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The abundantly expressed microRNA locus miR-144/451 regulates only about 100 target mRNAs during erythroid development

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE104455 | GEO | 2018/10/01

REPOSITORIES: GEO

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The abundantly expressed microRNA locus miR-144/451 regulates only about 100 target mRNAs during erythroid development (HITS-CLIP)

Project description:MicroRNAs inhibit gene expression by recruiting the RNA-induced silencing complex (RISC) to mRNAs in a process termed RNA interference (RNAi). While it is generally accepted that RNAi modulates gene expression pervasively, the number of mRNAs bound and repressed by miRNAs in vivo in individual cell types remains unknown, with estimates ranging from a few hundred genes to many thousands. We examined microRNA activities in primary cells by combining genetic loss of function with RNA-sequencing, quantitative proteomics and High-Throughput Sequencing of RNA isolated by Crosslinking Immunoprecipitation (HITS-CLIP), focusing on miR-144/451, the most highly expressed microRNA locus during red blood cell (RBC) formation. We show that Argonaute (Ago) protein binds over one thousand different mRNAs in a miR-144/451-dependent manner, accounting for one third of all Ago-bound mRNAs. However, only about 100 mRNAs are stabilized in RBC precursors after ablation of the miR-144/451 locus. Thus, Ago-miRNA complexes destabilize only a small subset of bound mRNAs, probably no more than a few hundred in erythroblasts under physiological conditions. Our integrated approach identified more than 50 new miR-144/451 target mRNAs, including Cox10, which facilitates assembly of the mitochondrial cytochrome c oxidase (COX) electron transport complex. Loss of miR-144/451 resulted in increased Cox10 expression, accumulation of the COX complex, and increased mitochondrial membrane potential with no change in mitochondrial mass. Thus, miR-144/451 represses mitochondrial respiration during erythropoiesis by inhibiting Cox10.

2018-10-01 | GSE104357 | GEO

The abundantly expressed microRNA locus miR-144/451 regulates only about 100 target mRNAs during erythroid development [RNA-seq]

2018-10-01 | GSE104447 | GEO

The abundantly expressed microRNA locus miR-144/451 regulates only about 100 target mRNAs during erythroid development [miRNA-seq]

2018-10-01 | GSE104441 | GEO

The miR-144/451 locus is required for erythroid homeostasis.

Project description:The process of erythropoiesis must be efficient and robust to supply the organism with red bloods cells both under condition of homeostasis and stress. The microRNA (miRNA) pathway was recently shown to regulate erythroid development. Here, we show that expression of the locus encoding miR-144 and miR-451 is strictly dependent on Argonaute 2 and is required for erythroid homeostasis. Mice deficient for the miR-144/451 cluster display a cell autonomous impairment of late erythroblast maturation, resulting in erythroid hyperplasia, splenomegaly, and a mild anemia. Analysis of gene expression profiles from wild-type and miR-144/451-deficient erythroblasts revealed that the miR-144/451 cluster acts as a "tuner" of gene expression, influencing the expression of many genes. MiR-451 imparts a greater impact on target gene expression than miR-144. Accordingly, mice deficient in miR-451 alone exhibited a phenotype indistinguishable from miR-144/451-deficient mice. Thus, the miR-144/451 cluster tunes gene expression to impart a robustness to erythropoiesis that is critical under conditions of stress.

| S-EPMC2901075 | biostudies-literature

The abundantly expressed microRNA locus miR-144/451 regulates only about 100 target mRNAs during erythroid development

Project description:The abundantly expressed microRNA locus miR-144/451 regulates only about 100 target mRNAs during erythroid development

| PRJNA412654 | ENA

The abundantly expressed microRNA locus miR-144/451 regulates only about 100 target mRNAs during erythroid development (HITS-CLIP)

Project description:The abundantly expressed microRNA locus miR-144/451 regulates only about 100 target mRNAs during erythroid development (HITS-CLIP)

| PRJNA412642 | ENA

The abundantly expressed microRNA locus miR-144/451 regulates only about 100 target mRNAs during erythroid development [RNA-seq]

Project description:The abundantly expressed microRNA locus miR-144/451 regulates only about 100 target mRNAs during erythroid development [RNA-seq]

| PRJNA412651 | ENA

The abundantly expressed microRNA locus miR-144/451 regulates only about 100 target mRNAs during erythroid development [miRNA-seq]

Project description:The abundantly expressed microRNA locus miR-144/451 regulates only about 100 target mRNAs during erythroid development [miRNA-seq]

| PRJNA412643 | ENA

CAP1, a target of miR-144/451, negatively regulates erythroid differentiation and enucleation.

Project description:The exact molecular mechanism underlying erythroblast enucleation has been a fundamental biological question for decades. In this study, we found that miR-144/451 critically regulated erythroid differentiation and enucleation. We further identified CAP1, a G-actin-binding protein, as a direct target of miR-144/451 in these processes. During terminal erythropoiesis, CAP1 expression declines along with gradually increased miR-144/451 levels. Enforced CAP1 up-regulation inhibits the formation of contractile actin rings in erythroblasts and prevents their terminal differentiation and enucleation. Our findings reveal a negative regulatory role of CAP1 in miR-144/451-mediated erythropoiesis and thus shed light on how microRNAs fine-tune terminal erythroid development through regulating actin dynamics.

| S-EPMC7933962 | biostudies-literature

Transcriptome analysis of miR-144/451-null bone marrow erythroid cells

Project description:microRNA miR-144/451 is highly expressed during erythropoiesis. We deleted the miR-144/451 gene locus in mice and compared the transcriptomes of miR-144/451-null bone marrow erythroid precursors to stage-matched wild-type control cells.

2010-07-15 | GSE21041 | GEO

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