk1 Couples Cell Cycle Restart To Cmentioning

confidence: 99%

The same, only different – DNA damage checkpoints and their reversal throughout the cell cycle

Shaltiël

Krenning

Bruinsma

et al. 2015

Journal of Cell Science

254

272

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Cell cycle checkpoints activated by DNA double-strand breaks (DSBs) are essential for the maintenance of the genomic integrity of proliferating cells. Following DNA damage, cells must detect the break and either transiently block cell cycle progression, to allow time for repair, or exit the cell cycle. Reversal of a DNA-damageinduced checkpoint not only requires the repair of these lesions, but a cell must also prevent permanent exit from the cell cycle and actively terminate checkpoint signalling to allow cell cycle progression to resume. It is becoming increasingly clear that despite the shared mechanisms of DNA damage detection throughout the cell cycle, the checkpoint and its reversal are precisely tuned to each cell cycle phase. Furthermore, recent findings challenge the dogmatic view that complete repair is a precondition for cell cycle resumption. In this Commentary, we highlight cell-cycle-dependent differences in checkpoint signalling and recovery after a DNA DSB, and summarise the molecular mechanisms that underlie the reversal of DNA damage checkpoints, before discussing when and how cell fate decisions after a DSB are made.

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Section: G2 Checkpoint Recovery -Plk1 Couples Cell Cycle Restart To Cmentioning

confidence: 99%

The same, only different – DNA damage checkpoints and their reversal throughout the cell cycle

Shaltiël

Krenning

Bruinsma

et al. 2015

Journal of Cell Science

254

272

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“…FACILITATES CHROMATIN TRANSCRIPTION is a histone chaperone that also mainly associates with H2A/H2B dimers. From the two human subunits, only SPT16 (but not the HMG boxcontaining SSRP1) is required for the efficient repair of UV light damage (Dinant et al, 2013;Oliveira et al, 2014). Both subunits have orthologs in Arabidopsis, and these are important for regular development (Lolas et al, 2010) and epigenetic regulation (Ikeda et al, 2011), but a link to DNA damage is not described.…”

Section: Histones and Histone Chaperones Connected With Ddrmentioning

confidence: 99%

DNA Damage Repair in the Context of Plant Chromatin

Donà

Scheid

2015

Plant Physiol.

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The integrity of DNA molecules is constantly challenged. All organisms have developed mechanisms to detect and repair multiple types of DNA lesions. The basic principles of DNA damage repair (DDR) in prokaryotes and unicellular and multicellular eukaryotes are similar, but the association of DNA with nucleosomes in eukaryotic chromatin requires mechanisms that allow access of repair enzymes to the lesions. This is achieved by chromatin-remodeling factors, and their necessity for efficient DDR has recently been demonstrated for several organisms and repair pathways. Plants share many features of chromatin organization and DNA repair with fungi and animals, but they differ in other, important details, which are both interesting and relevant for our understanding of genome stability and genetic diversity. In this Update, we compare the knowledge of the role of chromatin and chromatin-modifying factors during DDR in plants with equivalent systems in yeast and humans. We emphasize plant-specific elements and discuss possible implications.A DNA molecule in a eukaryotic chromosome has a diameter of 2 nm but a length in the range of centimeters. Being 10 7 times longer than it is wide would make it highly sensitive to breakage if it were not organized in compact and dynamic chromatin, with nucleosomes as basic units followed by multiple higher order levels of organization. Within this packaging, replication and transcription constitute an endogenous mechanical strain, while exposure of cells to physical or chemical hazard creates a wide range of DNA damage induced by external factors, including photoproducts, pyrimidine dimers, interstrand crosslinking, and single and double-strand breaks (DSBs). All organisms possess mechanisms that repair DNA molecules. DNA damage repair (DDR) systems for the various types of damage are overlapping as well as complementary, and their prevalence depends on the organism, the stage of the cell cycle, the site and the amount of damage, and the availability of intact templates. A coarse categorization distinguishes nucleotide excision repair, base excision repair, nonhomologous end joining (NHEJ), and homologous recombination (HR). Many schematic models for these DDR pathways describe the action and interaction of several repair components, but they are usually misleading in one aspect: DNA strands are illustrated as straight lines, neglecting the emerging role of chromatin for the location and the fate of DNA lesions. More realistically, we should envisage DNA lesions in the chromatin context like the leakage or burst of an in-ground pipe. Recognizing the defect, localizing it, excavating the broken parts, cleaning the ends, reconnecting them, and restoring the original state are mirrored in the subsequent steps of DDR: signaling, labeling, accessing, resecting, religating, and reassembling. Chromatin is expected to especially affect the access, resection, and restoration of the original arrangement, and several factors that can dissolve higher order structures, slide, evict, or exchange ...

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“…Furthermore, IRinduced RPA focus formation, which is likely to be CtIPdependent, was also attenuated in RNF20-depleted cells and in mutated NBS1-expressing cells at RNF20-binding sites, suggesting that the interaction between NBS1 and RNF20 participates in the regulation of DSB end-resection through DSB-induced chromatin remodeling. On the other hand, we also found SUPT16H, a subunit of the FACT complex, to be an RNF20-binding partner (Oliveira et al, 2014). SUPT16H directly interacts with the Cterminal RING domain of RNF20.…”

Section: Introductionmentioning

confidence: 60%

Chromatin modification and NBS1: their relationship in DNA double-strand break repair

2015

Self Cite

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The importance of chromatin modification, including histone modification and chromatin remodeling, for DNA double-strand break (DSB) repair, as well as transcription and replication, has been elucidated. Phosphorylation of H2AX to γ-H2AX is one of the first responses following DSB detection, and this histone modification is important for the DSB damage response by triggering several events, including the accumulation of DNA damage response-related proteins and subsequent homologous recombination (HR) repair. The roles of other histone modifications such as acetylation, methylation and ubiquitination have also been recently clarified, particularly in the context of HR repair. NBS1 is a multifunctional protein that is involved in various DNA damage responses. Its recently identified binding partner RNF20 is an E3 ubiquitin ligase that facilitates the monoubiquitination of histone H2B, a process that is crucial for recruitment of the chromatin remodeler SNF2h to DSB damage sites. Evidence suggests that SNF2h functions in HR repair, probably through regulation of end-resection. Moreover, several recent reports have indicated that SNF2h can function in HR repair pathways as a histone remodeler and that other known histone remodelers can also participate in DSB damage responses. On the other hand, information about the roles of such chromatin modifications and NBS1 in non-homologous end joining (NHEJ) repair of DSBs and stalled fork-related damage responses is very limited; therefore, these aspects and processes need to be further studied to advance our understanding of the mechanisms and molecular players involved.

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Histone chaperone FACT regulates homologous recombination by chromatin remodeling through interaction with RNF20

Cited by 51 publications

References 51 publications

The same, only different – DNA damage checkpoints and their reversal throughout the cell cycle

The same, only different – DNA damage checkpoints and their reversal throughout the cell cycle

DNA Damage Repair in the Context of Plant Chromatin

Chromatin modification and NBS1: their relationship in DNA double-strand break repair

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