SUMO and cellular adaptive mechanisms

Abstract

Stress response: how cells wrestle with SUMO disruption Cellular stress caused by disrupting attachment of the ubiquitous small ubiquitin-like modifier (SUMO) proteins, which are present in most organisms and regulate numerous DNA processes and stress responses by attaching to key proteins, results in some remarkable adaptations. Mark Hochstrasser at Yale University, New Haven, USA, and co-workers review how this “sumoylation” is reversed by protease enzymes, and how imbalances between sumoylation and desumoylation may be linked to diseases including cancer. When certain SUMO proteases are deliberately disrupted, the cells quickly become aneuploid, i.e., carry an abnormal number of chromosomes. These cells show severe growth defects, but over many generations they regain the normal number of chromosomes. They also undergo genetic changes that promote alternative mechanisms that compensate for losing the SUMO protease and facilitate the same efficient stress responses as the original cells.