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Identification of Setdb1 interaction proteins in neural stem cells

ABSTRACT: Setdb1 is an epigenetic factors catalyzing modification of H3K9me3. Expression of its gene is localized to embryonic neural cells during vertebrate embryogenesis, suggesting its role in regulating neural stemness. The project is to identify the interaction partners of Setdb1, by which Setdb1 regulates neural stemness in neural stem cells.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture

SUBMITTER: Ying Cao

LAB HEAD: Ying Cao

PROVIDER: PXD030453 | Pride | 2022-08-12

REPOSITORIES: Pride

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			Action	DRS
	20210113_08.wiff	Wiff
	20210113_08.wiff.scan	Wiff
	20210113_08_Cao_Ying_NE4C_IgG_ProteinSummary.txt	Txt
	20210113_09.wiff	Wiff
	20210113_09.wiff.scan	Wiff

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Publications

Neural stemness unifies cell tumorigenicity and pluripotent differentiation potential.

Zhang Min M Liu Yang Y Shi Lihua L Fang Lei L Xu Liyang L Cao Ying Y

The Journal of biological chemistry 20220604 7

Neural stemness is suggested to be the ground state of tumorigenicity and pluripotent differentiation potential. However, the relationship between these cell properties is unclear. Here, by disrupting the neural regulatory network in neural stem and cancer cells and by serial transplantation of cancer cells, we show that tumorigenicity and pluripotent differentiation potential are coupled cell properties unified by neural stemness. We show that loss of neural stemness via inhibition of SETDB1, a ...[more]

PMID: 35671824

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KDM4C epigenetically regulates and forms a feed-forward loop with ALDH1A3 to maintain gastric cancer stemness

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Post-transcriptional control of a stemness signature by RNA-binding 8 protein MEX3A regulates adult neurogenesis

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Impact of graded calorie restriction on mouse liver protein expression

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Genome-wide maps of chromatin state in wild-type and SetDB1 induced knockout mESCs

Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in mammalian cells and characterized genome-wide SetDB1 binding and H3K9 trimethylation (H3K9me3) profiles in mouse ES cells and uncovered two distinct classes of SetDB1 binding sites, termed solo and ensemble peaks. The solo peaks were devoid of H3K9me3 and enriched near developmental regulators while the ensemble peaks were associated with H3K9me3. A subset of the SetDB1 solo peaks, particularly those near neural development related genes, was found to be associated with Polycomb Repressive Complex 2 (PRC2) as well as PRC2-interacting proteins Jarid2 and Mtf2. Genetic deletion of Setdb1 dramatically reduced Ezh2 binding as well as histone 3 lysine 27 (H3K27) trimethylation level at SetDB1 solo peaks and facilitated neural differentiation. Furthermore, we found that H3K27me3 inhibits SetDB1 methyltransferase activity in vitro. The currently identified reciprocal action between SetDB1 and PRC2 reveals a novel mechanism underlying ES cell pluripotency and differentiation regulation. Examination of 2 different histone modifications in 2 cell status.

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