Evidence map›Paper›PMID 24833720›Full record

ArticleHuman molecular genetics2014

A feed-forward mechanism involving Drosophila fragile X mental retardation protein triggers a replication stress-induced DNA damage response.

Wenxin Zhang, Ying Cheng, Yujing Li, Zhenping Chen, Peng Jin, Dahua Chen

Open access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. FMRP promotes transcription-coupled homologous recombination via facilitating TET1-mediated m5C RNA modification demethylation.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Frontiers in genetics · 2019
    Review
  11. The Fragile X Protein and Genome Function.Molecular neurobiology · 2019
    Review
  12. Modeling Fragile X Syndrome inFrontiers in molecular neuroscience · 2018
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Wenxin ZhangState Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, PR China.
Ying ChengState Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, PR China Department of Human Genetics, Emory University School of Medicine, Atlanta, GA 30322, USA.
Yujing LiDepartment of Human Genetics, Emory University School of Medicine, Atlanta, GA 30322, USA.
Zhenping ChenState Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, PR China.
Peng JinDepartment of Human Genetics, Emory University School of Medicine, Atlanta, GA 30322, USA chendh@ioz.ac.cn peng.jin@emory.edu.
Dahua ChenState Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, PR China chendh@ioz.ac.cn peng.jin@emory.edu.
Chinese Academy of Sciences · CNEmory University · USInstitute of Zoology · CN

Funding

5-Hydroxymethylcytosine in NeurodevelopmentR01NS079625 · NINDS · EMORY UNIVERSITY · PI JIN, PENG · 2012 to 2016
$1.7M
NINDS NIH HHS NS079625
6 · The paper itself

Abstract

Fragile X syndrome, a common form of inherited mental retardation, is caused by loss of the fragile X mental retardation protein (FMRP). As a selective RNA-binding protein, FMRP is localized predominately in cytoplasm, where it regulates translational control. However, there is a small portion of FMRP present in the nucleus, and its function there has been elusive. Here, we show that Drosophila dFMR1 in nucleus is required for replication stress-induced H2Av phosphorylation in the DNA damage response (DDR). Replication stress could induce the expression of dFmr1 and promote the nuclear accumulation of dFMR1. We show that, upon the stimulation of replication stress, dFMR1 is associated with chromatin in a domain-specific manner, which is essential for its ability to induce the phosphorylation of H2Av. These results together reveal an unexpected nuclear role of FMRP in DDR and uncover a feed-forward mechanism by which dFmr1 and early DDR induced by replication stress reciprocally regulate each other, thereby synergistically triggering activity of the DDR signaling cascade.

Indexed as

DNA DamageDNA ReplicationAnimalsCell NucleusChromatinDrosophilaDrosophila ProteinsFragile X Messenger Ribonucleoprotein 1Gene Expression RegulationGerm CellsPhosphorylationProtein BindingProtein Interaction Domains and MotifsProtein TransportRNA, MessengerChromatinDrosophila ProteinsFMR1 protein, DrosophilaFragile X Messenger Ribonucleoprotein 1RNA, Messenger

Identifiers

PMID24833720
PMCPMC4159158
OpenAlexW2096157023

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.