Evidence map›Paper›PMID 31769059›Full record

ArticleThe EMBO journal2020

Histone H2A phosphorylation recruits topoisomerase IIα to centromeres to safeguard genomic stability.

Miao Zhang, Cai Liang, Qinfu Chen, Haiyan Yan, Junfen Xu, Hongxia Zhao, Xueying Yuan, Jingbo Liu, Shixian Lin, Weiguo Lu and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 46 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Miao ZhangMOE Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.
Cai LiangMOE Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.
Qinfu ChenMOE Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.
Haiyan YanMOE Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.
Junfen XuDepartment of Gynecologic Oncology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Hongxia ZhaoMOE Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.
Xueying YuanMOE Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.
Jingbo LiuMOE Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.
Shixian LinMOE Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.
Weiguo LuDepartment of Gynecologic Oncology, Women's Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China.
Fangwei WangMOE Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, Zhejiang, China.ORCID 0000-0001-5617-282X
Zhejiang University · CNWomen's Hospital, School of Medicine, Zhejiang University · CN

Funding

Fundamental Research Funds for the Central Universities in China 2014XZZX003-35Fundamental Research Funds for the Central Universities in China 2018QN81011National Key Research and Development Program of China 2017YFA0503600National Natural Science Foundation of China (NSFC) 31322032National Natural Science Foundation of China (NSFC) 31371359National Natural Science Foundation of China (NSFC) 31561130155National Natural Science Foundation of China (NSFC) 31571393National Natural Science Foundation of China (NSFC) 31771499National Natural Science Foundation of China (NSFC) 81702552Natural Science Foundation of Zhejiang Province LR13C070001Natural Science Foundation of Zhejiang Province LZ19C070001Royal Society Newton Advanced Fellowship NA140075
6 · The paper itself

Abstract

Chromosome segregation in mitosis requires the removal of catenation between sister chromatids. Timely decatenation of sister DNAs at mitotic centromeres by topoisomerase IIα (TOP2A) is crucial to maintain genomic stability. The chromatin factors that recruit TOP2A to centromeres during mitosis remain unknown. Here, we show that histone H2A Thr-120 phosphorylation (H2ApT120), a modification generated by the mitotic kinase Bub1, is necessary and sufficient for the centromeric localization of TOP2A. Phosphorylation at residue-120 enhances histone H2A binding to TOP2A in vitro. The C-gate and the extreme C-terminal region are important for H2ApT120-dependent localization of TOP2A at centromeres. Preventing H2ApT120-mediated accumulation of TOP2A at mitotic centromeres interferes with sister chromatid disjunction, as evidenced by increased frequency of anaphase ultra-fine bridges (UFBs) that contain catenated DNA. Tethering TOP2A to centromeres bypasses the requirement for H2ApT120 in suppressing anaphase UFBs. These results demonstrate that H2ApT120 acts as a landmark that recruits TOP2A to mitotic centromeres to decatenate sister DNAs. Our study reveals a fundamental role for histone phosphorylation in resolving centromere DNA entanglements and safeguarding genomic stability during mitosis.

Indexed as

Binding SitesCell LineCentromereChromosome SegregationDNADNA Topoisomerases, Type IIGenomic InstabilityHeLa CellsHistonesHumansPhosphorylationPoly-ADP-Ribose Binding ProteinsProtein Serine-Threonine KinasesThreonineBUB1 protein, humanDNADNA Topoisomerases, Type IIHistonesPoly-ADP-Ribose Binding ProteinsProtein Serine-Threonine KinasesThreonineTOP2A protein, humanBub1DNA decatenationhistone H2A phosphorylationSgo1TOP2A

Identifiers

PMID31769059
PMCPMC6996575
OpenAlexW2990783313

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.