N-WASP plays a critical role in fibroblast adhesion and spreading.
N-WASP (Neural Wiskott Aldrich Syndrome Protein) regulates actin polymerization by activating the Arp2/3 complex and promotes the formation of actin-rich structures such as filopodia. Such actin-rich structures play critical roles in cell adhesion and cell motility. Analysis of the adhesion properties of N-WASP+/+ and N-WASP-/- mouse embryonic fibroblasts to extracellular matrix proteins revealed that N-WASP is critical for cell adhesion to fibronectin. There was no significant difference in the localization of paxillin in the two cell lines, however the vinculin patches in WASP+/+ cells were thicker and more prominent than those in N-WASP-/- cells. The beta1 integrins in N-WASP+/+ cells were found in large clusters, while beta1 integrins were more dispersed in N-WASP-/- cells. The N-WASP-/- cells migrated more rapidly than N-WASP+/+ cells in a scratch migration assay. Thus, our data suggest that N-WASP deficiency leads to reduced adhesion to fibronectin and increased cell motility.
Misra
Ashish
A
School of Biological Sciences, Nanyang Technological University, 60 Nanyang Drive, Singapore 637551, Republic of Singapore.
Lim
Rina Pei Zhi
RP
Wu
Zhihao
Z
Thanabalu
Thirumaran
T
D000818:Animals; D002448:Cell Adhesion / Q000502:physiology*; D002460:Cell Line; D002465:Cell Movement / Q000502:physiology*; D005347:Fibroblasts / Q000166:cytology* / Q000502:physiology*; D051379:Mice; D051317:Wiskott-Aldrich Syndrome Protein, Neuronal / Q000378:metabolism*
C495772:Wasl protein, mouse; D051317:Wiskott-Aldrich Syndrome Protein, Neuronal