CD36 facilitates fatty acid uptake by dynamic palmitoylation-regulated endocytosis
Fatty acids (FAs) are essential nutrients, but how they are transported into cells remains unclear. Here, we show that FAs trigger caveolae-dependent CD36 internalization, which in turn delivers FAs into adipocytes. During the process, binding of FAs to CD36 activates its downstream kinase LYN, whic...
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| Published in | Nature communications Vol. 11; no. 1; pp. 4765 - 16 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
21.09.2020
Nature Portfolio |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Fatty acids (FAs) are essential nutrients, but how they are transported into cells remains unclear. Here, we show that FAs trigger caveolae-dependent CD36 internalization, which in turn delivers FAs into adipocytes. During the process, binding of FAs to CD36 activates its downstream kinase LYN, which phosphorylates DHHC5, the palmitoyl acyltransferase of CD36, at Tyr91 and inactivates it. CD36 then gets depalmitoylated by APT1 and recruits another tyrosine kinase SYK to phosphorylate JNK and VAVs to initiate endocytic uptake of FAs. Blocking CD36 internalization by inhibiting APT1, LYN or SYK abolishes CD36-dependent FA uptake. Restricting CD36 at either palmitoylated or depalmitoylated state eliminates its FA uptake activity, indicating an essential role of dynamic palmitoylation of CD36. Furthermore, blocking endocytosis by targeting LYN or SYK inhibits CD36-dependent lipid droplet growth in adipocytes and high-fat-diet induced weight gain in mice. Our study has uncovered a dynamic palmitoylation-regulated endocytic pathway to take up FAs.
The mechanistic details of fatty acid uptake into cells remains poorly understood. Here, the authors identify CD36 internalization via cavaeolae and demonstrate dynamic palmitoylationof CD36 is required for endocytic uptake of fatty acids. |
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| AbstractList | The mechanistic details of fatty acid uptake into cells remains poorly understood. Here, the authors identify CD36 internalization via cavaeolae and demonstrate dynamic palmitoylationof CD36 is required for endocytic uptake of fatty acids. Fatty acids (FAs) are essential nutrients, but how they are transported into cells remains unclear. Here, we show that FAs trigger caveolae-dependent CD36 internalization, which in turn delivers FAs into adipocytes. During the process, binding of FAs to CD36 activates its downstream kinase LYN, which phosphorylates DHHC5, the palmitoyl acyltransferase of CD36, at Tyr91 and inactivates it. CD36 then gets depalmitoylated by APT1 and recruits another tyrosine kinase SYK to phosphorylate JNK and VAVs to initiate endocytic uptake of FAs. Blocking CD36 internalization by inhibiting APT1, LYN or SYK abolishes CD36-dependent FA uptake. Restricting CD36 at either palmitoylated or depalmitoylated state eliminates its FA uptake activity, indicating an essential role of dynamic palmitoylation of CD36. Furthermore, blocking endocytosis by targeting LYN or SYK inhibits CD36-dependent lipid droplet growth in adipocytes and high-fat-diet induced weight gain in mice. Our study has uncovered a dynamic palmitoylation-regulated endocytic pathway to take up FAs. The mechanistic details of fatty acid uptake into cells remains poorly understood. Here, the authors identify CD36 internalization via cavaeolae and demonstrate dynamic palmitoylationof CD36 is required for endocytic uptake of fatty acids. Fatty acids (FAs) are essential nutrients, but how they are transported into cells remains unclear. Here, we show that FAs trigger caveolae-dependent CD36 internalization, which in turn delivers FAs into adipocytes. During the process, binding of FAs to CD36 activates its downstream kinase LYN, which phosphorylates DHHC5, the palmitoyl acyltransferase of CD36, at Tyr91 and inactivates it. CD36 then gets depalmitoylated by APT1 and recruits another tyrosine kinase SYK to phosphorylate JNK and VAVs to initiate endocytic uptake of FAs. Blocking CD36 internalization by inhibiting APT1, LYN or SYK abolishes CD36-dependent FA uptake. Restricting CD36 at either palmitoylated or depalmitoylated state eliminates its FA uptake activity, indicating an essential role of dynamic palmitoylation of CD36. Furthermore, blocking endocytosis by targeting LYN or SYK inhibits CD36-dependent lipid droplet growth in adipocytes and high-fat-diet induced weight gain in mice. Our study has uncovered a dynamic palmitoylation-regulated endocytic pathway to take up FAs.Fatty acids (FAs) are essential nutrients, but how they are transported into cells remains unclear. Here, we show that FAs trigger caveolae-dependent CD36 internalization, which in turn delivers FAs into adipocytes. During the process, binding of FAs to CD36 activates its downstream kinase LYN, which phosphorylates DHHC5, the palmitoyl acyltransferase of CD36, at Tyr91 and inactivates it. CD36 then gets depalmitoylated by APT1 and recruits another tyrosine kinase SYK to phosphorylate JNK and VAVs to initiate endocytic uptake of FAs. Blocking CD36 internalization by inhibiting APT1, LYN or SYK abolishes CD36-dependent FA uptake. Restricting CD36 at either palmitoylated or depalmitoylated state eliminates its FA uptake activity, indicating