Abstract
Micronuclei are small, aberrant nuclear compartments containing mis-segregated chromosomes or chromosomal fragments. During telophase, dysfunctional micronuclear envelope reassembly leaves the micronuclear envelope highly unstable and rupture-prone. Following rupture, micronuclei attempt to repair membrane gaps, but the process is typically unsuccessful and may promote the invasion of ER tubules into the interior of micronuclei. These abnormalities cause ruptured micronuclei to accumulate significant DNA damage in the form of both single-stranded DNA and double-stranded breaks. Because micronuclei are capable of promoting genome instability, it is essential to understand the sources of DNA damage and the mechanism through which it arises in these structures. In this review, I will explore the causes and consequences of micronuclear envelope rupture, beginning with the processes surrounding improper micronuclear envelope reassembly. I will then discuss micronuclear envelope rupture, attempted micronuclear envelope repair and its consequences, and the proposed causes of micronuclear DNA damage.
Highlights
The nuclear envelope (NE) maintains a semi-permeable barrier encompassing the nucleoplasm and consists of two lipid bilayers, the inner and outer nuclear membranes (INM and ONM, respectively), which are the primary regulators of compartmentalization [1]
Multiple studies have observed an association between RPA accumulation and micronuclear envelope (mNE) repair pathway proteins: knockdown of each LEMD2, CHMP7, and CHMP4B diminishes micronuclear RPA presence [33, 50], suggesting that single-stranded DNA (ssDNA) arises as a result of ESCRT-III activity or endoplasmic reticulum (ER) tubule invasion
I have discussed the origins of micronuclear DNA damage through five key processes: improper mNE reassembly, MN rupture, attempted mNE repair, ER tubule invasion, and accumulation of ssDNA and double-stranded breaks (DSBs)
Summary
The nuclear envelope (NE) maintains a semi-permeable barrier encompassing the nucleoplasm and consists of two lipid bilayers, the inner and outer nuclear membranes (INM and ONM, respectively), which are the primary regulators of compartmentalization [1]. I will discuss defects in mNE repair processes, possible causes of ER tubule invasion of MN, and alternative NE repair pathways. The study found that stabilization of MTs with Paclitaxel, a MT depolymerization inhibitor, prevents non-core protein assembly at PN chromosome regions covered by MTs. loosening MT bundling through inhibition of the kinesin KIF4 [42] reversed micronuclear reassembly defects.
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