Faithful propagation of life requires coordination of DNA replication and segregation with cell growth and division. In bacteria, this results in cell size homeostasis and periodicity in replication and division. The situation is perturbed under stress such as DNA damage, which induces filamentation as cell cycle progression is blocked to allow for repair. Mechanisms that release this morphological state for re-entry into wild type growth are unclear. Here we show that damage-induced filaments divide asymmetrically, producing short daughter cells that tend to be devoid of damage and have wild type size and growth dynamics. The Min system primarily determines division site location in the filament, with additional regulation of division completion by chromosome segregation. Collectively, we propose that coordination between chromosome (and specifically segregation and cell division may result in asymmetric division in damage-induced filaments and facilitate recovery from a stressed state.