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Updated: Feb 26, 2026

Detection of Nuclear Blebbing and DNA Leakage in Mammalian Cells by Immunofluorescence
Published on: January 17, 2025
Nucleocytoplasmic transport in cells with progerin-induced defective nuclear lamina
Gianmarco Ferri1, Barbara Storti2, Ranieri Bizzarri2
1NEST, Scuola Normale Superiore and Istituto Nanoscienze-CNR, Piazza San Silvestro 12, 56127 Pisa, Italy; Center for Nanotechnology Innovation @ NEST, Istituto Italiano di Tecnologia, Piazza San Silvestro 12, 56127 Pisa, Italy.
Abstract:
Recent data indicate that nuclear lamina (NL) plays a relevant role in many fundamental cellular functions. The peculiar role of NL in cells is dramatically demonstrated by the Hutchinson-Gilford progeria syndrome (HGPS), an inherited laminopathy that causes premature, rapid aging shortly after birth. In HGPS, a mutant form of Lamin A (progeria) leads to a dysmorphic NL structure, but how this perturbation is transduced into cellular changes is still largely unknown. Owing to the close structural relationship between NL and the Nuclear Pore Complex (NPC), in this work we test whether HGPS affects passive and active nucleo-cytoplasmic shuttling of cargoes by means of an established model based of fluorescence recovery after photobleaching. Our findings clearly demonstrate that dysmorphic NL is decoupled from the dynamic characteristics of passive and active transport towards and from the nucleus, as well as from the binding affinity of transport protein mediators.
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