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TPX2 Amplification-Driven Aberrant Mitosis in Long-Term Cultured Human Embryonic Stem Cells

ABSTRACT: TPX2 Amplification-Driven Aberrant Mitosis in Long-Term Cultured Human Embryonic Stem Cells

PROVIDER: PRJNA704811 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13782509_1.fastq.gz	Fastqsanger.gz
	SRR13782509_2.fastq.gz	Fastqsanger.gz
	SRR13782510_1.fastq.gz	Fastqsanger.gz
	SRR13782510_2.fastq.gz	Fastqsanger.gz
	SRR13782511_1.fastq.gz	Fastqsanger.gz

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TPX2 Amplification-Driven Aberrant Mitosis in Long-Term Cultured Human Embryonic Stem Cells

Project description:Although human embryonic stem cells (hESCs) are equipped with highly effective machinery for the maintenance of genome integrity, the frequency of genetic aberrations during long-term in vitro hESC culture has been a serious issue that raises concerns over their safety in future clinical applications. By passaging hESCs over a broad range of timepoints, we found that mitotic aberrations, such as the delay of mitosis, multipolar centrosomes, and chromosome mis-segregation, were increased in the late-passaged hESCs (LP-hESCs) in parallel with polyploidy compared to early-passaged hESCs (EP-hESCs). Through high-resolution genome-wide approaches and by following transcriptome analysis, we found that LP-hESCs with a minimal amplicon in chromosome 20q11.21 highly expressed TPX2 (targeting protein for Xklp2), a key protein for governing spindle assembly and cancer malignancy. Consistent with these findings, the inducible expression of TPX2 in EP-hESCs reproduced aberrant mitotic events, such as the delay of mitotic progression, spindle stability, misaligned chromosomes, and polyploidy. This data suggests that the amplification and increased transcription of the TPX2 gene at 20q11.21 could contribute to an increase in aberrant mitosis due to altered spindle dynamics.

2021-02-26 | GSE167495 | GEO

RecBCD Coordinates Repair of Two Ends at a DNA Double-Strand Break, Preventing Aberrant Chromosome Amplification [ChIP-seq]

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The inability to disassemble Rad51 nucleoprotein filaments leads to aberrant mitosis and cell death

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Dynamic role of Rotatin in mitosis, ciliogenesis and nucleokinesis correlates with variable mutant cerebral phenotypes.

Project description:Recessive mutations in RTTN, encoding centrosome associated protein Rotatin, were originally identified as cause of polymicrogyria, a cortical malformation. With time a wide variety of other brain malformations has been ascribed to RTTN mutations, such as primary microcephaly. However, the function of Rotatin is largely unknown and the molecular disease mechanism underlying these malformations has not yet been elucidated. Here, we report four novel families identified by high throughput sequencing, one of them with a novel deep intronic variant. We reviewed RTTN-related disease phenotypes and defined the spectrum which includes intellectual disability (ID), short stature, microcephaly, lissencephaly, periventricular heterotopia, polymicrogyria and other malformations. Rotatin expression, function and cellular disease phenotype were studied in cultured primary skin fibroblasts from eight unrelated affected individuals. We found that Rotatin deficiency leads to abnormal centrosome amplification during mitosis, resulting in multipolar spindle formation, mitotic failure, increased apoptosis and aneuploidy. In non-dividing healthy cells, Rotatin localizes at the primary cilium, both at basal body and axoneme during ciliogenesis. Interestingly, interphase mutant cells show aberrant ciliogenesis. Proteomics analysis reveals that exogenous Rotatin in HEK293 cells interacts with the non-muscle cellular myosin complex (MYH9-MYH10-MYH14), which is essential for nucleokinesis during neuronal migration. In hiPSC-derived neurons, endogenous Rotatin localizes to the leading edge centrosome, which pulls the perinuclear cage during nucleokinesis, suggesting a pivotal role of Rotatin in neuronal migration. This study sheds light on the pleiotropic cellular functions of Rotatin, explaining disease spectrum linked to both neuronal proliferation and migration.

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H2A.Z Mapping During G0/G1 and Mitosis

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