Evidence map›Paper›PMID 34708458›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2021

Autophagy coordinates chondrocyte development and early joint formation in zebrafish.

Joanna J Moss, Martina Wirth, Sharon A Tooze, Jon D Lane, Chrissy L Hammond

Open access · hybridAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  5. Review
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  10. [IRE1Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2022
    Article
  11. Article
  12. Article
  13. Autophagy coordinates chondrocyte development and early joint formation in zebrafish.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    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

5 authors at 2 institutions in 1 country.

Joanna J MossSchool of Biochemistry, University of Bristol, Bristol, UK.ORCID 0000-0003-1690-6512
Martina WirthMolecular Cell Biology of Autophagy, The Francis Crick Institute, London, UK.ORCID 0000-0002-3210-8644
Sharon A ToozeMolecular Cell Biology of Autophagy, The Francis Crick Institute, London, UK.ORCID 0000-0002-2182-3116
Jon D LaneSchool of Biochemistry, University of Bristol, Bristol, UK.ORCID 0000-0002-6828-5888
Chrissy L HammondSchool of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, UK.ORCID 0000-0002-4935-6724
University of Bristol · GBThe Francis Crick Institute · GB

Funding

Cancer Research UK FC001187Cancer Research UK FC001999Francis Crick InstituteMedical Research Council FC001187Medical Research Council FC001999Versus Arthritis 21937Wellcome Trust 083474Wellcome Trust FC001187Wellcome Trust FC001999
6 · The paper itself

Abstract

Autophagy is a catabolic process responsible for the removal of waste and damaged cellular components by lysosomal degradation. It plays a key role in fundamental cell processes, including ER stress mitigation, control of cell metabolism, and cell differentiation and proliferation, all of which are essential for cartilage cell (chondrocyte) development and survival, and for the formation of cartilage. Correspondingly, autophagy dysregulation has been implicated in several skeletal disorders such as osteoarthritis and osteoporosis. To test the requirement for autophagy during skeletal development in zebrafish, we generated an atg13 CRISPR knockout zebrafish line. This line showed a complete loss of atg13 expression, and restricted autophagic activity in vivo. In the absence of autophagy, chondrocyte maturation was accelerated, with chondrocytes exhibiting signs of premature hypertrophy. Focussing on the jaw element, autophagy disruption affected joint articulation causing restricted mouth opening. This gross behavioural phenotype corresponded with a failure to thrive, and death in homozygote atg13 nulls within 17 days. Taken together, our results are consistent with autophagy contributing to the timely regulation of chondrocyte maturation and for extracellular matrix formation.

Indexed as

ChondrogenesisAnimalsAutophagyAutophagy-Related ProteinsCell DifferentiationChondrocytesJointsZebrafishAutophagy-Related ProteinsAtg13autophagychondrocytesjointszebrafish

Identifiers

PMID34708458
PMCPMC9670821
OpenAlexW3208719246

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.