The actomyosin network is influenced by NMHC IIA and regulated by CrpF46, which is involved in controlling cell migration
- Beijing Key Laboratory of Gene Resource and Molecular Development, College of Life Sciences, Beijing Normal University, Beijing 100875, PR (China)
- School of Pharmacology and Biology, University of South China, Hunan Province Cooperative innovation Center for Molecular Target New Drug Study, Hengyang 421001, PR (China)
- The Institute of Medical Biotechnology (IMB) of the Chinese Academy of Medical Sciences, Beijing 100050, PR (China)
- AbMax Biotechnology Co., Beijing 101111, PR (China)
Highlights: • Crp{sup F46} knockdown in cells hindered cell migration. • Crp{sup F46} knockdown disturbed MT arrangement and centrosomal reorientation. • Crp{sup F46} knockdown induced weak stress fiber formation. • Crp{sup F46} interacted with NMHC IIA with its three coiled-coil domains. • Myosin filaments are regulated by Crp{sup F46} associated with phosphorylation of myosin. When a cell migrates, the centrosome positions between the nucleus and the leading edge of migration via the microtubule system. The protein Crp{sup F46} (centrosome-related protein F46) has a known role during mitosis and centrosome duplication. However, how Crp{sup F46} efficiently regulates centrosome-related cell migration is unclear. Here, we report that knockdown of Crp{sup F46} resulted in the disruption of microtubule arrangement, with impaired centrosomal reorientation, and slowed down cell migration. In cells that express low levels of Crp{sup F46}, stress fibers were weakened, which could be rescued by recovering Flag-Crp{sup F46}. We also found that Crp{sup F46} interacted with non-muscle myosin high chain IIA (NMHC IIA) and that its three coiled-coil domains are pivotal for its binding to NMHC IIA. Additionally, analyses of phosphorylation of NMHC IIA and RLC (regulatory light chain) demonstrated that Crp{sup F46} was associated with myosin IIA during filament formation. Indirect immunofluorescence images indicated that NM IIA filaments were inhibited when Crp{sup F46} was under-expressed. Thus, Crp{sup F46} regulates cell migration by centrosomal reorientation and altering the function of the actomyosin network by controlling specific phosphorylation of myosin.
- OSTI ID:
- 23082327
- Journal Information:
- Experimental Cell Research, Vol. 373, Issue 1-2; Other Information: Copyright (c) 2018 Elsevier Inc. All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); ISSN 0014-4827
- Country of Publication:
- United States
- Language:
- English
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