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Biology subjects

Figueroa, S.

Publications and source records attributed to Figueroa, S..

2 recordsLinked to original sources

Biomolecular condensates at the nuclear pore basket maintain global chromatin organization

Nuclear pore complexes are the only gateway between the nucleus and cytoplasm in eukaryotic cells during interphase. Specificity of transport is ensured by a size-dependent permeability barrier, which has so far been attributed to intrinsically disordered phenylalanine-glycine (FG) repeat- containing nucleoporins located in the central channel of the nuclear pores. We show that the coiled-coil domain of the main component of the nuclear pore basket, the non-FG protein TPR, encompasses intrinsically disordered regions. This "disordered coiled-coil domain" allows it to form biomolecular condensates in vivo, drives mechanical exclusion of heterochromatin, and defines a new permeability barrier at the nuclear basket. This work therefore highlights unconventional properties of coiled-coil domains at the nuclear pore basket and bridges the biophysics of such domains with nuclear architecture, chromatin spatial organization and nucleocytoplasmic transport.

cell biology↗

Changes in nuclear and actin mechanics from G1 to G2 affect nuclear integrity

The structural integrity of the nucleus is dependent on nuclear mechanical elements of chromatin and lamins to resist antagonistic actin cytoskeleton forces. Imbalance results in nuclear blebbing, rupture, and cellular dysfunction found in many human diseases. We used Fluorescent Ubiquitin Cell Cycle Indicator (FUCCI) cells to determine how cell cycle changes affect the nucleus and actin force balance. While nuclear blebs are present equally throughout interphase, nuclear blebs form predominantly in G1 and then persist into G2 due to increased actin-based nuclear confinement and focal adhesion density in G1 vs. G2 cells. Upon artificial confinement, G2 nuclei ruptured more than G1 nuclei. Single nucleus micromanipulation force measurements confirmed that G1 nuclei are stronger than G2 nuclei in both the chromatin-based and lamin-based nuclear stiffness regimes. Decreased nuclear stiffness can be explained by loss of peripheral H3K9me3 from G1 to G2, recapitulated by H3K9me3 inhibition via Chaetocin. Cell cycle-based changes in nuclear and actin mechanics impact nuclear integrity and shape.

cell biology↗