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Role of RBMX in the post-transcriptional control of homeotic genes

ABSTRACT: Role of RBMX in the post-transcriptional control of homeotic genes

PROVIDER: PRJNA485413 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7695680.fastq.gz	Fastqsanger.gz
	SRR7695690.fastq.gz	Fastqsanger.gz
	SRR7695700.fastq.gz	Fastqsanger.gz
	SRR7695710.fastq.gz	Fastqsanger.gz
	SRR7695681.fastq.gz	Fastqsanger.gz

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Role of RBMX in the post-transcriptional control of homeotic genes

Project description:Wild-type and RBMX-knockdown HEK293 cells where profiled at the transcriptome and translatome levels for the expression of 50 homeotic genes. Targeted RNA-seq libraries were built and sequenced on an Illumina MiSeq machine to allow for accurate gene expression quantification of this specific set of genes. To assess the binding of RBMX to the same set of mRNAs, RNA immunoprecipitation was also performed on HIS-HA tagged RBMX expressing HEK293 cells.

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Project description:RNA binding proteins (RBPs) are key arbiters of post-transcriptional regulation that have been found to be dysregulated in hematological malignancies. Here, we identify the RBP RBMX and its retrogene RBMXL1 to be required for murine and human myeloid leukemogenesis. RBMX/L1 are overexpressed in acute myeloid leukemia (AML) primary patients compared to healthy individuals, and RBMX/L1 loss delayed leukemia development. Complex chromosomal karyotyping analysis and assay for transposase-accessible chromatin sequencing demonstrated that RBMX/L1 loss led to significant changes in chromatin accessibility and compaction. We found that RBMX/L1 directly binds to mRNAs and affects transcription of multiple loci, including the heterochromatin protein 1 alpha (HP1a) mRNA. Using single molecule resolution RNA fluorescence in situ hybridization, we uncovered that RBMX/L1 controls the nascent transcription of the HP1a locus. Forced HP1a expression rescued the RBMX/L1 depletion effects on cell growth and apoptosis. Overall, we determine that RBMX/L1 control leukemia cell survival by regulating chromatin state through its downstream target HP1a. These findings illuminate a novel mechanism for RBPs directly promoting transcription and suggest RBMX/L1 as well as HP1a as potential novel therapeutic targets in myeloid malignancies.

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