Oxydative stress alters nuclear shape through lamins dysregulation: A route to senescence

Progeroid phenotypes are mainly encountered in 2 types of syndromes: in laminopathies, which are characterized by nuclear shape abnormalities due to laminA alteration, and in DNA damageresponse defect syndromes. Because laminA dysregulation leads to DNA damages, it has been proposed that senescenceoccurs in both types of syndromes through the accumulation of damages. We recently showed that elevated oxidative stress is responsible for laminB1 accumulation, nuclear shape alteration and senescencein the DDR syndrome, ataxia telangiectasia(A-T). Interestingly, overexpression of laminB1 in wild type cells is sufficient to induce senescencewithout the induction of DNA damages. Here, we will discuss the importance of controlling the laminslevel in order for maintenance nuclear architecture and we will comment the relationships of laminswith other senescencemechanisms. Finally, we will describe emerging data reportingredox control by lamins, leading us to propose a general mechanism by which reactive oxygen species can induce senescencethrough lamindysregulation and NSA.