First Author | Ishiguro K | Year | 2000 |
Journal | J Biol Chem | Volume | 275 |
Issue | 8 | Pages | 5249-52 |
PubMed ID | 10681494 | Mgi Jnum | J:60596 |
Mgi Id | MGI:1353707 | Doi | 10.1074/jbc.275.8.5249 |
Citation | Ishiguro K, et al. (2000) Syndecan-4 deficiency impairs focal adhesion formation only under restricted conditions. J Biol Chem 275(8):5249-52 |
abstractText | Two domains of fibronectin deliver two different but cooperative signals required for focal adhesion formation. The signal from the cell-binding domain is mediated by integrins, whereas the signal from the heparin-binding domain is recognized by heparan sulfate proteoglycans, of which syndecan-4 has been hypothesized to be involved in focal adhesion formation. We generated mice deficient in syndecan-4 to study its role directly. Even in fibroblasts from syndecan-4-deficient mice, focal adhesions were formed, and actin fibers terminated normally at focal adhesions when they were cultured on coverslips coated with fibronectin or with a mixture of its cell-binding and heparin-binding fragments. However, when the cells were cultured on the cell-binding fragment and the heparin-binding fragment was added to the medium, focal adhesion formation was impaired in the syndecan-4 null fibroblasts as compared with that in wild-type cells. Therefore, syndecan-4 is essential for promoting focal adhesion formation only when the signal of the heparin-binding domain of fibronectin is delivered as a soluble form, most probably from the apical surface. When the signal is delivered as a substratum-bound form, other molecule(s) also participate(s) in the signal reception. |