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Shp2 contributes to the regulation of nuclear shape and cellular viscoelasticity in response to substrate spatial cues

Cell polarization can be guided by substrate topology through space constraints and adhesion induction, which are part of cellular mechanosensing pathways. Here, we demonstrated that protein tyrosine phosphatase Shp2 plays a crucial role in mediating the response of cells to substrate spatial cues....

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Published in:Biochemical and biophysical research communications 2024-08, Vol.721, p.150144-150144, Article 150144
Main Authors: Chen, Yin-Quan, Lee, Hsin-Chang, Lee, Hsiao-Hui
Format: Article
Language:English
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Summary:Cell polarization can be guided by substrate topology through space constraints and adhesion induction, which are part of cellular mechanosensing pathways. Here, we demonstrated that protein tyrosine phosphatase Shp2 plays a crucial role in mediating the response of cells to substrate spatial cues. When compared to cells spreading on surfaces coated uniformly with fibronectin (FN), cells attached to 10 μm-width FN-strip micropattern (MP), which provides spatial cues for uniaxial spreading, exhibited elongated focal adhesions (FAs) and aligned stress fibers in the direction of the MP. As a result of uniaxial cell spreading, nuclei became elongated, dependent on ROCK-mediated actomyosin contractility. Additionally, intracellular viscoelasticity also increased. Shp2-deficient cells did not display elongated FAs mediated by MP, well-aligned stress fibers, or changes in nuclear shape and intracellular viscoelasticity. Overall, our data suggest that Shp2 is involved in regulating FAs and the actin cytoskeleton to modulate nuclear shape and intracellular physical properties in response to substrate spatial cues. •Shp2 is involved in cytoskeletal regulation in response to substrate spatial cues.•Nuclear elongation induced by substrate spatial cues is impaired in Shp2-deficient MEFs.•Shp2 is actively involved in modulating intracellular viscoelastic properties.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2024.150144