ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR150/076/SRR15048676/SRR15048676_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR150/078/SRR15048678/SRR15048678_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR150/078/SRR15048678/SRR15048678_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR150/077/SRR15048677/SRR15048677_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR150/079/SRR15048679/SRR15048679_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR150/076/SRR15048676/SRR15048676_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR150/077/SRR15048677/SRR15048677_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR150/079/SRR15048679/SRR15048679_1.fastq.gzprimaryOK200GenomicsOral Molecular Pathology, Tokushima Universityhttps://www.ebi.ac.uk/ena/browser/view/PRJNA744074Homo sapiensDuring mitosis, the chromosomal passenger complex (CPC) that is formed by Aurora-B, INCENP, Survivin, and Borealin ensures the faithful segregation of the chromosomes into daughter cells. We previously have shown that CPC activity was terminated by the anaphase promoting complex/cyclosome (APC/C) and its cofactor Cdh1 via ubiquitylation of Borealin and Aurora-B during the G1 phase of somatic cells. On the other hand, protein levels of Borealin and Aurora-B were stable during cell cycle progression due to high levels of Emi1, which keep APC/CCdh1 inactive in embryonal carcinoma (EC) cells. During retinoic acid-induced differentiation of EC cells, these proteins were downregulated by APC/CCdh1-mediated ubiquitylation. Interestingly, CPC proteins form a complex with Aurora-B kinase activity even in interphase of EC cells. Significantly, inhibition of CPC activity by either knockdown of Borealin or Aurora-B and Aurora-B kinase inhibitor treatment induced spontaneous differentiation of EC cells. In conclusion, sustained CPC activity plays a critical role in maintenance of the undifferentiated state of pluripotent stem cells. We therefore propose an interphase role of the CPC in regulating embryonic pluripotency. Overall design: Embryonal carcinoma cell line NCC-IT-A3 cells were cultured for 4 days with or without 100nM Barasertib, which was Aurora-B specific inhibitor. Collected RNAs were analyzed by RNA-seqENAfalseTranscriptome analysis of NCC-IT-A3 cells by Barasertib treatmentTranscriptome analysis of NCC-IT-A3 cells by Barasertib treatment2025-09-242021-07-10PRJNA744074GSE1795039606