Senescent cells form nuclear foci that contain the 26S proteasome

The proteasome plays a central role in intracellular protein degradation. Age-dependent decline in protea-some activity is associated with cellular senescence and organismal aging; however, the mechanism by which the proteasome plays a role in senescent cells remains elusive. Here, we show that nuclear foci that contain the proteasome and exhibit liquid-like properties are formed in senescent cells. The formation of senescence-associated nuclear proteasome foci (SANPs) is dependent on ubiquitination and RAD23B, similar to previously known nuclear proteasome foci, but also requires proteasome activity. RAD23B knock-down suppresses SANP formation and increases mitochondrial activity, leading to reactive oxygen species production without affecting other senescence traits such as cell-cycle arrest and cell morphology. These findings suggest that SANPs are an important feature of senescent cells and uncover a mechanism by which the proteasome plays a role in senescent cells.

Automated summary

Proteasome plays a role in senescent cells by forming nuclear foci with liquid-like properties. These foci, known as senescence-associated nuclear proteasome foci (SANPs), require ubiquitination, RAD23B, and proteasome activity for their formation. Knock-down of RAD23B suppresses SANP formation and alters mitochondrial activity, resulting in increased reactive oxygen species production.