an essential role of dynamic palmitoylation of CD36. Furthermore, blocking endocytosis by targeting LYN or SYK inhibits CD36-dependent lipid droplet growth in adipocytes and high-fat-diet induced weight gain in mice. Our study has uncovered a dynamic palmitoylation-regulated endocytic pathway to take up FAs. Fatty acids (FAs) are essential nutrients, but how they are transported into cells remains unclear. Here, we show that FAs trigger caveolae-dependent CD36 internalization, which in turn delivers FAs into adipocytes. During the process, binding of FAs to CD36 activates its downstream kinase LYN, which phosphorylates DHHC5, the palmitoyl acyltransferase of CD36, at Tyr91 and inactivates it. CD36 then gets depalmitoylated by APT1 and recruits another tyrosine kinase SYK to phosphorylate JNK and VAVs to initiate endocytic uptake of FAs. Blocking CD36 internalization by inhibiting APT1, LYN or SYK abolishes CD36-dependent FA uptake. Restricting CD36 at either palmitoylated or depalmitoylated state eliminates its FA uptake activity, indicating an essential role of dynamic palmitoylation of CD36. Furthermore, blocking endocytosis by targeting LYN or SYK inhibits CD36-dependent lipid droplet growth in adipocytes and high-fat-diet induced weight gain in mice. Our study has uncovered a dynamic palmitoylation-regulated endocytic pathway to take up FAs. |
| ArticleNumber | 4765 |
| Author | Zhao, Tong-Jin Wang, Xu Zhao, Ning Chen, Shuai Huang, Xi Hao, Jian-Wei Liang, Bin Lai, Xiao-Ying Li, Cheng-Bin Wang, Juan Guo, Huiling Sun, Hui-Hui Li, Yi-Fan Xie, Changchuan Hong, Lixin Zhao, Yin-Yue Wang, Hong-Rui |
| Author_xml | – sequence: 1 givenname: Jian-Wei surname: Hao fullname: Hao, Jian-Wei organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University – sequence: 2 givenname: Juan surname: Wang fullname: Wang, Juan organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Institute of Metabolism and Integrative Biology, Fudan University – sequence: 3 givenname: Huiling surname: Guo fullname: Guo, Huiling organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University – sequence: 4 givenname: Yin-Yue surname: Zhao fullname: Zhao, Yin-Yue organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University – sequence: 5 givenname: Hui-Hui surname: Sun fullname: Sun, Hui-Hui organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University – sequence: 6 givenname: Yi-Fan surname: Li fullname: Li, Yi-Fan organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University – sequence: 7 givenname: Xiao-Ying surname: Lai fullname: Lai, Xiao-Ying organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University – sequence: 8 givenname: Ning surname: Zhao fullname: Zhao, Ning organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University – sequence: 9 givenname: Xu surname: Wang fullname: Wang, Xu organization: Institute of Metabolism and Integrative Biology, Fudan University – sequence: 10 givenname: Changchuan surname: Xie fullname: Xie, Changchuan organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University – sequence: 11 givenname: Lixin surname: Hong fullname: Hong, Lixin organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University – sequence: 12 givenname: Xi surname: Huang fullname: Huang, Xi organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University – sequence: 13 givenname: Hong-Rui orcidid: 0000-0002-2916-8849 surname: Wang fullname: Wang, Hong-Rui organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, State-Province Joint Engineering Laboratory of Targeted Drugs from Natural Products, Xiamen University – sequence: 14 givenname: Cheng-Bin surname: Li fullname: Li, Cheng-Bin organization: Center for Life Sciences, School of Life Sciences, Yunnan University – sequence: 15 givenname: Bin surname: Liang fullname: Liang, Bin organization: Center for Life Sciences, School of Life Sciences, Yunnan University – sequence: 16 givenname: Shuai surname: Chen fullname: Chen, Shuai email: chenshuai@nju.edu.cn organization: State Key Laboratory of Pharmaceutical Biotechnology, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University – sequence: 17 givenname: Tong-Jin orcidid: 0000-0001-6861-3071 surname: Zhao fullname: Zhao, Tong-Jin email: zhaotj@fudan.edu.cn organization: State Key Laboratory of Cellular Stress Biology, School of Life Sciences, Xiamen University, Institute of Metabolism and Integrative Biology, Fudan University, State-Province Joint Engineering Laboratory of Targeted Drugs from Natural Products, Xiamen University |
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| Snippet | Fatty acids (FAs) are essential nutrients, but how they are transported into cells remains unclear. Here, we show that FAs trigger caveolae-dependent CD36... The mechanistic details of fatty acid uptake into cells remains poorly understood. Here, the authors identify CD36 internalization via cavaeolae and... |
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| Title | CD36 facilitates fatty acid uptake by dynamic palmitoylation-regulated endocytosis |
| URI | https://link.springer.com/article/10.1038/s41467-020-18565-8 https://www.proquest.com/docview/2444881769 https://pubmed.ncbi.nlm.nih.gov/PMC7505845 https://doaj.org/article/475bc3befce0421399240b3b2a58b6c8 |
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