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Gene expression analysis in HeLa Kyoto cells upon knockdown of JAZF1

ABSTRACT: The goal was the investigation of JAZF1's possible role in regulating gene expression. RNA-seq analysis revealed that depletion of JAZF1 results in transcriptome changes that affect, among others, ribosome biogenesis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE163214 | GEO | 2021/01/16

REPOSITORIES: GEO

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Genome-wide ChIP-seq analysis of H2A.Z and H2A.Zac in HeLa Kyoto cells upon knockdown of JAZF1

Project description:The goal was to investigate genome-wide if JAZF1 influences the deposition as well as the acetylation of the histone variant H2A.Z. ChIP-seq analysis revealed that depletion of JAZF1 leads to reduced acetylation of H2A.Z at specific sites.

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Gene expression analysis in HeLa Kyoto cells upon knockdown of JAZF1

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Genome-wide ChIP-seq analysis of H2A.Z and H2A.Zac in HeLa Kyoto cells upon knockdown of JAZF1

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Small molecule RBI2 disrupts ribosome biogenesis through pre-rRNA depletion

Project description:In all domains of life, the rate of protein synthesis is directly linked to the rates of cell growth and proliferation. Consequently, highly proliferative cancer cells are especially sensitive to perturbations in ribosome biogenesis. While ribosome synthesis and cancer have a well-established relationship, only recently has ribosome biogenesis drawn interest as a cancer therapeutic target. Here, we have exploited the relationship between ribosome biogenesis and cancer cell proliferation by using a potent ribosome biogenesis inhibitor: RBI2 (Ribosome Biogenesis Inhibitor 2) to perturb cancer cell growth and viability. We demonstrate that RBI2 significantly decreases cell viability in malignant melanoma cells and breast cancer cell lines. Treatment with RBI2 dramatically and rapidly decreases ribosomal RNA (rRNA) synthesis, without affecting the occupancy of RNA polymerase I (Pol I) on the ribosomal DNA template. Next-generation RNA sequencing (RNA-seq) reveals that RBI2 and previously described ribosome biogenesis inhibitor CX-5461 induce distinct changes in the transcriptome. Investigation of the content of the pre-rRNAs through RT-qPCR reveals an increase in polyadenylation of cellular rRNA after treatment with RBI2, a known pathway by which rRNA degradation occurs. Northern blotting revealed that RBI2 does not appear to impair or alter rRNA processing. Collectively, these data suggest that RBI2 inhibits rRNA synthesis distinctly from other previously described ribosome biogenesis inhibitors, potentially through a novel pathway that upregulates turnover of premature rRNAs.

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