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http://purl.uniprot.org/citations/31264311http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31264311http://www.w3.org/2000/01/rdf-schema#comment"

Objectives

A high rate of chromosome aneuploidy is exhibited in in vitro fertilization (IVF)-derived embryos. Our previous experiments suggested that reactive oxygen species (ROS) can activate Mad2, a key protein in the spindle assembly checkpoint (SAC), and delay the first mitotic, providing time to prevent the formation of embryonic aneuploidy. We aimed to determine whether mitotic kinase Aurora B was involved in the SAC function to prevent aneuploidy in IVF-derived embryos.

Materials and methods

We analysed aneuploidy formation and repair during embryo pre-implantation via 4',6-diamidino-2-phenylindole (DAPI) staining and karyotype analysis. We assessed Aurora B activation by immunofluorescence and investigated the effect of Aurora B inhibition on embryo injury-related variables, such as embryonic development, ROS levels, mitochondrial membrane potential and γH2AX-positive expression.

Results

We observed the expression and phosphorylation of Thr232 in Aurora B in oxidative stress-induced zygotes. Moreover, inhibition of Aurora B caused chromosome mis-segregation, abnormal spindle structures, abnormal chromosome number and reduced expression of Mad2 in IVF embryos. Our results suggest that Aurora B causes mitotic arrest and participates in SAC via Mad2 and H3S10P, which is required for self-correction of aneuploidies.

Conclusions

We demonstrate here that oxidative stress-induced DNA damage triggers Aurora B-mediated activation of SAC, which prevents aneuploidy at the first mitotic cleavage in early mouse IVF embryos."xsd:string
http://purl.uniprot.org/citations/31264311http://purl.org/dc/terms/identifier"doi:10.1111/cpr.12657"xsd:string
http://purl.uniprot.org/citations/31264311http://purl.uniprot.org/core/author"Huang Y."xsd:string
http://purl.uniprot.org/citations/31264311http://purl.uniprot.org/core/author"Li Z."xsd:string
http://purl.uniprot.org/citations/31264311http://purl.uniprot.org/core/author"Li J."xsd:string
http://purl.uniprot.org/citations/31264311http://purl.uniprot.org/core/author"Xiao W."xsd:string
http://purl.uniprot.org/citations/31264311http://purl.uniprot.org/core/author"Lin E."xsd:string
http://purl.uniprot.org/citations/31264311http://purl.uniprot.org/core/author"Ha S."xsd:string
http://purl.uniprot.org/citations/31264311http://purl.uniprot.org/core/date"2019"xsd:gYear
http://purl.uniprot.org/citations/31264311http://purl.uniprot.org/core/name"Cell Prolif"xsd:string
http://purl.uniprot.org/citations/31264311http://purl.uniprot.org/core/pages"e12657"xsd:string
http://purl.uniprot.org/citations/31264311http://purl.uniprot.org/core/title"Aurora B prevents aneuploidy via MAD2 during the first mitotic cleavage in oxidatively damaged embryos."xsd:string
http://purl.uniprot.org/citations/31264311http://purl.uniprot.org/core/volume"52"xsd:string
http://purl.uniprot.org/citations/31264311http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31264311
http://purl.uniprot.org/citations/31264311http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/31264311
http://purl.uniprot.org/uniprot/#_O70126-mappedCitation-31264311http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/31264311
http://purl.uniprot.org/uniprot/O70126http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/31264311