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A global screening identifies chromatin-enriched RNA-binding proteins and the transcriptional regulatory activity of QKI5 during monocytic differentiation

ABSTRACT: Background: Cellular RNA binding proteins (RBPs) have multiple roles in post-transcriptional control, and some have been shown to bind DNA. However, the global localization and the general chromatin-binding ability of RBPs have not been well-characterized and remain undefined in hematopoietic cells. Results: We first provided a full view of RBPs’ distribution pattern in nucleus and screened for chromatin-enriched RBPs (Che-RBPs) in different human cells. Subsequently, by generating ChIP-seq, CLIP-seq and RNA-seq datasets and conducting combined analysis, the transcriptional regulatory potential of certain hematopoietic Che-RBPs were predicted and from which quaking (QKI5) emerged as a potential transcriptional activator during monocytic differentiation. QKI5 was over-represented in gene promoter regions, independent of RNA or transcription factors. Furthermore, promoter-occupied QKI5 activated the transcription of several critical monocytic differentiation-associated genes, including CXCL2, IL16 and PTPN6. Finally, we showed that the differentiation-promoting activity of QKI5 is largely dependent on CXCL2, irrespective of its RNA-binding capacity. Conclusions: Our study indicates that Che-RBPs are versatile factors that orchestrate gene expression in different cellular contexts, and identifies QKI5, a classic RBP regulating RNA processing, as a novel transcriptional activator during monocytic differentiation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE178800 | GEO | 2023/06/23

REPOSITORIES: GEO

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Nuclear fractionation reveals chromatin-enriched RNA binding proteins and transcriptional regulatory activity of QKI5 during monocytic differentiation

Project description:Background: Cellular RNA binding proteins (RBPs) have multiple roles in post-transcriptional control, and some are shown to bind DNA. However, the global localization and the general chromatin-binding ability of RBPs are not well-characterized and remain undefined in hematopoietic cells. Results: We first provide a full view of RBPs' distribution pattern in the nucleus and screen for chromatin-enriched RBPs (Che-RBPs) in different human cells. Subsequently, by generating ChIP-seq, CLIP-seq and RNA-seq datasets and conducting combined analysis, the transcriptional regulatory potential of certain hematopoietic Che-RBPs are predicted. From this analysis, quaking (QKI5) emerges as a potential transcriptional activator during monocytic differentiation. QKI5 is over-represented in gene promoter regions, independent of RNA or transcription factors. Furthermore, DNA-bound QKI5 activates the transcription of several critical monocytic differentiation-associated genes, including CXCL2, IL16 and PTPN6. Finally, we show that the differentiation promoting activity of QKI5 is largely dependent on CXCL2, irrespective of its RNA binding capacity. Conclusions: Our study indicates that Che-RBPs are versatile factors that orchestrate gene expression in different cellular contexts, and identifies QKI5, a classic RBP regulating RNA processing, as a novel transcriptional activator during monocytic differentiation.

2021-09-09 | GSE161943 | GEO

QKI5-regulated miRNAs

Project description:microRNAs (miRNAs) accomplish a remarkable variety of biological functions. Their expression is tightly controlled, and the final production of a miRNA is dependent on the cooperation of multiple mechanisms and their net effect. Here we show that miR-124-1 is transcriptionally activated during erythroid differentiation by GATA-1, however its post-transcriptional processing is attenuated. We found that QKI5 binds to a distal QKI response element (QRE) embedded in the primary transcript of miR-124-1 (pri-124-1) and modulates Microprocessor function by direct association with DGCR8. Strikingly, Microprocessor recruitment to pri-124-1 is disrupted upon RNAi-mediated depletion of QKI5, consistent with the decrease in mature miR-124. Moreover, addition of QKI5 increases the conversion efficiency of pri-124-1 in cell-free extracts. For erythropoiesis, the decreased QKI5 leads to attenuated Microprocessor-mediated processing of pri-124-1, which confers the exquisite miRNA abundance necessary for development. This regulation also gives rise to a unique miRNA signature required for normal erythropoiesis. Thus, this QKI5-regulated miRNA processing may represent a common paradigm for erythroid development, and specifically, it may serve as a post-transcriptional fault security to prevent misexpression of certain miRNAs, that is essential for the establishment of particular gene expression patterns during development. Two samples are analyzed: K562 cells transduced with GFP lentivirus; and K562 cells transduced with QKI5-overexpressing lentivirus.

