Evidence map›Paper›PMID 20700435›Full record

ArticlePLoS genetics2010

A developmental timing switch promotes axon outgrowth independent of known guidance receptors.

Katherine Olsson-Carter, Frank J Slack

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

38 citing papers in PubMed, 58 citations in OpenAlex.

  1. 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
  2. A developmental timer coordinates organism-wide microRNA transcription.bioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Review
  5. Two intrinsic timing mechanisms set start and end times for dendritic arborization of a nociceptive neuron.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. The multifaceted roles of microRNAs in differentiation.Current opinion in cell biology · 2020
    Review
  10. The MakorineLife · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Timing of neuronal plasticity in development and aging.Wiley interdisciplinary reviews. Developmental biology · 2018
    Review
  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

2 authors at 1 institution in 1 country.

Katherine Olsson-CarterDepartment of Molecular, Cellular, and Developmental Biology, Yale University, New Haven, Connecticut, USA.
Frank J Slack
Yale University · US

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM007499 · NIGMS · YALE UNIVERSITY · PI CARLSON, JOHN R, REINKE, VALERIE J · 1985 to 2022
$13.9M
Heterochronic control of development and lifespanR01GM064701 · NIGMS · YALE UNIVERSITY · PI SLACK, FRANK J. · 2002 to 2010
$2.0M
Genetic control of timing of neuronal differentiationF31NS050981 · NINDS · YALE UNIVERSITY · PI CARTER, KATHERINE O · 2004 to 2005
$58k
NIGMS NIH HHS GM 064701NIGMS NIH HHS R01 GM064701NIGMS NIH HHS T32 GM007499NIGMS NIH HHS T32 GM07499NINDS NIH HHS F31 NS050981NINDS NIH HHS F31 NS050981-01
6 · The paper itself

Abstract

To form functional neuronal connections, axon outgrowth and guidance must be tightly regulated across space as well as time. While a number of genes and pathways have been shown to control spatial features of axon development, very little is known about the in vivo mechanisms that direct the timing of axon initiation and elongation. The Caenorhabditis elegans hermaphrodite specific motor neurons (HSNs) extend a single axon ventrally and then anteriorly during the L4 larval stage. Here we show the lin-4 microRNA promotes HSN axon initiation after cell cycle withdrawal. Axons fail to form in lin-4 mutants, while they grow prematurely in lin-4-overexpressing animals. lin-4 is required to down-regulate two inhibitors of HSN differentiation--the transcriptional regulator LIN-14 and the "stemness" factor LIN-28--and it likely does so through a cell-autonomous mechanism. This developmental switch depends neither on the UNC-40/DCC and SAX-3/Robo receptors nor on the direction of axon growth, demonstrating that it acts independently of ventral guidance signals to control the timing of HSN axon elongation.

Indexed as

Cell DifferentiationAnimalsAxonsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell Adhesion MoleculesGene Expression RegulationMicroRNAsMotor NeuronsNerve Tissue ProteinsNuclear ProteinsReceptors, ImmunologicRepressor ProteinsRoundabout ProteinsCaenorhabditis elegans ProteinsCell Adhesion MoleculesLIN-14 protein, C elegansLIN-28 protein, C eleganslin-4 microRNA, C elegansMicroRNAsNerve Tissue ProteinsNuclear ProteinsReceptors, ImmunologicRepressor ProteinsRoundabout ProteinsUNC-40 protein, C elegans

Identifiers

PMID20700435
PMCPMC2916846
OpenAlexW1966075007

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.