Potential for micronuclear turnover through autophagy secretion pathway

TL;DR

This study explores how micronuclei, byproducts of genomic instability, are released through autophagy and influence microglial behavior.

Contribution

The paper introduces a novel mechanism by which damaged micronuclei are secreted via the autophagy pathway to microglia.

Findings

Micronuclei are recognized by autophagy regulatory factors and may be secreted.

Micronuclei released by neurons are transferred to microglia, influencing their characteristics.

MN release is linked to developmental stress and autophagy secretion pathways.

Abstract

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.

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