Evidence map›Paper›PMID 22619389›Full record

ArticleDevelopment (Cambridge, England)2012

Dauer larva quiescence alters the circuitry of microRNA pathways regulating cell fate progression in C. elegans.

Xantha Karp, Victor Ambros

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
0.9field-weighted citation impact, top 33% 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

33 citing papers in PubMed, 53 citations in OpenAlex.

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  13. The multifaceted roles of microRNAs in differentiation.Current opinion in cell biology · 2020
    Review
  14. Review
  15. microPublication biology · 2020
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  16. Regulation of nuclear-cytoplasmic partitioning by theDevelopment (Cambridge, England) · 2019
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  17. Article
  18. Article
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  20. Epidermal Remodeling inGenetics · 2019
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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

2 authors at 1 institution in 1 country.

Xantha KarpProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.
Victor Ambros
University of Massachusetts Chan Medical School · US

Funding

PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
GENETIC CONTROL OF NEMATODE DEVELOPMENTR01GM034028 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI AMBROS, VICTOR · 1985 to 2018
$7.0M
Developmental Regulation of MicroRNA ExpressionR01GM088365 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI AMBROS, VICTOR · 2009 to 2010
$771k
Genetics of postdauer developmental timing in C elegansF32GM073307 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KARP, XANTHA · 2005 to 2007
$143k
BIOCHEMISTRY AND GENETICS OF LIPOAMIDE DEHYDROGENASER01GM030428 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI SOKATCH, JOHN R · 1985 to 1994
–
Howard Hughes Medical InstituteNIDDK NIH HHS DK32520NIDDK NIH HHS P30 DK032520NIGMS NIH HHS F32 GM073307NIGMS NIH HHS F32 GM73307NIGMS NIH HHS R01 GM034028NIGMS NIH HHS R01 GM088365NIGMS NIH HHS R01GM088365NIGMS NIH HHS R01GM30428
6 · The paper itself

Abstract

In C. elegans larvae, the execution of stage-specific developmental events is controlled by heterochronic genes, which include those encoding a set of transcription factors and the microRNAs that regulate the timing of their expression. Under adverse environmental conditions, developing larvae enter a stress-resistant, quiescent stage called 'dauer'. Dauer larvae are characterized by the arrest of all progenitor cell lineages at a stage equivalent to the end of the second larval stage (L2). If dauer larvae encounter conditions favorable for resumption of reproductive growth, they recover and complete development normally, indicating that post-dauer larvae possess mechanisms to accommodate an indefinite period of interrupted development. For cells to progress to L3 cell fate, the transcription factor Hunchback-like-1 (HBL-1) must be downregulated. Here, we describe a quiescence-induced shift in the repertoire of microRNAs that regulate HBL-1. During continuous development, HBL-1 downregulation (and consequent cell fate progression) relies chiefly on three let-7 family microRNAs, whereas after quiescence, HBL-1 is downregulated primarily by the lin-4 microRNA in combination with an altered set of let-7 family microRNAs. We propose that this shift in microRNA regulation of HBL-1 expression involves an enhancement of the activity of lin-4 and let-7 microRNAs by miRISC modulatory proteins, including NHL-2 and LIN-46. These results illustrate how the employment of alternative genetic regulatory pathways can provide for the robust progression of progenitor cell fates in the face of temporary developmental quiescence.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCarrier ProteinsCell LineageDisorders of Sex DevelopmentDown-RegulationGene Expression Regulation, DevelopmentalGene Regulatory NetworksLarvaMicroRNAsModels, BiologicalPhenotypeRNA-Induced Silencing ComplexSignal TransductionAdaptor Proteins, Signal TransducingCaenorhabditis elegans ProteinsCarrier Proteinslet-7 microRNA, C elegansLin-46 protein, C elegansMicroRNAsNHL-2 protein, C elegansRNA-Induced Silencing Complex

Identifiers

PMID22619389
PMCPMC3357911
OpenAlexW2005676064

What OpenQuestion holds

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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.