Abstract
While micronuclei (MN) store extranuclear DNA and cause genome instability, the effects of nuclear envelope (NE) assembly defects associated with MN on genome instability remain largely unknown. Here, we investigated the NE protein distribution in MN using HeLa human cervical cancer cells. Under the standard condition and two pharmacological culture conditions, we found that three types of NE protein assemblies were associated with MN: 1) intact NE assembly, in which both core and non-core NE proteins were evenly present; 2) type I assembly, in which only core NE proteins were detectable; and 3) type II assembly in which a region deficient for both core and non-core NE proteins existed and a pattern recognition receptor, cyclic guanosine monophos-phate-adenosine monophosphate synthase, was frequently detected. Our findings provide experimental settings and a method of grouping MN-associated NE defects, which may be helpful for researchers who are interested in regulation of genome and nuclear organization relevant to cancer development.
Highlights
In most eukaryotic cells, genomic DNA is enclosed in the nucleus and the boundary of the nucleus is the nuclear envelope (NE) [1]
Under the standard condition and two pharmacological culture conditions, we found that three types of NE protein assemblies were associated with MN: 1) intact NE assembly, in which both core and non-core NE proteins were evenly present; 2) type I assembly, in which only core NE proteins were detectable; and 3) type II assembly in which a region deficient for both core and non-core NE proteins existed and a pattern recognition receptor, cyclic guanosine monophosphate-adenosine monophosphate synthase, was frequently detected
Our findings describe pharmacological cell culture conditions to induce MN and a method to differentiate NE defects associated with MN, providing insights into quality control of MN and cell fate decisions of MN-containing cells, which are relevant to regulation of genome instability and cancer development
Summary
In most eukaryotic cells, genomic DNA is enclosed in the nucleus and the boundary of the nucleus is the nuclear envelope (NE) [1]. Core NE proteins can be assembled more efficiently around miss-segregated chromosomes than non-core NE proteins, leading to NE protein assembly defects in MN [8]. Their findings concerning NE assemblies associated with MN provide a new perspective to assess the linkage between NE assembly defects and cell fate decisions of MN-containing cells, they may have overlooked other types of NE assembly defects that might regulate such decisions. Our findings describe pharmacological cell culture conditions to induce MN and a method to differentiate NE defects associated with MN, providing insights into quality control of MN and cell fate decisions of MN-containing cells, which are relevant to regulation of genome instability and cancer development
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