Rev7/Mad2B plays a critical role in the assembly of a functional mitotic spindle

Bhat, Audesh; Wu, Zhaojia; Maher, Veronica M.; McCormick, J. Justin; Xiao, Wei

doi:10.1080/15384101.2015.1120922

Cited by 32 publications

(31 citation statements)

References 46 publications

(91 reference statements)

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“…To further refine REV7 interactors, we intersected our data with previously reported proteomic profiling of REV7 (Nelson et al, 1999;Chen & Fang, 2001;Weterman et al, 2001;Guo et al, 2003;Iwai et al, 2007;Zhang et al, 2007;Hong et al, 2009;Medendorp et al, 2009;Tissier et al, 2010;Vermeulen et al, 2010;Listovsky & Sale, 2013;Rolland et al, 2014;Huttlin et al, 2015Huttlin et al, , 2017. Using this methodology, we obtained 11 high-confidence REV7 interactors (Figs 1B and EV1E), including the chromosome alignmentmaintaining phosphoprotein (CHAMP1), a kinetochore-microtubule attachment protein that has been recently linked to REV7 and its role during mitotic progression (Itoh et al, 2011), and the cell-division cycle protein 20 (CDC20), a critical activator of the anaphasepromoting complex (APC/C) that allows chromatid separation and entrance into anaphase (Chen & Fang, 2001;Listovsky & Sale, 2013;Bhat et al, 2015). However, whether these high-confidence REV7 interactors play any role in the DSB response remains unresolved.…”

Section: Resultsmentioning

confidence: 99%

SHLD 2/ FAM 35A co‐operates with REV 7 to coordinate DNA double‐strand break repair pathway choice

et al. 2018

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DNA double‐strand breaks (DSBs) can be repaired by two major pathways: non‐homologous end‐joining (NHEJ) and homologous recombination (HR). DNA repair pathway choice is governed by the opposing activities of 53BP1, in complex with its effectors RIF1 and REV7, and BRCA1. However, it remains unknown how the 53BP1/RIF1/REV7 complex stimulates NHEJ and restricts HR to the S/G2 phases of the cell cycle. Using a mass spectrometry (MS)‐based approach, we identify 11 high‐confidence REV7 interactors and elucidate the role of SHLD2 (previously annotated as FAM35A and RINN2) as an effector of REV7 in the NHEJ pathway. FAM35A depletion impairs NHEJ‐mediated DNA repair and compromises antibody diversification by class switch recombination (CSR) in B cells. FAM35A accumulates at DSBs in a 53BP1‐, RIF1‐, and REV7‐dependent manner and antagonizes HR by limiting DNA end resection. In fact, FAM35A is part of a larger complex composed of REV7 and SHLD1 (previously annotated as C20orf196 and RINN3), which promotes NHEJ and limits HR. Together, these results establish SHLD2 as a novel effector of REV7 in controlling the decision‐making process during DSB repair.

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Section: Resultsmentioning

confidence: 99%

SHLD 2/ FAM 35A co‐operates with REV 7 to coordinate DNA double‐strand break repair pathway choice

et al. 2018

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“…To further refine REV7 interactors, we intersected our data with previously reported proteomic profiling of REV7 (Nelson et al, 1999;Chen and Fang, 2001;Weterman et al, 2001;Guo et al, 2003;Iwai et al, 2007;Zhang et al, 2007;Hong et al, 2009;Medendorp et al, 2009;Tissier et al, 2010;Vermeulen et al, 2010;Listovsky and Sale, 2013); Rolland et al (2014); (Huttlin et al, 2015;Huttlin et al, 2017). Using this methodology, we obtained 11 high-confidence REV7 interactors ( including the chromosome alignment-maintaining phosphoprotein (CHAMP1), a kinetochore-microtubule attachment protein that has been recently linked to REV7 and its role during mitotic progression (Itoh et al, 2011), as well as the cell-division cycle protein 20 (CDC20), a critical activator of the anaphase promoting complex (APC/C) that allows chromatid separation and entrance into anaphase (Chen and Fang, 2001;Listovsky and Sale, 2013;Bhat et al, 2015).…”

