Evidence map›Paper›PMID 34128978›Full record

ArticleDevelopment (Cambridge, England)2021

The molecular complex of ciliary and golgin protein is crucial for skull development.

Hiroyuki Yamaguchi, Matthew D Meyer, Li He, Lakmini Senavirathna, Sheng Pan, Yoshihiro Komatsu

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
  5. Review
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  8. Review
  9. Article
  10. Disruption of Trip11 in cranial neural crest cells is associated with increased ER and Golgi stress contributing to skull defects in mice.Developmental dynamics : an official publication of the American Association of Anatomists · 2022
    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

6 authors at 4 institutions in 1 country.

Hiroyuki YamaguchiDepartment of Pediatrics, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Matthew D MeyerShared Equipment Authority, Rice University, Houston, TX 77005, USA.
Li HeDepartment of Pediatrics, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Lakmini SenavirathnaThe Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Sheng PanThe Brown Foundation Institute of Molecular Medicine, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Yoshihiro KomatsuDepartment of Pediatrics, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.ORCID 0000-0003-3115-1437
Brown Foundation · USThe University of Texas Health Science Center at Houston · USRice University · USThe University of Texas MD Anderson Cancer Center · US

Funding

The role of BMP signaling in craniofacial cartilage developmentR01DE025897 · NIDCR · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI KOMATSU, YOSHIHIRO · 2017 to 2021
$1.8M
NIDCR NIH HHS R01 DE025897Uehara Memorial FoundationUniversity of Texas Health Science Center at Houston
6 · The paper itself

Abstract

Intramembranous ossification, which consists of direct conversion of mesenchymal cells to osteoblasts, is a characteristic process in skull development. One crucial role of these osteoblasts is to secrete collagen-containing bone matrix. However, it remains unclear how the dynamics of collagen trafficking is regulated during skull development. Here, we reveal the regulatory mechanisms of ciliary and golgin proteins required for intramembranous ossification. During normal skull formation, osteoblasts residing on the osteogenic front actively secreted collagen. Mass spectrometry and proteomic analysis determined endogenous binding between ciliary protein IFT20 and golgin protein GMAP210 in these osteoblasts. As seen in Ift20 mutant mice, disruption of neural crest-specific GMAP210 in mice caused osteopenia-like phenotypes due to dysfunctional collagen trafficking. Mice lacking both IFT20 and GMAP210 displayed more severe skull defects compared with either IFT20 or GMAP210 mutants. These results demonstrate that the molecular complex of IFT20 and GMAP210 is essential for the intramembranous ossification during skull development.

Indexed as

AnimalsCalcification, PhysiologicCarrier ProteinsCell DifferentiationCell ProliferationCollagenCytoskeletal ProteinsGolgi ApparatusGolgi Matrix ProteinsMiceMice, KnockoutNeural CrestOsteoblastsOsteogenesisProteomicsSkullCarrier ProteinsCollagenCytoskeletal ProteinsGolgi Matrix ProteinsIft20 protein, mouseTRIP11 protein, mouseCollagenCranial neural crest cellsGolgi microtubule associated protein 210Intraflagellar transport 20MouseSkull

Identifiers

PMID34128978
PMCPMC8276989
OpenAlexW3172418207

What OpenQuestion holds

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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.