#2 Using a genetic system to induce controlled errors during mitosis we demonstrate that chromosome segregation errors alter nuclear shape and its mechanical properties. These abnormalities rapidly trigger the p53 checkpoint, preventing aneuploid cells from proliferating. #3 We further identified the molecular mechanisms that sense these nuclear mechanical and shape abnormalities by showing that these changes are sensed by the mTORC2 complex and the ATR protein which subsequently activate p53. #4 We also found that this surveillance mechanism is activated in aging-related setting, such as in a disease condition called progeria, which is characterized by altered assembly of the nuclear lamina at the cellular level