Evidence map›Paper›PMID 25032706›Full record

ArticlePLoS genetics2014

LIN-42, the Caenorhabditis elegans PERIOD homolog, negatively regulates microRNA transcription.

Roberto Perales, Dana M King, Cristina Aguirre-Chen, Christopher M Hammell

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 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

32 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Article
  3. A molecular timer couples organism-wide temporal identity to developmental checkpoints.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. A developmental timer coordinates organism-wide microRNA transcription.bioRxiv : the preprint server for biology · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Temporal scaling inProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  16. Article
  17. Article
  18. Article
  19. The multifaceted roles of microRNAs in differentiation.Current opinion in cell biology · 2020
    Review
  20. Article
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

4 authors at 1 institution in 1 country.

Roberto PeralesCold Spring Harbor Laboratory, Cold Spring Harbor, New York, United States of America.
Dana M KingCold Spring Harbor Laboratory, Cold Spring Harbor, New York, United States of America.
Cristina Aguirre-ChenCold Spring Harbor Laboratory, Cold Spring Harbor, New York, United States of America.
Christopher M HammellCold Spring Harbor Laboratory, Cold Spring Harbor, New York, United States of America.
Cold Spring Harbor Laboratory · US

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
NCI NIH HHS 5P30CA045508NCI NIH HHS P30 CA045508NIH HHS P40 OD010440
6 · The paper itself

Abstract

During C. elegans development, microRNAs (miRNAs) function as molecular switches that define temporal gene expression and cell lineage patterns in a dosage-dependent manner. It is critical, therefore, that the expression of miRNAs be tightly regulated so that target mRNA expression is properly controlled. The molecular mechanisms that function to optimize or control miRNA levels during development are unknown. Here we find that mutations in lin-42, the C. elegans homolog of the circadian-related period gene, suppress multiple dosage-dependent miRNA phenotypes including those involved in developmental timing and neuronal cell fate determination. Analysis of mature miRNA levels in lin-42 mutants indicates that lin-42 functions to attenuate miRNA expression. Through the analysis of transcriptional reporters, we show that the upstream cis-acting regulatory regions of several miRNA genes are sufficient to promote highly dynamic transcription that is coupled to the molting cycles of post-embryonic development. Immunoprecipitation of LIN-42 complexes indicates that LIN-42 binds the putative cis-regulatory regions of both non-coding and protein-coding genes and likely plays a role in regulating their transcription. Consistent with this hypothesis, analysis of miRNA transcriptional reporters in lin-42 mutants indicates that lin-42 regulates miRNA transcription. Surprisingly, strong loss-of-function mutations in lin-42 do not abolish the oscillatory expression patterns of lin-4 and let-7 transcription but lead to increased expression of these genes. We propose that lin-42 functions to negatively regulate the transcriptional output of multiple miRNAs and mRNAs and therefore coordinates the expression levels of genes that dictate temporal cell fate with other regulatory programs that promote rhythmic gene expression.

Indexed as

Transcription, GeneticAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell DifferentiationCell LineageGene Expression Regulation, DevelopmentalMicroRNAsMutationRNA, MessengerTranscription FactorsCaenorhabditis elegans ProteinsLIN-42 protein, C elegansMicroRNAsRNA, MessengerTranscription Factors

Identifiers

PMID25032706
PMCPMC4102445
OpenAlexW2130079085

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.