Evidence map›Paper›PMID 33621320›Full record

ArticleNucleic acids research2021

Role of CxxC-finger protein 1 in establishing mouse oocyte epigenetic landscapes.

Qian-Qian Sha, Ye-Zhang Zhu, Yunlong Xiang, Jia-Li Yu, Xiao-Ying Fan, Yan-Chu Li, Yun-Wen Wu, Li Shen, Heng-Yu Fan

Abstract read
In one paragraph

Article in Nucleic acids research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. CRL4Cellular and molecular life sciences : CMLS · 2024
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. ASH1L contributes to oocyte apoptosis by regulating DNA damage.American journal of physiology. Cell physiology · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. Article
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

9 authors.

Qian-Qian ShaFertility Preservation Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital, Guangzhou 510317, China.
Ye-Zhang ZhuLife Sciences Institute, Zhejiang University, Hangzhou 310058, China.
Yunlong XiangCenter for Stem Cell Biology and Regenerative Medicine, MOE Key Laboratory of Bioinformatics, THU-PKU Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing, China.
Jia-Li YuLife Sciences Institute, Zhejiang University, Hangzhou 310058, China.
Xiao-Ying FanBioland Laboratory (Guangzhou Regenerative Medicine and Health GuangDong Laboratory), Guangzhou 510005, China.
Yan-Chu LiFertility Preservation Laboratory, Reproductive Medicine Center, Guangdong Second Provincial General Hospital, Guangzhou 510317, China.
Yun-Wen WuLife Sciences Institute, Zhejiang University, Hangzhou 310058, China.
Li ShenLife Sciences Institute, Zhejiang University, Hangzhou 310058, China.
Heng-Yu FanLife Sciences Institute, Zhejiang University, Hangzhou 310058, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During oogenesis, oocytes gain competence and subsequently undergo meiotic maturation and prepare for embryonic development; trimethylated histone H3 on lysine-4 (H3K4me3) mediates a wide range of nuclear events during these processes. Oocyte-specific knockout of CxxC-finger protein 1 (CXXC1, also known as CFP1) impairs H3K4me3 accumulation and causes changes in chromatin configurations. This study investigated the changes in genomic H3K4me3 landscapes in oocytes with Cxxc1 knockout and the effects on other epigenetic factors such as the DNA methylation, H3K27me3, H2AK119ub1 and H3K36me3. H3K4me3 is overall decreased after knocking out Cxxc1, including both the promoter region and the gene body. CXXC1 and MLL2, which is another histone H3 methyltransferase, have nonoverlapping roles in mediating H3K4 trimethylation during oogenesis. Cxxc1 deletion caused a decrease in DNA methylation levels and affected H3K27me3 and H2AK119ub1 distributions, particularly at regions with high DNA methylation levels. The changes in epigenetic networks implicated by Cxxc1 deletion were correlated with the transcriptional changes in genes in the corresponding genomic regions. This study elucidates the epigenetic changes underlying the phenotypes and molecular defects in oocytes with deleted Cxxc1 and highlights the role of CXXC1 in orchestrating multiple factors that are involved in establishing the appropriate epigenetic states of maternal genome.

Indexed as

Epigenesis, GeneticAnimalsCells, CulturedDNA MethylationFemaleGene DeletionGenomeHistone CodeHistonesMiceMice, Inbred C57BLOocytesPromoter Regions, GeneticTrans-ActivatorsTranscription, GeneticCxxc1 protein, mouseHistonesTrans-Activators

Identifiers

PMID33621320
PMCPMC7969028

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Registered trials

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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.