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Talin2-mediated traction force drives matrix degradation and cell invasion

Qi, L, Jafari, N, Chen, Z, Li, L, Hyto?nen, VP, Goult, Benjamin T, Zhan, C-G, Huang, C (2016) Talin2-mediated traction force drives matrix degradation and cell invasion. Journal of Cell Science, 129 (19). pp. 3661-3674. ISSN 0021-9533. (doi:10.1242/jcs.185959) (KAR id:57608)

Abstract

Talin binds to ?-integrin tails to activate integrins, regulating cell migration, invasion and metastasis. There are two talin genes, TLN1 and TLN2, encoding talin1 and talin2, respectively. Talin1 regulates focal adhesion dynamics, cell migration and invasion, whereas the biological function of talin2 is not clear and, indeed, talin2 has been presumed to function redundantly with talin1. Here, we show that talin2 has a much stronger binding to ?-integrin tails than talin1. Replacement of talin2 Ser339 with Cys significantly decreased its binding to ?1-integrin tails to a level comparable to that of talin1. Talin2 localizes at invadopodia and is indispensable for the generation of traction force and invadopodium-mediated matrix degradation. Ablation of talin2 suppressed traction force generation and invadopodia formation, which were restored by re-expressing talin2 but not talin1. Furthermore, re-expression of wild-type talin2 (but not talin2S339C) in talin2-depleted cells rescued development of traction force and invadopodia. These results suggest that a strong interaction of talin2 with integrins is required to generate traction, which in turn drives invadopodium-mediated matrix degradation, which is key to cancer cell invasion.

Item Type: Article
DOI/Identification number: 10.1242/jcs.185959
Subjects: Q Science > QH Natural history > QH581.2 Cell Biology
Divisions: Divisions > Division of Natural Sciences > Biosciences
Funders: [37325] UNSPECIFIED
Depositing User: Ben Goult
Date Deposited: 01 Oct 2016 16:06 UTC
Last Modified: 04 Mar 2024 16:32 UTC
Resource URI: https://kar.kent.ac.uk/id/eprint/57608 (The current URI for this page, for reference purposes)

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