Evidence map›Paper›PMID 25167051›Full record

ArticlePLoS genetics2014

The TRIM-NHL protein LIN-41 controls the onset of developmental plasticity in Caenorhabditis elegans.

Cristina Tocchini, Jeremy J Keusch, Sarah B Miller, Susanne Finger, Heinz Gut, Michael B Stadler, Rafal Ciosk

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 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

49 citing papers in PubMed, 73 citations in OpenAlex.

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  11. Multiple Roles of TRIM21 in Virus Infection.International journal of molecular sciences · 2023
    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

7 authors at 2 institutions in 1 country.

Cristina TocchiniFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland; University of Basel, Basel, Switzerland.
Jeremy J KeuschFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Sarah B MillerFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Susanne FingerFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland; University of Basel, Basel, Switzerland.
Heinz GutFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Michael B StadlerFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland; Swiss Institute of Bioinformatics, Basel, Switzerland.
Rafal CioskFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Friedrich Miescher Institute · CHUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mechanisms controlling cell fate determination and reprogramming are fundamental for development. A profound reprogramming, allowing the production of pluripotent cells in early embryos, takes place during the oocyte-to-embryo transition. To understand how the oocyte reprogramming potential is controlled, we sought Caenorhabditis elegans mutants in which embryonic transcription is initiated precociously in germ cells. This screen identified LIN-41, a TRIM-NHL protein and a component of the somatic heterochronic pathway, as a temporal regulator of pluripotency in the germline. We found that LIN-41 is expressed in the cytoplasm of developing oocytes, which, in lin-41 mutants, acquire pluripotent characteristics of embryonic cells and form teratomas. To understand LIN-41 function in the germline, we conducted structure-function studies. In contrast to other TRIM-NHL proteins, we found that LIN-41 is unlikely to function as an E3 ubiquitin ligase. Similar to other TRIM-NHL proteins, the somatic function of LIN-41 is thought to involve mRNA regulation. Surprisingly, we found that mutations predicted to disrupt the association of LIN-41 with mRNA, which otherwise compromise LIN-41 function in the heterochronic pathway in the soma, have only minor effects in the germline. Similarly, LIN-41-mediated repression of a key somatic mRNA target is dispensable for the germline function. Thus, LIN-41 appears to function in the germline and the soma via different molecular mechanisms. These studies provide the first insight into the mechanism inhibiting the onset of embryonic differentiation in developing oocytes, which is required to ensure a successful transition between generations.

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell DifferentiationCellular ReprogrammingEmbryonic DevelopmentEmbryo, NonmammalianGene Expression Regulation, DevelopmentalGerm CellsMutationOocytesRNA, MessengerTranscription FactorsUbiquitin-Protein LigasesCaenorhabditis elegans ProteinsLIN-41 protein, C elegansRNA, MessengerTranscription FactorsUbiquitin-Protein Ligases

Identifiers

PMID25167051
PMCPMC4148191
OpenAlexW1988179224

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.