The small G-proteins Rac1 and Cdc42 are essential for myoblast fusion in the mouse
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
Standard
The small G-proteins Rac1 and Cdc42 are essential for myoblast fusion in the mouse. / Vasyutina, Elena; Martarelli, Benedetta; Brakebusch, Cord; Wende, Hagen; Birchmeier, Carmen.
I: Proceedings of the National Academy of Science of the United States of America, Bind 106, Nr. 22, 2009, s. 8935-40.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
Harvard
APA
Vancouver
Author
Bibtex
}
RIS
TY - JOUR
T1 - The small G-proteins Rac1 and Cdc42 are essential for myoblast fusion in the mouse
AU - Vasyutina, Elena
AU - Martarelli, Benedetta
AU - Brakebusch, Cord
AU - Wende, Hagen
AU - Birchmeier, Carmen
N1 - Keywords: Animals; Cell Fusion; Drosophila; Evolution, Molecular; Mice; Mice, Transgenic; Mutagenesis; Myoblasts, Skeletal; cdc42 GTP-Binding Protein; rac1 GTP-Binding Protein
PY - 2009
Y1 - 2009
N2 - Rac1 and Cdc42 are small G-proteins that regulate actin dynamics and affect plasma membrane protrusion and vesicle traffic. We used conditional mutagenesis in mice to demonstrate that Rac1 and Cdc42 are essential for myoblast fusion in vivo and in vitro. The deficit in fusion of Rac1 or Cdc42 mutant myoblasts correlates with a deficit in the recruitment of actin fibers and vinculin to myoblast contact sites. Comparison of the changes observed in mutant myogenic cells indicates that Rac1 and Cdc42 function in a nonredundant and not completely overlapping manner during the fusion process. Our genetic analysis demonstrates thus that the function of Rac in myoblast fusion is evolutionarily conserved from insects to mammals and that Cdc42, a molecule hitherto not implicated in myoblast fusion, is essential for the fusion of murine myoblasts.
AB - Rac1 and Cdc42 are small G-proteins that regulate actin dynamics and affect plasma membrane protrusion and vesicle traffic. We used conditional mutagenesis in mice to demonstrate that Rac1 and Cdc42 are essential for myoblast fusion in vivo and in vitro. The deficit in fusion of Rac1 or Cdc42 mutant myoblasts correlates with a deficit in the recruitment of actin fibers and vinculin to myoblast contact sites. Comparison of the changes observed in mutant myogenic cells indicates that Rac1 and Cdc42 function in a nonredundant and not completely overlapping manner during the fusion process. Our genetic analysis demonstrates thus that the function of Rac in myoblast fusion is evolutionarily conserved from insects to mammals and that Cdc42, a molecule hitherto not implicated in myoblast fusion, is essential for the fusion of murine myoblasts.
U2 - 10.1073/pnas.0902501106
DO - 10.1073/pnas.0902501106
M3 - Journal article
C2 - 19443691
VL - 106
SP - 8935
EP - 8940
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 22
ER -
ID: 12866257