2015-05-06 | E-GEOD-57363 | biostudies-arrayexpress

QKI5-regulated miRNAs

2015-05-06 | GSE57363 | GEO

Nuclear fractionation reveals chromatin-enriched RNA binding proteins and transcriptional regulatory activity of QKI5 during monocytic differentiation

Project description:Nuclear fractionation reveals chromatin-enriched RNA binding proteins and transcriptional regulatory activity of QKI5 during monocytic differentiation

| PRJNA679956 | ENA

Qki5 CLIP in E14.5 mouse brain

Project description:Mouse brains at E14.5 wild-type were subjected to HITS-CLIP to identify Qki5-binding positions on RNA.

2017-12-08 | GSE103247 | GEO

Mass spectrometry (MS) datasets of QKI5 co-immunoprecipitation samples in THP-1 cells

Project description:We performed QKI5 co-immunoprecipitation followed by MS analysis to identify QKI5-interacting proteins in THP-1 cells.

2021-09-27 | PXD028743 | Pride

Expression data from Che-1 (AATF) depleted HCT 116 cell line

Project description:Che-1 is a RNA Polymerase II binding protein involved in the regulation of gene transcription. Che-1 emerges as an important adaptor that connects transcriptional regulation, cell-cycle progression, checkpoint control, and apoptosis. We have observed that Che-1 depletion sensitizes cells to chemotherapy. We used microarrays analysis to investigate classes of genes regulated by Che-1. Total RNA was extracted from control and Che-1 depleted HCT 116 cells 48 hours after transient transfection of siRNA.

2013-03-12 | E-GEOD-45009 | biostudies-arrayexpress

Expression data from Che-1 (AATF) depleted HCT 116 cell line

2013-03-12 | GSE45009 | GEO

AATF interactome in human Kms27 cells

Project description:Multiple myeloma is a hematological neoplasm of plasma cells characterized by an abnormal production of immunoglobulins. Che-1/AATF (Che-1) is an RNA binding protein involved in transcription regulation and highly expressed in this malignancy. In order to better characterize its functions in this type of disease, we performed co-immunoprecipitation experiments coupled with a mass-spec analysis by using total MM Kms27 cell lysates. From this analysis we were able to identify more than 600 proteins significantly enriched in Che-1 precipitates. As expected from its role in ribosomal RNA maturation, the Che-1 interactome contains numerous proteins involved in pre-rRNA processing and several ribosomal proteins. Notably, among other proteins interacting with Che-1, we identified many essential components of the paraspeckle which play an important role in the regulation of gene expression.

2022-08-03 | PXD026659 | Pride

Che-1 modulates the decision between cell cycle arrest and apoptosis by its binding to p53.

Project description:The tumor suppressor p53 is mainly involved in the transcriptional regulation of a large number of growth-arrest- and apoptosis-related genes. However, a clear understanding of which factor/s influences the choice between these two opposing p53- dependent outcomes remains largely elusive. We have previously described that in response to DNA damage, the RNA polymerase II binding protein Che-1/AATF transcriptionally activates p53. Here, we show that Che-1 binds directly p53. This interaction essentially occurs in the first hours of DNA damage, whereas it is lost when cells undergo to apoptosis in response to post-transcriptional modifications. Moreover, Che-1 sits in a ternary complex with p53 and the oncosuppressor Brca1. Accordingly, our analysis of genome-wide chromatin occupancy by p53 revealed that p53/Che1 interaction results in preferential transactivation of growth-arrest p53 target genes over its pro-apoptotic target genes. Notably, exposure of Che-1+/- mice to ionizing radiations resulted in enhanced apoptosis of thymocytes, compared to wild-type mice. These results confirm Che-1 as an important regulator of p53 activity and suggest Che-1 to be a promising yet attractive drug target for cancer therapy.

2015-06-01 | GSE60267 | GEO

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