Evidence map›Paper›PMID 21343362›Full record

ArticleDevelopment (Cambridge, England)2011

synMuv B proteins antagonize germline fate in the intestine and ensure C. elegans survival.

Lisa N Petrella, Wenchao Wang, Caroline A Spike, Andreas Rechtsteiner, Valerie Reinke, Susan Strome

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

73 citing papers in PubMed, 105 citations in OpenAlex.

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  18. A chromodomain protein mediates heterochromatin-directed piRNA expression.Proceedings of the National Academy of Sciences of the United States of America · 2021
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13 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

6 authors at 3 institutions in 1 country.

Lisa N PetrellaDepartment of Molecular, Cell and Developmental Biology, University of California Santa Cruz, Santa Cruz, CA 95064, USA.
Wenchao Wang
Caroline A Spike
Andreas Rechtsteiner
Valerie Reinke
Susan Strome
Indiana University Bloomington · USUniversity of California, Santa Cruz · USYale University · US

Funding

IMMUNOLOGIC STUDY OF GERM GRANULES IN C. ELEGANS EMBRY0SR01GM034059 · NIGMS · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI STROME, SUSAN · 1985 to 2020
$8.9M
Chromatin Regulation in C. elegans Germline DevelopmentF32GM083548 · NIGMS · UNIVERSITY OF CALIFORNIA SANTA CRUZ · PI PETRELLA, LISA NICOLE · 2008 to 2010
$149k
Assembly and function of germ granules in C. elegansF32GM069084 · NIGMS · INDIANA UNIVERSITY BLOOMINGTON · PI SPIKE, CAROLINE A · 2003 to 2003
$42k
NIGMS NIH HHS F32 GM069084NIGMS NIH HHS F32 GM083548NIGMS NIH HHS GM083548NIGMS NIH HHS GM34059NIGMS NIH HHS GM69084NIGMS NIH HHS R01 GM034059
6 · The paper itself

Abstract

Previous studies demonstrated that a subset of synMuv B mutants ectopically misexpress germline-specific P-granule proteins in their somatic cells, suggesting a failure to properly orchestrate a soma/germline fate decision. Surprisingly, this fate confusion does not affect viability at low to ambient temperatures. Here, we show that, when grown at high temperature, a majority of synMuv B mutants irreversibly arrest at the L1 stage. High temperature arrest (HTA) is accompanied by upregulation of many genes characteristic of germ line, including genes encoding components of the synaptonemal complex and other meiosis proteins. HTA is suppressed by loss of global regulators of germline chromatin, including MES-4, MRG-1, ISW-1 and the MES-2/3/6 complex, revealing that arrest is caused by somatic cells possessing a germline-like chromatin state. Germline genes are preferentially misregulated in the intestine, and necessity and sufficiency tests demonstrate that the intestine is the tissue responsible for HTA. We propose that synMuv B mutants fail to erase or antagonize an inherited germline chromatin state in somatic cells during embryonic and early larval development. As a consequence, somatic cells gain a germline program of gene expression in addition to their somatic program, leading to a mixed fate. Somatic expression of germline genes is enhanced at elevated temperature, leading to developmentally compromised somatic cells and arrest of newly hatched larvae.

Indexed as

AnimalsAnimals, Genetically ModifiedCaenorhabditis elegansCaenorhabditis elegans ProteinsCell LineageEmbryo, NonmammalianGene Expression ProfilingGene Expression Regulation, DevelopmentalGenes, HelminthGerm CellsIntestinal MucosaIntestinesLarvaLife Cycle StagesMicroarray AnalysisSurvivalCaenorhabditis elegans Proteins

Identifiers

PMID21343362
PMCPMC3042865
OpenAlexW2128541738

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.