Evidence map›Paper›PMID 25404322›Full record

ReviewProceedings of the National Academy of Sciences of the United States of America2015

Genomic imprinting, action, and interaction of maternal and fetal genomes.

Eric B Keverne

Open access · bronzeAbstract readReview
In one paragraph

Review in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.4field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
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  3. Review
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  7. Review
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  9. Article
  10. The model of "genetic compartments": a new insight into reproductive genetics.Journal of assisted reproduction and genetics · 2019
    Review
  11. Article
  12. Review
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  14. Review
  15. Article
  16. Review
  17. Epigenetic changes in the developing brain: Effects on behavior.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  18. 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

1 author at 1 institution in 1 country.

Eric B KeverneSub-Department of Animal Behaviour, University of Cambridge, Cambridge CB23 8AA, United Kingdom ebk10@cam.ac.uk.
University of Cambridge · GB

Funding

Biotechnology and Biological Sciences Research Council
6 · The paper itself

Abstract

Mammalian viviparity (intrauterine development of the fetus) introduced a new dimension to brain development, with the fetal hypothalamus and fetal placenta developing at a time when the fetal placenta engages hypothalamic structures of the maternal generation. Such transgenerational interactions provide a basis for ensuring optimal maternalism in the next generation. This success has depended on genomic imprinting and a biased role of the matriline. Maternal methylation imprints determine parent of origin expression of genes fundamental to both placental and hypothalamic development. The matriline takes a further leading role for transgenerational reprogramming of these imprints. Developmental errors are minimized by the tight control that imprinted genes have on regulation of downstream evolutionary expanded gene families important for placental and hypothalamic development. Imprinted genes themselves have undergone purifying selection, providing a framework of stability for in utero development with most growth variance occurring postnatally. Mothers, not fathers, take the lead in the endocrinological and behavior adaptations that nurture, feed, and protect the infant. In utero coadaptive development of the placenta and hypothalamus has thus required a concomitant development to ensure male masculinization. Only placental male mammals evolved the sex determining SRY, which activates Sox9 for testes formation. SRY is a hybrid gene of Dgcr8 expressed in the developing placenta and Sox3 expressed in hypothalamic development. This hybridization of genes that take their origin from the placenta and hypothalamus has enabled critical in utero timing for the development of fetal Leydig cells, and hence testosterone production for hypothalamic masculinization.

Indexed as

Sex CharacteristicsAdaptation, BiologicalAnimalsFemaleGene Expression Regulation, DevelopmentalGenomic ImprintingGenomic InstabilityHumansHypothalamusMaleMammalsPlacentaPregnancydevelopmentgenomic imprintinggenomic reprogramminghypothalamusplacenta

Identifiers

PMID25404322
PMCPMC4460494
OpenAlexW1967095727

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.