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MacroH2A2 modulates the self-renewal of glioblastoma cells

ABSTRACT: MacroH2A2 modulates the self-renewal of glioblastoma cells

PROVIDER: PRJNA873932 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21209133_1.fastq.gz	Fastqsanger.gz
	SRR21209133_2.fastq.gz	Fastqsanger.gz
	SRR21209134_1.fastq.gz	Fastqsanger.gz
	SRR21209134_2.fastq.gz	Fastqsanger.gz
	SRR21209135_1.fastq.gz	Fastqsanger.gz

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MacroH2A2 modulates the self-renewal of glioblastoma cells

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Project description:Cell lines geneticially engineered to undergo conditional asymmetric self-renewal were used to identify genes whose expression is asymmetric self-renewal associated (ASRA). Non-random sister chromatid segregation occurs concordantly with asymmetric self-renewal in these cell lines. Asymmetric self-renewal occurs when murine embryo fibroblasts that are otherwise p53-null are induced to express physiological levels of wildtype p53 protein (Asym). To distinguish p53-responsive genes that also require induction of asymmetric self renewal (i.e., ASRA genes) and/or non-random sister chromatid segregation for change, an additional control cell line, which continues to symmetrically self-renew (with random sister chromatid segregation) even when p53 is induced, was also compared (Symp53). This congenic cell line constitutively expresses the type II inosine monophosphate dehydrogenase (IMPDH II; the rate-limiting enzmye for guanine ribonucleotide biosynthesis) and, thereby, prevents p53-induced asymmetric self-renewal and non-random sister chromatid segregation. Three biological replicates of asymmetrically self-renewing cultures (Asym1-3) were compared with cultures that were symmetrically self-renewing - either because they did not express p53 (3 biological replicates, Sym1-3) or they expressed constitutive IMPDH II (i.e., not regulated by p53) as well as p53 (2 biological replicates, Symp53_1 and 2.)

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