Shyam B. Khatau

TL;DR: It is found that the shape of the nucleus is tightly regulated by the underlying cell adhesion geometry, and its nuclear shape-determining function is disrupted in cells from mouse models of accelerated aging and muscular dystrophy with distorted nuclei caused by alterations of A-type lamins.

TL;DR: Both the mechanical properties of the cytOSkeleton and cytoskeleton-based processes, including cell motility, coupled MTOC and nucleus dynamics, and cell polarization, depend critically on the integrity of the nuclear lamina, which suggest the existence of a functional mechanical connection between the nucleus and the cytos skeleton.

TL;DR: Results indicate a new function for emerin in cell polarization and suggest that laminopathies are not directly associated with cells' inability to polarize, but rather with cytoplasmic softening and weakened adhesion mediated by the disruption of the LINC complex across the nuclear envelope.

TL;DR: The results establish the perinuclear actin cap and associated ACAFAs as major mediators of cellular mechanosensing and a critical element of the physical pathway that transduce mechanical cues all the way to the nucleus.

TL;DR: This work shows that only a small subset of actin fibers, those forming the perinuclear actin cap that wraps around the nucleus, form in response to low physiological mechanical stresses in adherent fibroblasts, and identifies additional roles for lamin A/C of the nuclear lamina and linkers of nucleus to cytoskeleton (LINC) molecules nesprin2giant and nesPRin3, which anchor actincap fibers to the nucleus.