Evidence map›Paper›PMID 35947946›Full record

ArticleCell reports2022

The developmentally timed decay of an essential microRNA family is seed-sequence dependent.

Bridget F Donnelly, Bing Yang, Acadia L Grimme, Karl-Frédéric Vieux, Chen-Yu Liu, Lecong Zhou, Katherine McJunkin

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
4.2field-weighted citation impact, top 4% 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

39 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Linking miRNAs to decay.Genes & development · 2026
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  8. Genes & development · 2026
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  9. bioRxiv : the preprint server for biology · 2026
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  17. Widespread destabilization ofRNA (New York, N.Y.) · 2024
    Article
  18. Article
  19. Article
  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

7 authors at 2 institutions in 1 country.

Bridget F DonnellyLaboratory of Cellular and Developmental Biology, NIDDK Intramural Research Program, 50 South Drive, Bethesda, MD 20892, USA; Johns Hopkins University Department of Biology, 3400 N. Charles Street, Baltimore, MD 21218, USA.
Bing YangLaboratory of Cellular and Developmental Biology, NIDDK Intramural Research Program, 50 South Drive, Bethesda, MD 20892, USA.
Acadia L GrimmeLaboratory of Cellular and Developmental Biology, NIDDK Intramural Research Program, 50 South Drive, Bethesda, MD 20892, USA; Johns Hopkins University Department of Biology, 3400 N. Charles Street, Baltimore, MD 21218, USA.
Karl-Frédéric VieuxLaboratory of Cellular and Developmental Biology, NIDDK Intramural Research Program, 50 South Drive, Bethesda, MD 20892, USA.
Chen-Yu LiuLaboratory of Cellular and Developmental Biology, NIDDK Intramural Research Program, 50 South Drive, Bethesda, MD 20892, USA.
Lecong ZhouLaboratory of Cellular and Developmental Biology, NIDDK Intramural Research Program, 50 South Drive, Bethesda, MD 20892, USA.
Katherine McJunkinLaboratory of Cellular and Developmental Biology, NIDDK Intramural Research Program, 50 South Drive, Bethesda, MD 20892, USA. Electronic address: mcjunkin@nih.gov.
National Institute of Diabetes and Digestive and Kidney Diseases · USJohns Hopkins University · US

Funding

Biological functions and post-transcriptional regulation of microRNAsZIADK075147 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI MCJUNKIN, KATHERINE · 2018 to 2025
$14.4M
Engineering HCC-selective PET agentZIABC011800 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI ESCORCIA, FREDDY · 2018 to 2025
$10.6M
Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
Biological functions and post-transcriptional regulation of microRNAsZIIDK075147 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI MCJUNKIN, KATHERINE · 2017 to 2017
$1.3M
Intramural NIH HHS Z99 DK999999Intramural NIH HHS ZIA DK075147Intramural NIH HHS ZII DK075147NIH HHS P40 OD010440
6 · The paper itself

Abstract

MicroRNA (miRNA) abundance is tightly controlled by regulation of biogenesis and decay. Here, we show that the mir-35 miRNA family undergoes selective decay at the transition from embryonic to larval development in C. elegans. The seed sequence of the miRNA is necessary and largely sufficient for this regulation. Sequences outside the seed (3' end) regulate mir-35 abundance in the embryo but are not necessary for sharp decay at the transition to larval development. Enzymatic modifications of the miRNA 3' end are neither prevalent nor correlated with changes in decay, suggesting that miRNA 3' end display is not a core feature of this mechanism and further supporting a seed-driven decay model. Our findings demonstrate that seed-sequence-specific decay can selectively and coherently regulate all redundant members of a miRNA seed family, a class of mechanism that has great biological and therapeutic potential for dynamic regulation of a miRNA family's target repertoire.

Indexed as

Caenorhabditis elegans ProteinsMicroRNAsAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsMicroRNAsMIRN35 microRNA, C elegansC. elegansCP: Cell biologyCP: Developmental biologydevelopmental transitionsEBAX-1embryonic developmentmicroRNAmir-35mir-35-41mir-35 familymiRNAmiRNA decaymiRNA degradationmiRNA tailingmiRNA turnoverpost-transcriptional regulationtarget-directed miRNA degradationTDMDZSWIM8

Identifiers

PMID35947946
PMCPMC9413084
OpenAlexW4290767706

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.