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Expression data from Fus/TLS-null KSL hematopoietic stem/progenitor cells

ABSTRACT: Fus is the gene for a member of the FET family of RNA-binding proteins often involved in chromosomal translocations to generate oncogenic fusion genes in human cancers. Fus participates in multiple cellular functions, including RNA processing and transport, transcriptional regulation, and genome integrity. We uncovered its critical role in the maintenance of hematopoietic stem cells (HSCs). Fus-/- fetal livers developed normally except for a mild reduction in numbers of colony-forming cells compared to the wild type. The proliferation and differentiation of Fus-/- hematopoietic progenitors were normal in vitro. However, the number of colony-forming cells present in long-term cocultures of Fus-/- hematopoietic progenitors and stromal cells was significantly reduced. Fus-/- HSCs had an impaired long-term repopulating capacity and failed to repopulate in tertiary recipient mice. Fus-/- HSCs were highly susceptible to radiation both in vitro and in vivo and showed retardation of radiation-induced DNA damage repair. These findings define Fus as a novel regulator of HSCs and implicate it in stress-resistance and maintenance of the genomic integrity of HSCs. Therefore, it would be of importance to analyze the gene expression profiles of Fus-knockout hematopoietic stem/progenitor cells to understand its role in HSCs.

ORGANISM(S): Mus musculus

PROVIDER: GSE18853 | GEO | 2009/11/03

SECONDARY ACCESSION(S): PRJNA121095

REPOSITORIES: GEO

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Expression data from Fus/TLS-null KSL hematopoietic stem/progenitor cells

Project description:Fus is the gene for a member of the FET family of RNA-binding proteins often involved in chromosomal translocations to generate oncogenic fusion genes in human cancers. Fus participates in multiple cellular functions, including RNA processing and transport, transcriptional regulation, and genome integrity. We uncovered its critical role in the maintenance of hematopoietic stem cells (HSCs). Fus-/- fetal livers developed normally except for a mild reduction in numbers of colony-forming cells compared to the wild type. The proliferation and differentiation of Fus-/- hematopoietic progenitors were normal in vitro. However, the number of colony-forming cells present in long-term cocultures of Fus-/- hematopoietic progenitors and stromal cells was significantly reduced. Fus-/- HSCs had an impaired long-term repopulating capacity and failed to repopulate in tertiary recipient mice. Fus-/- HSCs were highly susceptible to radiation both in vitro and in vivo and showed retardation of radiation-induced DNA damage repair. These findings define Fus as a novel regulator of HSCs and implicate it in stress-resistance and maintenance of the genomic integrity of HSCs. Therefore, it would be of importance to analyze the gene expression profiles of Fus-knockout hematopoietic stem/progenitor cells to understand its role in HSCs. Purified wild-type and Fus–/– KSL cells from BM of recipient mice repopulated with wild-type and Fus–/– fetal liver cells were subjected to RNA extraction and hybridization on Affymetrix microarrays. Data were obtained from dublicate samples.

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