An aggregation-prone region in talin controls talin self-interactions and regulates integrin adhesion complex dynamics.

Mechanical unfolding of talin R11 exposes an embedded cryptic Aggregation-Prone Region 1 (APR1) that enables high-affinity talin–talin interactions and force-dependent self-association.

• Why it matters: The molecular basis of the proposed second integrin-binding site in talin rod R11–R12 is unclear, and how talin’s mechanosensing is translated into adhesion remodeling needs direct mechanisms.
• What they did: The study mapped an APR within Helix50, showed isolated APR1 forms amyloid-like fibers in vitro, used APR1-disrupting gatekeeper mutations to suppress fiber formation and self-association, and tested cellular recruitment and adhesion dynamics.
• The result: APR1-dependent recruitment occurs independently of focal adhesions and integrins, vinculin disrupts preexisting talin assemblies, and blocking APR1 does not prevent adhesion formation but yields larger, talin-rich adhesions with altered assembly dynamics and signaling.

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