Evidence map›Paper›PMID 9294199›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

Structure of the imprinted mouse Snrpn gene and establishment of its parental-specific methylation pattern.

R Shemer, Y Birger, A D Riggs, A Razin

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
9.5field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 196 citations in OpenAlex.

  1. Article
  2. Fertile androgenetic mice generated by targeted epigenetic editing of imprinting control regions.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  12. Genomic imprinting in mammals.Cold Spring Harbor perspectives in biology · 2014
    Review
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  15. Article
  16. Review
  17. Article
  18. Temporal and developmental requirements for the Prader-Willi imprinting center.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

R ShemerDepartment of Cellular Biochemistry, Hebrew University Hadassah Medical School, P.O. Box 12272, Jerusalem, 91120, Israel. shemer@md2.huji.ac.il
Y Birger
A D Riggs
A Razin
City of Hope · US

Funding

TRANSCRIPTION AND MODIFICATION OF CHROMATIN DNAR01GM020483 · NIGMS · HEBREW UNIVERSITY OF JERUSALEM · PI CEDAR, HOWARD · 1985 to 2005
$1.0M
SECRETION OF CTX PHAGE--GENETIC &MOLECULAR REQUIREMENTSF32GM020483 · NIGMS · TUFTS MEDICAL CENTER · PI DAVIS, BRIGID M · 2000 to 2001
$73k
NIGMS NIH HHS F32 GM020483NIGMS NIH HHS GM 20483NIGMS NIH HHS R01 GM020483
6 · The paper itself

Abstract

The mouse Snrpn gene encodes the Smn protein, which is involved in RNA splicing. The gene maps to a region in the central part of chromosome 7 that is syntenic to the Prader-Willi/Angelman syndromes (PWS-AS) region on human chromosome 15q11-q13. The mouse gene, like its human counterpart, is imprinted and paternally expressed, primarily in brain and heart. We provide here a detailed description of the structural features and differential methylation pattern of the gene. We have identified a maternally methylated region at the 5' end (DMR1), which correlates inversely with the Snrpn paternal expression. We also describe a region at the 3' end of the gene (DMR2) that is preferentially methylated on the paternal allele. Analysis of Snrpn mRNA levels in a methylase-deficient mouse embryo revealed that maternal methylation of DMR1 may play a role in silencing the maternal allele. Yet both regions, DMR1 and DMR2, inherit the parental-specific methylation profile from the gametes. This methylation pattern is erased in 12.5-days postcoitum (dpc) primordial germ cells and reestablished during gametogenesis. DMR1 is remethylated during oogenesis, whereas DMR2 is remethylated during spermatogenesis. Once established, these methylation patterns are transmitted to the embryo and maintained, protected from methylation changes during embryogenesis and cell differentiation. Transfections of DMR1 and DMR2 into embryonic stem cells and injection into pronuclei of fertilized eggs reveal that embryonic cells lack the capacity to establish anew the differential methylation pattern of Snrpn. That all PWS patients lack DMR1, together with the overall high resemblance of the mouse gene to the human SNRPN, offers an excellent experimental tool to study the regional control of this imprinted chromosomal domain.

Indexed as

DNA MethylationGenomic ImprintingRibonucleoproteins, Small NuclearAllelesAnimalsAutoantigensBase SequenceCells, CulturedDNA, ComplementaryEmbryonic DevelopmentFemaleFertilizationMaleMiceMolecular Sequence DataPregnancyAutoantigensDNA, ComplementaryRibonucleoproteins, Small NuclearsnRNP Core ProteinsSNRPN protein, human

Identifiers

PMID9294199
PMCPMC23351
OpenAlexW1986011018

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.