Internalization of the TGF-β type I receptor into caveolin-1 and EEA1 double-positive early endosomes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2015-06

AUTHORS

Kangmin He, Xiaohua Yan, Nan Li, Song Dang, Li Xu, Bing Zhao, Zijian Li, Zhizhen Lv, Xiaohong Fang, Youyi Zhang, Ye-Guang Chen

ABSTRACT

Endocytosis and intracellular sorting of transforming growth factor-β (TGF-β) receptors play an important regulatory role in TGF-β signaling. Two major endocytic pathways, clathrin- and caveolae-mediated endocytosis, have been reported to independently mediate the internalization of TGF-β receptors. In this study, we demonstrate that the clathrin- and caveolae-mediated endocytic pathways can converge during TGF-β receptor endocytic trafficking. By tracking the intracellular dynamics of fluorescently-labeled TGF-β type I receptor (TβRI), we found that after mediating TβRI internalization, certain clathrin-coated vesicles and caveolar vesicles are fused underneath the plasma membrane, forming a novel type of caveolin-1 and clathrin double-positive vesicles. Under the regulation of Rab5, the fused vesicles are targeted to early endosomes and thus deliver the internalized TβRI to the caveolin-1 and EEA1 double-positive early endosomes (caveolin-1-positive early endosomes). We further showed that the caveolin-1-positive early endosomes are positive for Smad3/SARA, Rab11 and Smad7/Smurf2, and may act as a multifunctional device for TGF-β signaling and TGF-β receptor recycling and degradation. Therefore, these findings uncover a novel scenario of endocytosis, the direct fusion of clathrin-coated and caveolae vesicles during TGF-β receptor endocytic trafficking, which leads to the formation of the multifunctional sorting device, caveolin-1-positive early endosomes, for TGF-β receptors. More... »

PAGES

738

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/cr.2015.60

DOI

http://dx.doi.org/10.1038/cr.2015.60

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1010266487

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25998683


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