ArticleCell proliferation2016
F-actin rearrangement is regulated by mTORC2/Akt/Girdin in mouse fertilized eggs.
Article in Cell proliferation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Genome sequencing reveals CCDC88A variants in malformations of cortical development and immune dysfunction.Human molecular genetics · 2025Article
- Taenia solium excretory secretory proteins (ESPs) suppresses TLR4/AKT mediated ROS formation in human macrophages via hsa-miR-125.PLoS neglected tropical diseases · 2023Article
- WAVE2 Regulates Actin-Dependent Processes Induced by the B Cell Antigen Receptor and Integrins.Cells · 2023Article
- mTORC2 regulates auditory hair cell structure and function.iScience · 2023Article
- mTORC2 interactome and localization determine aggressiveness of high-grade glioma cells through association with gelsolin.Scientific reports · 2023Article
- [CCL18 Promotes the Invasion of Lung Adenocarcinoma through ANXA2].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2021Article
- The DISC1-Girdin complex - a missing link in signaling to the T cell cytoskeleton.Journal of cell science · 2020Article
- High Dosages of Equine Chorionic Gonadotropin Exert Adverse Effects on the Developmental Competence of IVF-Derived Mouse Embryos and Cause Oxidative Stress-Induced Aneuploidy.Frontiers in cell and developmental biology · 2020Article
- Review
- Construction of Chitosan-Zn-Based Electrochemical Biosensing Platform for Rapid and Accurate Assay of Actin.Sensors (Basel, Switzerland) · 2018Article
- Cell Migration in Microfabricated 3D Collagen Microtracks is Mediated through the Prometastatic Protein Girdin.Cellular and molecular bioengineering · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mouse fertilized eggs, correct assembly and distribution of the actin cytoskeleton are intimately related to cleavage in early-stage embryos. However, in mouse fertilized eggs, mechanisms and involved factors responsible for regulating the actin cytoskeleton are poorly defined. In this study, mTORC2, PKB/Akt and Girdin were found to modulate division of mouse fertilized eggs by regulating distribution of the actin cytoskeleton. RNA interference (RNAi)-mediated depletion of mTORC2, Akt1 or Girdin disrupted F-actin rearrangement and strongly inhibited egg development. PKB/Akt has been proven to be a downstream target of the mTORC2 signalling pathway. Girdin, a newly found actin cross-linker, has been proven to be a downstream target of the Akt signalling pathway. Furthermore, phosphorylation of both Akt1 and girdin was affected by knockdown of mTORC2. Akt1 positively regulated development of the mouse fertilized eggs by girdin-mediated F-actin rearrangement. Thus it seems that girdin could be a downstream target of the Akt1-mediated signalling pathway. Collectively, this study aimed to prove participation of mTORC2/Akt in F-actin assembly in early-stage cleavage of mouse fertilized eggs via the function of girdin.
objectivesIn mouse fertilized eggs, the proper assembly and distribution of actin cytoskeleton is intimately related with the cleavage of early-stage embryo. However, in mammals, especially in mouse fertilized eggs, the mechanisms and involved factors responsible for regulating the actin cytoskeleton are poorly defined. The aim of this study was to determine the role of mTORC2,PKB/Akt and Girdin in early development of fertilized mouse eggs, via regulating the distribution of actin cytoskeleton. MATERIALS AND
methodsChanges of F-actin after treatting with mTORC2 shRNA, Akt siRNA or Girdin siRNA were observed by Immunofluorescence staining and laser-scanning confocal microscopy. Levels of phosphorylated Girdin at Se1417 were detected by Western immunoblotting. Percentages of cells undergoing division were determined by counting, using a dissecting microscope.
resultsRNA interference (RNAi)-mediated depletion of mTORC2, Akt1 or Girdin disrupts F-actin rearrangement, and remarkably inhibited the development of mouse-fertilized eggs. PKB/Akt has been proved to be a downstream target of the mTORC2 signaling pathway. Girdin, the newly found actin-cross linker, has been proved to be a downstream target of the Akt signaling pathway. Furthermore phosphorylation of both Akt1 and Girdin were affected by knockdown of mTORC2. Akt1 positively regulates the development of mouse-fertilized eggs by Girdin mediated F-actin rearrangement. Girdin could be a downstream target of the Akt1-mediated signaling pathway.
conclusionsCollectively, this study aimed to prove the participation of mTORC2/Akt in F-actin assembling in early-stage cleavage of mouse fertilized eggs via the function of Girdin.
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