scholarly journals Appl1andAppl2are Expendable for Mouse Development But Are Essential for HGF-Induced Akt Activation and Migration in Mouse Embryonic Fibroblasts

2015 ◽  
Vol 231 (5) ◽  
pp. 1142-1150 ◽  
Author(s):  
Yinfei Tan ◽  
Xiaoban Xin ◽  
Francis J. Coffey ◽  
David L. Wiest ◽  
Lily Q. Dong ◽  
...  
Keyword(s):  
Mouse Development ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Akt Activation ◽  
And Migration

scholarly journals Replacing nonmuscle myosin 2A with myosin 2C1 permits gastrulation but not placenta vascular development in mice

2018 ◽  
Vol 29 (19) ◽  
pp. 2326-2335
Author(s):  
Yingfan Zhang ◽  
Chengyu Liu ◽  
Robert S. Adelstein ◽  
Xuefei Ma
Keyword(s):  
Homologous Recombination ◽  
Focal Adhesions ◽  
Nonmuscle Myosin ◽  
Developmentally Delayed ◽  
Mouse Development ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Heavy Chains ◽  
Vascular Formation

Three paralogues of nonmuscle myosin 2 (NM 2A, 2B, and 2C) are expressed in mammals, and the heavy chains are the products of three different genes (Myh9, Myh10, and Myh14, respectively). NM 2A and 2B are essential for mouse development, while 2C is not. Studies on NM 2C are limited and the in vivo function of this paralogue is not clear. Using homologous recombination, cDNA encoding nonmuscle myosin heavy chain 2C1 fused with GFP was introduced into the first coding exon of Myh9, replacing NM 2A expression with NM 2C1 expression in mice. In contrast to A–/A– embryos, which die by embryonic day (E) 6.5, AC1*gfp/AC1*gfp embryos survive through E8.5, demonstrating that NM 2C1 can support mouse development beyond gastrulation. At E9.5 and E10.5, however, AC1*gfp/AC1*gfp embryos are developmentally delayed, with abnormalities in placental vascular formation. The defect in vascular formation is confirmed in allantois explants from AC1*gfp/AC1*gfp embryos. Thus, NM 2C1 cannot support normal placental vascular formation. In addition, AC1*gfp/AC1*gfp mouse embryonic fibroblasts (MEFs) migrate rapidly but with impaired persistence and develop smaller, less mature focal adhesions than A+/A+ MEFs. This is attributed to enhanced NM 2C1 actomyosin stability and different NM 2C1 subcellular localization than in NM 2A.

scholarly journals Protein 4.1G Regulates Cell Adhesion, Spreading, and Migration of Mouse Embryonic Fibroblasts through the β1 Integrin Pathway

2015 ◽  
Vol 291 (5) ◽  
pp. 2170-2180 ◽  
Author(s):  
Lixiang Chen ◽  
Ting Wang ◽  
Yaomei Wang ◽  
Jingxin Zhang ◽  
Yuanming Qi ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Β1 Integrin ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
And Migration

scholarly journals Specificity Protein 2 (Sp2) Is Essential for Mouse Development and Autonomous Proliferation of Mouse Embryonic Fibroblasts

PLoS ONE ◽  
2010 ◽  
Vol 5 (3) ◽  
pp. e9587 ◽  
Author(s):  
Frank Baur ◽  
Kerstin Nau ◽  
Dennis Sadic ◽  
Lena Allweiss ◽  
Hans-Peter Elsässer ◽  
...  
Keyword(s):  
Mouse Development ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Specificity Protein

scholarly journals The Dioxin Receptor Regulates the Constitutive Expression of the Vav3 Proto-Oncogene and Modulates Cell Shape and Adhesion

2009 ◽  
Vol 20 (6) ◽  
pp. 1715-1727 ◽  
Author(s):  
Jose M. Carvajal-Gonzalez ◽  
Sonia Mulero-Navarro ◽  
Angel Carlos Roman ◽  
Vincent Sauzeau ◽  
Jaime M. Merino ◽  
...  
Keyword(s):  
Cell Shape ◽  
Constitutive Expression ◽  
Focal Adhesions ◽  
Stress Fibers ◽  
Cell Area ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Null Phenotype ◽  
And Migration ◽  
Dioxin Receptor

The dioxin receptor (AhR) modulates cell plasticity and migration, although the signaling involved remains unknown. Here, we report a mechanism that integrates AhR into these cytoskeleton-related functions. Immortalized and mouse embryonic fibroblasts lacking AhR (AhR−/−) had increased cell area due to spread cytoplasms that reverted to wild-type morphology upon AhR re-expression. The AhR-null phenotype included increased F-actin stress fibers, depolarized focal adhesions, and enhanced spreading and adhesion. The cytoskeleton alterations of AhR−/− cells were due to down-regulation of constitutive Vav3 expression, a guanosine diphosphate/guanosine triphosphate exchange factor for Rho/Rac GTPases and a novel transcriptional target of AhR. AhR was recruited to the vav3 promoter and maintained constitutive mRNA expression in a ligand-independent manner. Consistently, AhR−/− fibroblasts had reduced Rac1 activity and increased activation of the RhoA/Rho kinase (Rock) pathway. Pharmacological inhibition of Rac1 shifted AhR+/+ fibroblasts to the null phenotype, whereas Rock inhibition changed AhR-null cells to the AhR+/+ morphology. Knockdown of vav3 transcripts by small interfering RNA induced cytoskeleton defects and changes in adhesion and spreading mimicking those of AhR-null cells. Moreover, vav3−/− MEFs, as AhR−/− mouse embryonic fibroblasts, had increased cell area and enhanced stress fibers. By modulating Vav3-dependent signaling, AhR could regulate cell shape, adhesion, and migration under physiological conditions and, perhaps, in certain pathological states.

Deletion of Gremlin1 increases cell proliferation and migration responses in mouse embryonic fibroblasts

2012 ◽  
Vol 24 (4) ◽  
pp. 889-898 ◽  
Author(s):  
Simon P. Curran ◽  
Fionnuala B. Hickey ◽  
Alan Watson ◽  
Catherine Godson ◽  
Derek P. Brazil
Keyword(s):  
Cell Proliferation ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Regulation of c-Fos Gene Expression by NF-κB: A p65 Homodimer Binding Site in Mouse Embryonic Fibroblasts but Not Human HEK293 Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e84062 ◽  
Author(s):  
Yu-Cheng Tu ◽  
Duen-Yi Huang ◽  
Shine-Gwo Shiah ◽  
Jang-Shiun Wang ◽  
Wan-Wan Lin
Keyword(s):  
Gene Expression ◽  
Binding Site ◽  
Hek293 Cells ◽  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts

scholarly journals Introduction of Mouse Embryonic Fibroblasts into Early Embryos: From Confusion to Constructive Discussion. Comment on Savatier, P. Introduction of Mouse Embryonic Fibroblasts into Early Embryos Causes Reprogramming and (Con)fusion. Cells 2021, 10, 772

Cells ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 1534
Author(s):  
Krystyna Żyżyńska-Galeńska ◽  
Jolanta Karasiewicz ◽  
Agnieszka Bernat
Keyword(s):  
Mouse Embryonic Fibroblasts ◽  
Embryonic Fibroblasts ◽  
Early Embryos ◽  
Constructive Discussion

We would like to address the issues raised by Pierre Savatier in “Introduction of Mouse Embryonic Fibroblasts into Early Embryos Causes Reprogramming and (Con)Fusion” [...]

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