Section: Mapping Of Rev7 Proximal/interacting Partners Relevant For Dmentioning

confidence: 99%

“…While the opposing role of 53BP1 and BRCA1 in DNA repair pathway choice has been extensively scrutinized over the past years, it remains largely unclear how the 53BP1 downstream effectors, namely REV7, promote NHEJ and antagonize BRCA1-mediated HR in G1 phase of the cell cycle (Boersma et al, 2015;Xu et al, 2015). REV7 is an adaptor protein that has been described for its role in mitotic progression through the control of both the activity of the spindle assembly checkpoint (SAC) and the formation of a functional anaphase-promoting complex/cyclosome-Cdc20 (APC/C) (Cahill et al, 1999;Listovsky and Sale, 2013;Bhat et al, 2015). In parallel, REV7 is a well-defined player in DNA translesion synthesis (TLS) (reviewed in (Waters et al, 2009)) as well as DSB repair by HR as part of a complex composed of the deoxycytidyl (dCMP) transferase REV1 and the catalytic subunit of the DNA polymerase ζ, REV3L (Sharma et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

FAM35A co-operates with REV7 to coordinate DNA double-strand break repair pathway choice

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Heath

et al. 2018

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“…It also physically interacts with proteins required for mitosis, such as RAN and CLTA . Additionally, the distinct subcellular distribution patterns of Rev3 and Rev7 during G2/M phase in mitotic cells and further characterization of roles of Rev7 during G2/M phase suggests a Rev3‐ and checkpoint‐independent role for Rev7 during mitosis . Furthermore, Rev7 has been recently reported to inhibit double‐strand break resection for homologous recombination .…”

Section: Introductionmentioning

confidence: 98%

Rev7, the regulatory subunit of Polζ, undergoes UV‐induced and Cul4‐dependent degradation

et al. 2017

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In eukaryotic cells, Rev7 interacts with Rev3 and functions as a regulatory subunit of Polf, a translesion DNA synthesis (TLS) polymerase. In addition to its role in TLS, mammalian Rev7, also known as Mad2B/Mad2L2, participates in multiple cellular activities including cell cycle progression and double-strand break repair through its interaction with several proteins. Here we show that in mammalian cells, Rev7 undergoes ubiquitin/proteasomemediated degradation upon UV irradiation in a time-dependent manner. We identified the Rev7 N-terminal destruction box as the degron and Cul4A/B as putative E3 ligases in this process. We also show that the nucleotide excision repair (NER) pathway protein HR23B physically interacts and colocalizes with Rev7 in the nuclear foci after UV irradiation and protects Rev7 from accelerated degradation. Furthermore, a similar Rev7 degradation profile was observed in cells treated with the UV-mimetic agent 4-nitroquinoline 1-oxide but not with cisplatin or camptothecin, suggesting a role of the NER pathway protein(s) in UV-induced Rev7 degradation. These data and the observation that cells deficient in Rev7 are sensitized to UV irradiation while excessive Rev7 protects cells from UV-induced DNA damage provide a new insight into the potential interplay between TLS and NER.

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Rev7/Mad2B plays a critical role in the assembly of a functional mitotic spindle

Cited by 32 publications

References 46 publications

SHLD 2/ FAM 35A co‐operates with REV 7 to coordinate DNA double‐strand break repair pathway choice

SHLD 2/ FAM 35A co‐operates with REV 7 to coordinate DNA double‐strand break repair pathway choice

FAM35A co-operates with REV7 to coordinate DNA double-strand break repair pathway choice

Rev7, the regulatory subunit of Polζ, undergoes UV‐induced and Cul4‐dependent degradation

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