ArticleBiophysical journal2025
The mechanism of nesprin-2 accumulation at the nucleus front during confined cell migration.
Article in Biophysical journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Nuclear mechanobiology in confined cell migration.Nucleus (Austin, Tex.) · 2026Review
- Periodic confined cell migration drives partially reversible chromatin reorganization in cancer cell lines.Communications biology · 2026Article
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7 authors.
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Abstract
Cell migration through constrictions is essential for many physiological processes. During this confined cell migration, the protein nesprin-2, which links the cytoskeletal network to the nucleus, can accumulate at the front of the nucleus. However, up to now, the exact mechanism of this accumulation is unknown. Here, we further investigate this accumulation mechanism. We quantify the spatial distribution of nesprin-2, actin, and the proteins SUN1 and SUN2, which are inner-nuclear-membrane proteins that bind to nesprin-2. We observe that SUN2 shows the same frontal accumulation as nesprin-2, but SUN1 does not. Based on the spatial protein distributions and the homology between the actin-binding domains of nesprin-2 and the well characterized actin-binding protein α-actinin-4, we hypothesize that strengthening of the nesprin-actin bond upon increasing actin pulling force induces frontal nesprin-2 accumulation. This force-strengthening behavior is known as catch-bond binding. Based on this catch-bond hypothesis, we develop a simple physical model that qualitatively reproduces the experimentally observed nesprin-2 profiles. We try to further test the catch-bond hypothesis by using a specific point mutation to abrogate the catch-bond behavior in mininesprin-2 constructs. These chimeric constructs consist of the N-terminal actin-binding domains and the C-terminal SUN-binding domain of nesprin-2. The experimentally measured distribution of the mininesprin-2 mutant agrees well with the model prediction on this mutation effect. All in all, our work builds an important foundation to unravel the mechanism of frontal nesprin-2 accumulation during confined cell migration.
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