ArticlePloS one2010
Sec24D-dependent transport of extracellular matrix proteins is required for zebrafish skeletal morphogenesis.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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Who cites it
91 citing papers in PubMed, 143 citations in OpenAlex.
- Site-specific glycosylation of Sec24D and myoferlin recruit ERGIC to ER exit sites for collagen trafficking.Nature communications · 2026Article
- Elucidating the impact of a synonymous SEC24D variant on aberrant splicing in a patient with cole-carpenter syndrome 2.Journal of human genetics · 2026Article
- Succinate supplementation ameliorates musculoskeletal defects caused by PLOD3 mutations in a BCARD syndrome model.Genome medicine · 2026Article
- Towards a unified framework for the function of endoplasmic reticulum exit sites.Nature reviews. Molecular cell biology · 2025Review
- Review
- SEC24D depletion induces osteogenic differentiation deficiency by inactivating the ATF6/TGF-β/Runx2 regulatory loop.Communications biology · 2025Article
- SEC24C deficiency causes trafficking and glycosylation abnormalities in an epileptic encephalopathy with cataracts and dyserythropoeisis.JCI insight · 2025Article
- [Research progress on collagen secretion mechanisms in scarring].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025Review
- Review
- Article
- Self-Assembled Nanoparticles with Well-Defined Oligosaccharide Promote Osteogenesis by Regulating Golgi Stress Response.Advanced healthcare materials · 2025Article
- Zebrafish Models for Skeletal and Extraskeletal Osteogenesis Imperfecta Features: Unveiling Pathophysiology and Paving the Way for Drug Discovery.Calcified tissue international · 2024Review
- Detection of selective sweep in European wild sheep breeds.3 Biotech · 2024Article
- Transforming growth factor beta signaling and craniofacial development: modeling human diseases in zebrafish.Frontiers in cell and developmental biology · 2024Review
- Conventional and Unconventional Protein Secretion in Yeast and Animal Cells.Methods in molecular biology (Clifton, N.J.) · 2024Review
- Rare variant modifier analysis identifies variants in SEC24D associated with orofacial cleft subtypes.Human genetics · 2023Article
- Article
- Rare genetic variants inmedRxiv : the preprint server for health sciences · 2023Article
- KLHL12 can form large COPII structures in the absence of CUL3 neddylation.Molecular biology of the cell · 2023Article
- AP-4 loss in CRISPR-edited zebrafish affects early embryo development.Advances in biological regulation · 2023Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Protein transport from endoplasmic reticulum (ER) to Golgi is primarily conducted by coated vesicular carriers such as COPII. Here, we describe zebrafish bulldog mutations that disrupt the function of the cargo adaptor Sec24D, an integral component of the COPII complex. We show that Sec24D is essential for secretion of cartilage matrix proteins, whereas the preceding development of craniofacial primordia and pre-chondrogenic condensations does not depend on this isoform. Bulldog chondrocytes fail to secrete type II collagen and matrilin to extracellular matrix (ECM), but membrane bound receptor beta1-Integrin and Cadherins appear to leave ER in Sec24D-independent fashion. Consequently, Sec24D-deficient cells accumulate proteins in the distended ER, although a subset of ER compartments and Golgi complexes as visualized by electron microscopy and NBD C(6)-ceramide staining appear functional. Consistent with the backlog of proteins in the ER, chondrocytes activate the ER stress response machinery and significantly upregulate BiP transcription. Failure of ECM secretion hinders chondroblast intercalations thus resulting in small and malformed cartilages and severe craniofacial dysmorphology. This defect is specific to Sec24D mutants since knockdown of Sec24C, a close paralog of Sec24D, does not result in craniofacial cartilage dysmorphology. However, craniofacial development in double Sec24C/Sec24D-deficient animals is arrested earlier than in bulldog/sec24d, suggesting that Sec24C can compensate for loss of Sec24D at initial stages of chondrogenesis, but Sec24D is indispensable for chondrocyte maturation. Our study presents the first developmental perspective on Sec24D function and establishes Sec24D as a strong candidate for cartilage maintenance diseases and craniofacial birth defects.
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Registered trials
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.