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TCP11L2 promotes bovine skeletal muscle‐derived satellite cell migration and differentiation via FMNL2
Author(s) -
Li Shuang,
Wang Zhiqi,
Tong Huili,
Li Shufeng,
Yan Yunqin
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29617
Subject(s) - microbiology and biotechnology , immunofluorescence , immunoprecipitation , actin , formins , cell migration , cellular differentiation , in vitro , biology , cell , chemistry , cell culture , cytoskeleton , actin cytoskeleton , immunology , gene , antibody , biochemistry , genetics
T‐complex 11 like 2 (TCP11L2) is a protein containing a serine‐rich region in its N‐terminal region. However, the function of TCP11L2 is unclear. Here, we showed that TCP11L2 expression gradually increased during muscle‐derived satellite cell (MDSC) differentiation in vitro, reaching a peak on Day 3, which is the migration and fusion stage of MDSCs. Using CRISPR/dCas9 gene‐editing technology to elevate or repress the expression of TCP11L2, we also showed that TCP11L2 promoted MDSC differentiation. Moreover, wound‐healing assays showed that TCP11L2 promoted the migration of MDSCs during differentiation. Additionally, immunofluorescence analyses showed that TCP11L2 was mainly distributed around the microfilament and microtubules. Furthermore, the expression of TCP11L2 affected the expression of actin‐related protein 2/3 (ARP2/3) complex. Co‐immunoprecipitation assays and immunofluorescence analysis showed that TCP11L2 interacted with formin‐like 2 (FMNL2). This protein promoted migration of bovine MDSCs by affecting the expression of ARP2/3. Finally, the activities of TCP11L2 during MDSC differentiation and migration were blocked when FMNL2 was inhibited. Taken together, our data established that TCP11L2 interacted with FMNL2 to promote MDSC migration and differentiation.