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题名: G beta 1 is required for neutrophil migration in zebrafish
作者: Ke, Wenfan1; Ye, Ding1, 3; Mersch, Kacey1; Xu, Hui1, 4; Chen, Songhai2; Lin, Fang1, 5
关键词: Cell migration ; Neutrophil ; G protein ; G beta 1 ; Imaging
刊名: DEVELOPMENTAL BIOLOGY
发表日期: 2017-08-01
DOI: 10.1016/j.ydbio.2017.05.024
卷: 428, 期:1, 页:135-147
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology ; Life Sciences & Biomedicine
类目[WOS]: Developmental Biology
研究领域[WOS]: Developmental Biology
英文摘要: Signaling mediated by G protein-coupled receptors (GPCRs) is essential for the migration of cells toward chemoattractants. The recruitment of neutrophils to injured tissues in zebrafish larvae is a useful model for studying neutrophil migration and trafficking in vivo. Indeed, the study of this process led to the discovery that PI3Ky is required for the polarity and motility of neutrophils, features that are necessary for the directed migration of these cells to wounds. However, the mechanism by which PI3Ky is activated remains to be determined. Here we show that signaling by specifically the heterotrimeric G protein subunit G beta 1 is critical for neutrophil migration in response to wounding. In embryos treated with small-molecule inhibitors of G beta y signaling, neutrophils failed to migrate to wound sites. Although both the G beta 1 and G beta 4 isoforms are expressed in migrating neutrophils, only deficiency for the former (morpholino-based knockdown) interfered with the directed migration of neutrophils towards wounds. The G beta 1 deficiency also impaired the ability of cells to change cell shape and reduced their general motility, defects that are similar to those in neutrophils deficient for PI3Ky. Transplantation assays showed that the requirement for G beta 1 in neutrophil migration is cell autonomous. Finally, live imaging revealed that G beta 1 is required for polarized activation of PI3K, and for the actin dynamics that enable neutrophil migration. Collectively, our data indicate that Gill signaling controls proper neutrophil migration by activating PI3K and modulating actin dynamics. Moreover, they illustrate a role for a specific G beta isoform in chemotaxis in vivo.
关键词[WOS]: BETA-GAMMA-SUBUNITS ; SIGNALING CONTROLS ; CELL-MIGRATION ; TRANSGENIC ZEBRAFISH ; BACTERIAL-INFECTION ; ACTIN CYTOSKELETON ; LATERAL-LINE ; GASTRULATION ; CHEMOTAXIS ; RECEPTOR
语种: 英语
项目资助者: NIH/NCRR(K99R00RR024119) ; National Science Foundation(IOS-1354457) ; NIH(R01GM094255) ; (AHA10GRNT3620015)
WOS记录号: WOS:000406255300010
ISSN号: 0012-1606
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内容类型: 期刊论文
URI标识: http://ir.ihb.ac.cn/handle/342005/29335
Appears in Collections:鱼类生物学及渔业生物技术研究中心_期刊论文

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作者单位: 1.Univ Iowa, Carver Coll Med, Dept Anat & Cell Biol, Iowa City, IA 52242 USA
2.Univ Iowa, Dept Pharmacol, Carver Coll Med, Iowa City, IA 52242 USA
3.Chinese Acad Sci, Inst Hydrobiol, State Key Lab Freshwater Ecol & Biotechnol, Wuhan 430072, Hubei, Peoples R China
4.Nantong Univ, Jiangsu Key Lab Neural Regenerat, Med Sch, Nantong 226001, Jiangsu, Peoples R China
5.Univ Virginia, Dept Biol, Charlottesville, VA 22903 USA
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