PTRN‐1/CAMSAP promotes CYK‐1/formin‐dependent actin polymerization during endocytic recycling |
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Authors: | Jing Zhang Shuai Liu Hang Liu Jinghu Gao Xin Zhou Juan Chen Anbing Shi |
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Affiliation: | 1. Department of Biochemistry and Molecular Biology, School of Basic Medicine and the Collaborative Innovation Center for Brain Science, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China;2. Institute for Brain Research, Huazhong University of Science and Technology, Wuhan, Hubei, China;3. Key Laboratory of Neurological Disease of National Education Ministry, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China |
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Abstract: | Cargo sorting and membrane carrier initiation in recycling endosomes require appropriately coordinated actin dynamics. However, the mechanism underlying the regulation of actin organization during recycling transport remains elusive. Here we report that the loss of PTRN‐1/CAMSAP stalled actin exchange and diminished the cytosolic actin structures. Furthermore, we found that PTRN‐1 is required for the recycling of clathrin‐independent cargo hTAC‐GFP. The N‐terminal calponin homology (CH) domain and central coiled‐coils (CC) region of PTRN‐1 can synergistically sustain the flow of hTAC‐GFP. We identified CYK‐1/formin as a binding partner of PTRN‐1. The N‐terminal GTPase‐binding domain (GBD) of CYK‐1 serves as the binding interface for the PTRN‐1 CH domain. The presence of the PTRN‐1 CH domain promoted CYK‐1‐mediated actin polymerization, which suggests that the PTRN‐1‐CH:CYK‐1‐GBD interaction efficiently relieves autoinhibitory interactions within CYK‐1. As expected, the overexpression of the CYK‐1 formin homology domain 2 (FH2) substantially restored actin structures and partially suppressed the hTAC‐GFP overaccumulation phenotype in ptrn‐1 mutants. We conclude that the PTRN‐1 CH domain is required to stimulate CYK‐1 to facilitate actin dynamics during endocytic recycling. |
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Keywords: | actin
Caenorhabditis elegans
CYK‐1/formin endocytic recycling PTRN‐1/CAMSAPs |
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