Abstract

Contact inhibition of locomotion (CIL) occurs when a cell ceases moving in the same direction following contact with another cell. Homotypic and heterotypic CIL occur between cells of the same and different types, respectively. Using Abercrombie's confronted explants assay we studied the effect of changing Rac1 or RhoA activities on heterotypic CIL between NIH3T3 and chicken heart fibroblasts. Both dominant active (L61) and dominant negative (N17) Rac1 expressed in NIH3T3 cells resulted in loss of heterotypic CIL. N17Rac1 expression caused RhoA activation. Increasing RhoA activity directly (V14RhoA) or indirectly (downregulation of N-cadherin or p120-catenin) also resulted in loss of CIL. High RhoA activity has been associated with tumour invasion and our results are consistent with loss of heterotypic CIL playing a role.

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Publisher Full Text

Authors

Anear E, Parish RW

Institution

Department of Botany, La Trobe University, Melbourne 3086, Australia.

Source

FEBS letters 586:9 2012 May 7 pg 1330-5

MeSH

Actins
Animals
Cadherins
Catenins
Cell Movement
Chickens
Contact Inhibition
Down-Regulation
Mice
NIH 3T3 Cells
Protein Multimerization
Protein Structure, Quaternary
cdc42 GTP-Binding Protein
rac1 GTP-Binding Protein
rho-Associated Kinases
rhoA GTP-Binding Protein

Pub Type(s)

Journal Article

Language

eng

PubMed ID

22498500