ArticleCellular and molecular life sciences : CMLS2021
Noncanonical ER-Golgi trafficking and autophagy of endogenous procollagen in osteoblasts.
Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 24 citations in OpenAlex.
- Inhibition of EED enhances osteogenic differentiation and bone formation: a potential therapeutic strategy for osteogenesis imperfecta.JBMR plus · 2026Article
- Site-specific glycosylation of Sec24D and myoferlin recruit ERGIC to ER exit sites for collagen trafficking.Nature communications · 2026Article
- LC3 and GABARAP independent autophagy of misfolded procollagen in mouse osteoblasts.Autophagy · 2025Article
- Collagen IV biosynthesis: Intracellular choreography of post-translational modifications.Matrix biology : journal of the International Society for Matrix Biology · 2025Review
- Collagen Biosynthesis and Its Molecular Ensemble: What Remains Unexplored.Biochemistry · 2025Review
- The ACBD3 protein coordinates ER-Golgi contacts to enable productive TBEV infection.Journal of virology · 2025Article
- Collagen fibril formation at the plasma membrane occurs independently from collagen secretion.Wellcome open research · 2025Article
- The p24-family and COPII subunit SEC24C facilitate the clearance of alpha1-antitrypsin Z from the endoplasmic reticulum to lysosomes.Molecular biology of the cell · 2024Article
- Mechanisms of autophagy and their implications in dermatological disorders.Frontiers in immunology · 2024Review
- COPI Vesicle Disruption Inhibits Mineralization via mTORC1-Mediated Autophagy.International journal of molecular sciences · 2023Article
- Sorting and Export of Proteins at the Endoplasmic Reticulum.Cold Spring Harbor perspectives in biology · 2023Review
- The emerging mechanisms and functions of microautophagy.Nature reviews. Molecular cell biology · 2023Review
- KLHL12 can form large COPII structures in the absence of CUL3 neddylation.Molecular biology of the cell · 2023Article
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- Bone Formation in 2D Culture of Primary Cells.JBMR plus · 2023Article
- ER, Mitochondria, and ISR Regulation by mt-HSP70 and ATF5 upon Procollagen Misfolding in Osteoblasts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- ER-phagy: mechanisms, regulation, and diseases connected to the lysosomal clearance of the endoplasmic reticulum.Physiological reviews · 2022Review
- 4PBA reduces growth deficiency in osteogenesis imperfecta by enhancing transition of hypertrophic chondrocytes to osteoblasts.JCI insight · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Secretion and quality control of large extracellular matrix proteins remain poorly understood and debated, particularly transport intermediates delivering folded proteins from the ER to Golgi and misfolded ones to lysosomes. Discrepancies between different studies are related to utilization of exogenous cargo, off-target effects of experimental conditions and cell manipulation, and identification of transport intermediates without tracing their origin and destination. To address these issues, here we imaged secretory and degradative trafficking of type I procollagen in live MC3T3 osteoblasts by replacing a region encoding N-propeptide in endogenous Col1a2 gDNA with GFP cDNA. We selected clones that produced the resulting fluorescent procollagen yet had normal expression of key osteoblast and ER/cell stress genes, normal procollagen folding, and normal deposition and mineralization of extracellular matrix. Live-cell imaging of these clones revealed ARF1-dependent transport intermediates, which had no COPII coat and delivered procollagen from ER exit sites (ERESs) to Golgi without stopping at ER-Golgi intermediate compartment (ERGIC). It also confirmed ERES microautophagy, i.e., lysosomes engulfing ERESs containing misfolded procollagen. Beyond validating these trafficking models for endogenous procollagen, we uncovered a probable cause of noncanonical cell stress response to procollagen misfolding. Recognized and retained only at ERESs, misfolded procollagen does not directly activate the canonical UPR, yet it disrupts the ER lumen by blocking normal secretory export from the ER.
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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.