Endoplasmic reticulum disruption stimulates nuclear membrane mechanotransduction.

ABSTRACT: Cytosolic phospholipase A2 (cPLA₂) controls some of the most powerful inflammatory lipids in vertebrates by releasing their metabolic precursor, arachidonic acid, from the inner nuclear membrane (INM). Ca²⁺ and INM tension (T_INM) are thought to govern the interactions and activity of cPLA₂ at the INM. However, as compensatory membrane flow from the contiguous endoplasmic reticulum (ER) may prevent T_INM, the conditions permitting nuclear membrane mechanotransduction by cPLA₂ or other mediators remain unclear. To test whether the ER buffers T_INM, we created the genetically encoded, Ca²⁺-insensitive T_INM biosensor amphipathic lipid-packing domain inside the nucleus (ALPIN). Confocal time-lapse imaging of A

SUBMITTER: Shen Z 

PROVIDER: S-EPMC12807876 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature