Data from: Micronuclear collapse from oxidative damage

Chromosome-containing micronuclei are a hallmark of aggressive cancers.
Micronuclei frequently undergo irreversible collapse exposing their
enclosed chromatin to the cytosol. Micronuclear rupture catalyzes
chromosomal rearrangements, epigenetic abnormalities, and inflammation,
yet mechanisms governing micronuclear integrity are poorly understood.
Here we show that mitochondria-derived reactive oxygen species (ROS)
disrupt micronuclei by promoting a noncanonical function of the ESCRT-III
nuclear membrane repair complex protein, CHMP7. ROS retain CHMP7 in
micronuclei while disrupting its interaction with other ESCRT-III
components. Instead, ROS-induced cysteine oxidation promotes CHMP7
oligomerization and binding to the nuclear membrane protein LEMD2
disrupting micronuclear envelopes. We show that this ROS-CHMP7 axis
promotes chromosome shattering known to result from micronuclear rupture.
It also mediates micronuclear rupture under hypoxic conditions, linking
tumor hypoxia with downstream processes driving cancer progression.