Evidence map›Paper›PMID 26814574›Full record

ArticleeLife2016

Maternally provided LSD1/KDM1A enables the maternal-to-zygotic transition and prevents defects that manifest postnatally.

Jadiel A Wasson, Ashley K Simon, Dexter A Myrick, Gernot Wolf, Shawn Driscoll, Samuel L Pfaff, Todd S Macfarlan, David J Katz

Open access · goldAbstract read
In one paragraph

Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 92 citations in OpenAlex.

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  6. Ectopic transcription due to inherited histone methylation may interfere with the ongoing function of differentiated neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Jadiel A WassonDepartment of Cell Biology, Emory University School of Medicine, Atlanta, United States.
Ashley K SimonDepartment of Human Genetics, Emory University School of Medicine, Atlanta, United States.
Dexter A MyrickDepartment of Cell Biology, Emory University School of Medicine, Atlanta, United States.
Gernot WolfThe Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, United States.
Shawn DriscollHoward Hughes Medical Institute, The Salk Institute for Biological Studies, La Jolla, United States.
Samuel L PfaffHoward Hughes Medical Institute, The Salk Institute for Biological Studies, La Jolla, United States.
Todd S MacfarlanThe Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, United States.
David J KatzDepartment of Cell Biology, Emory University School of Medicine, Atlanta, United States.ORCID http://orcid.org/0000-0002-3040-1142
Emory University · USNational Institutes of Health · USSalk Institute for Biological Studies · US

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Ye Zheng · 1985 to 2026
$82.8M
Mechanisms of Mammalian Epigenome ReprogrammingZIAHD008933 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI MACFARLAN, TODD SCOTT · 2013 to 2025
$19.1M
Training Program in Biochemistry, Cell and Molecular BiologyT32GM008367 · NIGMS · EMORY UNIVERSITY · PI BOISE, LAWRENCE H., CORBETT, ANITA H. · 1990 to 2019
$5.6M
Post Baccalaureate Research Education ProgramR25GM089615 · NIGMS · EMORY UNIVERSITY · PI CHURCHWARD, GORDON G · 2010 to 2013
$1.1M
NCI NIH HHS P30 CA014195NIGMS NIH HHS R25 GM089615NIGMS NIH HHS T32 GM008367
6 · The paper itself

Abstract

Somatic cell nuclear transfer has established that the oocyte contains maternal factors with epigenetic reprogramming capacity. Yet the identity and function of these maternal factors during the gamete to embryo transition remains poorly understood. In C. elegans, LSD1/KDM1A enables this transition by removing H3K4me2 and preventing the transgenerational inheritance of transcription patterns. Here we show that loss of maternal LSD1/KDM1A in mice results in embryonic arrest at the 1-2 cell stage, with arrested embryos failing to undergo the maternal-to-zygotic transition. This suggests that LSD1/KDM1A maternal reprogramming is conserved. Moreover, partial loss of maternal LSD1/KDM1A results in striking phenotypes weeks after fertilization; including perinatal lethality and abnormal behavior in surviving adults. These maternal effect hypomorphic phenotypes are associated with alterations in DNA methylation and expression at imprinted genes. These results establish a novel mammalian paradigm where defects in early epigenetic reprogramming can lead to defects that manifest later in development.

Indexed as

Cell DifferentiationEmbryonic DevelopmentAnimalsDNA MethylationEpigenesis, GeneticGene Expression Regulation, DevelopmentalGenomic ImprintingHistone DemethylasesMiceOocytesZygoteHistone DemethylasesKDM1a protein, mousedevelopmental biologyepigeneticsgenomic imprintingKDM1aLSD1maternal effectmouseMZTstem cells

Identifiers

PMID26814574
PMCPMC4829428
OpenAlexW2254290007

What OpenQuestion holds

Textmetadata
LicenceCC0
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.