Evidence map›Paper›PMID 26527006›Full record

ArticleCell reports2015

TRIM28 Controls Genomic Imprinting through Distinct Mechanisms during and after Early Genome-wide Reprogramming.

Katherine A Alexander, Xu Wang, Maho Shibata, Andrew G Clark, María J García-García

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 54 citations in OpenAlex.

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  15. eLife · 2020
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  16. Article
  17. Methylation-directed glycosylation of chromatin factors represses retrotransposon promoters.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  18. Article
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Katherine A AlexanderDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.
Xu WangDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.
Maho ShibataDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.
Andrew G ClarkDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA.
María J García-GarcíaDepartment of Molecular Biology and Genetics, Cornell University, Ithaca, NY 14853, USA. Electronic address: garciamj@cornell.edu.
Cornell University · US

Funding

Developmental & Molecular Mechanisms Employed by Chato, KRAB Zinc Finger ProteinR01HD060581 · NICHD · CORNELL UNIVERSITY · PI GARCIA-GARCIA, MARIA J · 2010 to 2014
$1.4M
Research and Career Training in Vertebrate Developmental GenomicsT32HD057854 · NICHD · CORNELL UNIVERSITY · PI SCHIMENTI, JOHN C · 2010 to 2020
$1.3M
Zeiss LSM710 Confocal Microscope for Shared Imaging FacilityS10RR025502 · NCRR · CORNELL UNIVERSITY · PI WILLIAMS, REBECCA M · 2009 to 2009
$500k
NCRR NIH HHS S10 RR025502NCRR NIH HHS S10RR025502NICHD NIH HHS 5T32HD057854-04NICHD NIH HHS R01 HD060581NICHD NIH HHS R01HD060581NICHD NIH HHS T32 HD057854
6 · The paper itself

Abstract

Genomic imprinting depends on the establishment and maintenance of DNA methylation at imprinting control regions. However, the mechanisms by which these heritable marks influence allele-specific expression are not fully understood. By analyzing maternal, zygotic, maternal-zygotic, and conditional Trim28 mutants, we found that the transcription factor TRIM28 controls genomic imprinting through distinct mechanisms at different developmental stages. During early genome-wide reprogramming, both maternal and zygotic TRIM28 are required for the maintenance of methylation at germline imprints. However, in conditional Trim28 mutants, Gtl2-imprinted gene expression was lost despite normal methylation levels at the germline IG-DMR. These results provide evidence that TRIM28 controls imprinting after early embryonic reprogramming through a mechanism other than the maintenance of germline imprints. Additionally, our finding that secondary imprints were hypomethylated in TRIM28 mutants uncovers a requirement of TRIM28 after genome-wide reprogramming for interpreting germline imprints and regulating DNA methylation at imprinted gene promoters.

Indexed as

Cellular ReprogrammingGenomeGenomic ImprintingAnimalsDNA MethylationMiceMice, Inbred C57BLNuclear ProteinsRepressor ProteinsTripartite Motif-Containing Protein 28Nuclear ProteinsRepressor ProteinsTrim28 protein, mouseTripartite Motif-Containing Protein 28

Identifiers

PMID26527006
PMCPMC4644443
OpenAlexW1913498431

What OpenQuestion holds

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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.