Potential for micronuclear turnover through autophagy secretion pathway.

Micronuclei (MN) serve as well-established markers of genomic instability. MN arise from various stresses, such as segregation errors and mechanical stress, and are subsequently eliminated by the autophagy pathway. It has been suggested that MN are traditionally considered markers of cancer cells, often without recognized functional significance. Meanwhile, we recently discovered that MN act as mediators in regulating microglial characteristics. Neurons produce MN in response to migrating stress during the developmental stage and release them to the extracellular space, subsequently transferring them to microglia. In this study, we report the potential mechanisms underlying MN release through the autophagic secretion pathway. Our data show a possibility by which damaged MN are recognized autophagy regulatory factors, resulting in the propagation of MN to microglia.