Evidence map›Paper›PMID 30810530›Full record

ArticleeLife2019

Amplification of a broad transcriptional program by a common factor triggers the meiotic cell cycle in mice.

Mina L Kojima, Dirk G de Rooij, David C Page

Abstract read
In one paragraph

Article in eLife, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing 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

72 citing papers in PubMed.

  1. Article
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  5. MCT1 governs a metabolic checkpoint at pachytene during spermatogenesis.bioRxiv : the preprint server for biology · 2026
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12 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

3 authors.

Mina L KojimaWhitehead Institute, Cambridge, United States.ORCID 0000-0002-3387-8608
Dirk G de RooijWhitehead Institute, Cambridge, United States.ORCID 0000-0003-3932-4419
David C PageWhitehead Institute, Cambridge, United States.ORCID 0000-0001-9920-3411

Funding

PRE-DOCTORAL TRAINING IN THE BIOLOGICAL SCIENCEST32GM007287 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI BELL, STEPHEN P., KEATING, AMY E · 1985 to 2019
$40.8M
Howard Hughes Medical Institute InvestigatorNational Science Foundation Graduate Research FellowshipNIGMS NIH HHS T32 GM007287
6 · The paper itself

Abstract

The germ line provides the cellular link between generations of multicellular organisms, its cells entering the meiotic cell cycle only once each generation. However, the mechanisms governing this initiation of meiosis remain poorly understood. Here, we examined cells undergoing meiotic initiation in mice, and we found that initiation involves the dramatic upregulation of a transcriptional network of thousands of genes whose expression is not limited to meiosis. This broad gene expression program is directly upregulated by STRA8, encoded by a germ cell-specific gene required for meiotic initiation. STRA8 binds its own promoter and those of thousands of other genes, including meiotic prophase genes, factors mediating DNA replication and the G1-S cell-cycle transition, and genes that promote the lengthy prophase unique to meiosis I. We conclude that, in mice, the robust amplification of this extraordinarily broad transcription program by a common factor triggers initiation of meiosis.

Indexed as

Cell CycleGene Expression RegulationMeiosisAdaptor Proteins, Signal TransducingAnimalsDNAGene Regulatory NetworksGerm CellsMicePromoter Regions, GeneticProtein BindingAdaptor Proteins, Signal TransducingDNAStra8 protein, mousecell cyclechromosomesdevelopmental biologygene expressiongerm cellsmeiosismouseStra8transcription

Identifiers

PMID30810530
PMCPMC6392498

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.