Evidence map›Paper›PMID 24763381›Full record

ArticlePLoS genetics2014

Mutations in conserved residues of the C. elegans microRNA Argonaute ALG-1 identify separable functions in ALG-1 miRISC loading and target repression.

Anna Y Zinovyeva, Samir Bouasker, Martin J Simard, Christopher M Hammell, Victor Ambros

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

30 citing papers in PubMed, 46 citations in OpenAlex.

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  7. Modeling neurodevelopmental disorder-associated humanProceedings of the National Academy of Sciences of the United States of America · 2024
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  14. microRNA strand selection: Unwinding the rules.Wiley interdisciplinary reviews. RNA · 2021
    Review
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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

5 authors at 4 institutions in 2 countries.

Anna Y ZinovyevaProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, United States of America.
Samir BouaskerSt-Patrick Research Group in Basic Oncology, Hôtel-Dieu de Québec (Centre Hospitalier Universitaire de Québec), Laval University Cancer Research Centre, Quebec City, Québec, Canada.
Martin J SimardSt-Patrick Research Group in Basic Oncology, Hôtel-Dieu de Québec (Centre Hospitalier Universitaire de Québec), Laval University Cancer Research Centre, Quebec City, Québec, Canada.
Christopher M HammellCold Spring Harbor Laboratory, Cold Spring Harbor, New York, United States of America.
Victor AmbrosProgram in Molecular Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, United States of America.
University of Massachusetts Chan Medical School · USCentre hospitalier universitaire de Québec · CACold Spring Harbor Laboratory · USUniversité Laval · CA

Funding

Single-Cell Biology Shared ResourceP30CA045508 · NCI · COLD SPRING HARBOR LABORATORY · PI John Edward Moses · 1987 to 2026
$118.9M
Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
GENETIC CONTROL OF NEMATODE DEVELOPMENTR01GM034028 · NIGMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI AMBROS, VICTOR · 1985 to 2018
$7.0M
CIHR MOP-81186NCI NIH HHS P30 CA045508NIGMS NIH HHS NIH R01-GM34028NIGMS NIH HHS R01 GM034028NIH HHS P40 OD010440
6 · The paper itself

Abstract

microRNAs function in diverse developmental and physiological processes by regulating target gene expression at the post-transcriptional level. ALG-1 is one of two Caenorhabditis elegans Argonautes (ALG-1 and ALG-2) that together are essential for microRNA biogenesis and function. Here, we report the identification of novel antimorphic (anti) alleles of ALG-1 as suppressors of lin-28(lf) precocious developmental phenotypes. The alg-1(anti) mutations broadly impair the function of many microRNAs and cause dosage-dependent phenotypes that are more severe than the complete loss of ALG-1. ALG-1(anti) mutant proteins are competent for promoting Dicer cleavage of microRNA precursors and for associating with and stabilizing microRNAs. However, our results suggest that ALG-1(anti) proteins may sequester microRNAs in immature and functionally deficient microRNA Induced Silencing Complexes (miRISCs), and hence compete with ALG-2 for access to functional microRNAs. Immunoprecipitation experiments show that ALG-1(anti) proteins display an increased association with Dicer and a decreased association with AIN-1/GW182. These findings suggest that alg-1(anti) mutations impair the ability of ALG-1 miRISC to execute a transition from Dicer-associated microRNA processing to AIN-1/GW182 associated effector function, and indicate an active role for ALG/Argonaute in mediating this transition.

Indexed as

AllelesAmino Acid SequenceAnimalsArgonaute ProteinsCaenorhabditis elegansCaenorhabditis elegans ProteinsCarrier ProteinsConserved SequenceGene Expression Regulation, DevelopmentalMicroRNAsMolecular Sequence DataMutationRepressor ProteinsSequence AlignmentAIN-1 protein, C elegansArgonaute ProteinsCaenorhabditis elegans ProteinsCarrier ProteinsLIN-28 protein, C elegansMicroRNAsRepressor Proteins

Identifiers

PMID24763381
PMCPMC3998888
OpenAlexW2064864543

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.