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Rbm24 functions as a critical translational regulator to pretect crystallin proteins accumulation for lens transparency. RNA-seq data of 33 hpf rbm24a-/- and wildtype embryo, head explant

ABSTRACT: Rbm24 functions as a critical translational regulator to pretect crystallin proteins accumulation for lens transparency. RNA-seq data of 33 hpf rbm24a-/- and wildtype embryo, head explant

PROVIDER: PRJNA560923 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10004188_1.fastq.gz	Fastqsanger.gz
	SRR10004188_2.fastq.gz	Fastqsanger.gz
	SRR10004189_1.fastq.gz	Fastqsanger.gz
	SRR10004189_2.fastq.gz	Fastqsanger.gz

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Rbm24 functions as a critical translational regulator to pretect crystallin proteins accumulation for lens transparency. RNA-seq data of 33 hpf rbm24a-/- and wildtype embryo, head explant

Project description:This experiment is aimed to compare the transcriptomes of rbm24a mutant and wildtype at 33 hpf. As Rbm24a is an RNA binding protein, this comparation is suitable to obtain information on differential gene expression and alternative splicing. We found that the expression of most of the crystallin genes and many other lens specific genes are down regulated in rbm24a mutant, without changes in splicing patterns.

2020-02-29 | GSE136003 | GEO

Rbm24 functions as a critical translational regulator to pretect crystallin proteins accumulation for lens transparency. RNA-seq data of 33 hpf rbm24a-/- and wildtype zebrafish embryo

2020-02-29 | GSE136006 | GEO

Rbm24 functions as a critical translational regulator to pretect crystallin proteins accumulation for lens transparency. RNA-seq data of 33 hpf rbm24a-/- and wildtype zebrafish embryo

Project description:Rbm24 functions as a critical translational regulator to pretect crystallin proteins accumulation for lens transparency. RNA-seq data of 33 hpf rbm24a-/- and wildtype zebrafish embryo

| PRJNA560932 | ENA

rbm24a is an organizer component of germ plasm to determine germ cell fate

Project description:The formation of germ cells is a critical issue for the continuation of species. A large group of animals follow a preformation strategy to generate their primordial germ cells (PGCs). They produce a set of localized maternal mRNAs and proteins to form phase-separated germ plasm that functions as the PGC determinants, but the mechanisms underlying the assembly of germ plasm is poorly understood. This study identifies Rbm24a as an enssential localized germ plasm protein component that controls the formation of large and functional germ plasm granules. Rbm24a is complexed with Buc and interacts with germ plasm mRNAs, which determines the specific grasp of germ plasm mRNAs into the phase-separated aggregates. Rbm24a-absent granules fail to undergo kinesin-dependent transport towards the cleavage furrows, where small particles fuse into large ones. The loss of maternal rbm24a causes the complete degradation of germ plasm components and the disappearance of PGCs, resulting in totally sterile animals. Our work establishes that Rbm24 is a critical nucleating organizer component of germ plasm, highlighting an emerging common mechanism to read and recruit RNA component into phase-separated condensates.

2025-01-24 | GSE267406 | GEO

rbm24a is an organizer component of germ plasm to determine germ cell fate

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rbm24a is an organizer component of germ plasm to determine germ cell fate (202409 validation)

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Induced of RBM24 expression effect on nasopharyngeal carcinoma cells

Project description:RNA-binding proteins (RBPs) are key components in the determination of miRNA function, as they control different stages of miRNA biogenesis and their localization, degradation and activity. To further investigate the underlying mechanisms of RBM24 in nasopharyngeal carcinoma (NPC) carcinogenesis, we compared the miRNA expression profiles in RBM24 induced and control cells by using human miRNA microarray. Microarray analysis identified 11 commonly upregulated and 12 commonly downregulated miRNAs in RBM24 induced cells. Among the 23 miRNAs, miR-25 ranked highest of all the commonly upregulated genes sorted in ascending order according to fold change values. RBM24 expression was controlled by tetracycline-off system in NPC cells. microRNA profiling of RBM24 expression induced cells vs. repressed cells: The expression of RBM24 in HONE-1, 5-8F, and CNE-2 cells was induced by removing doxycycline or repressed by adding doxycycline.

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Rbm24 dictates mRNA recruitment for germ plasm assembly

Project description:Ribonucleoprotein (RNP) granules are the most common membrane-less biomolecular condensates. However, the mechanisms underlying their assembly are largely unknown. The aggregation of germ plasm determines the fate of primordial germ cells (PGCs) and serves as a model for RNP granule assembly. Here, we show that maternal RNA binding protein Rbm24a is the key factor governing specific sorting of mRNAs. Mechanistically, Rbm24a complexes with Buc and interacts to dictate the specific grasp of germ plasm mRNAs into phase-separated condensates. Germ plasm particles lacking Rbm24a and mRNAs fail to undergo kinesin-dependent transport towards the cleavage furrows where small granules fuse into large aggregates. Therefore, the loss of maternal Rbm24a causes a complete degradation of germ plasm and the disappearance of PGCs. These findings demonstrate that Rbm24a functions as a nucleating organizer of the germ plasm, highlighting an emerging mechanism for RNA-binding proteins in reading and recruiting RNA components into the phase-separated protein scaffold.

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AAV9 mediated overexpression of Rbm24 in wildtype C57/Bl6 mice

Project description:The RNA-binding protein Rbm24 has recently been identified as a pivotal splicing factor in the developing heart. Loss of Rbm24 in mice disrupts cardiac development by governing a large number of muscle- specific splicing events. Since Rbm24 knockout mice are embryonically lethal, the role of Rbm24 in the adult heart remained unexplored. Here, we used adeno-associated viruses (AAV9) to investigate the effect of increased Rbm24 levels in adult mouse heart. Using high-resolution microarrays, we found 893 differentially expressed genes and 1102 differential splicing events in 714 genes in hearts overexpressing Rbm24. We found splicing differences in cardiac genes, such as PDZ and Lim domain 5, Phospholamban, and Titin, but did not find splicing differences in previously identified embryonic splicing targets of Rbm24, such as skNAC, αNAC, and Coro6. Gene ontology enrichment analysis demonstrated increased expression of extracellular matrix (ECM)-related and immune response genes. Moreover, we found increased expression of Tgfβ-signaling genes, suggesting enhanced Tgfβ-signaling in these hearts. Ultimately, this increased activation of cardiac fibroblasts, as evidenced by robust expression of Periostin in the heart, and extensive cardiac fibrosis. These results indicate that Rbm24 may function as a regulator of cardiac fibrosis, potentially through the regulation of TgfβR1 and TgfβR2 expression.

2018-07-16 | GSE110991 | GEO

Induced of RBM24 expression effect on nasopharyngeal carcinoma cells

2016-03-13 | GSE66878 | GEO