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Microarray analysis of differential gene expression of whole testis extracts from transgenic Musashi-2 and transgenic Musashi-1 over-expression mice

ABSTRACT: Analysis of testis-specific over-expression of Musashi-1 and Musashi-2 at gene expression level. The hypothesis tested in the present study was that testis-specific over-expression of Musashi-1/Musashi-2 would result in differential gene expression profiles from the Wildtype control. Results provide important information of the genes affected by Musashi-2 overexpression during spermatogenesis. Total RNA obtained from whole adult testis of transgenic testis-specfic Musashi-1 and Musashi-2 overexpression mice compared to Wildtype (control) littermates. 4 replicates, 16 samples, 2 comparisons: Wt (Musashi-1) vs. TgMsi1 & Wt (Musashi-2) vs. TgMsi2

ORGANISM(S): Mus musculus

SUBMITTER: Jessie Sutherland

PROVIDER: E-GEOD-59358 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Microarray analysis of differential gene expression of whole testis extracts from transgenic Musashi-2 and transgenic Musashi-1 over-expression mice

Project description:Analysis of testis-specific over-expression of Musashi-1 and Musashi-2 at gene expression level. The hypothesis tested in the present study was that testis-specific over-expression of Musashi-1/Musashi-2 would result in differential gene expression profiles from the Wildtype control. Results provide important information of the genes affected by Musashi-2 overexpression during spermatogenesis.

2014-07-12 | GSE59358 | GEO

Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE16432: MSI2 regulates hematopoiesis and accelerates leukemogenesis GSE22773: Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (LK and MS12-inducible) GSE22774: Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (LSK and LK) GSE22775: Musashi 2 regulates normal hematopoiesis and accelerates leukemogenesis (Leukemia cell lines) Refer to individual Series

2010-07-21 | E-GEOD-22778 | biostudies-arrayexpress

Musashi interaction with poly(A) binding protein is required for activation of target mRNA translation

Project description:The Musashi family of mRNA translational regulators control both physiological and pathological stem cell self-renewal primarily by repressing targets that promote differentiation. In response to differentiation cues, Musashi can switch from a repressor to an activator of target mRNA translation. However, the molecular events that distinguish Musashi-mediated translational activation from repression are not understood. We have previously reported that Musashi function is required for the maturation of Xenopus oocytes, and specifically for translational activation of specific dormant maternal mRNAs. Here, we employed mass spectrometry to identify cellular factors necessary for Musashi-dependent mRNA translational activation. We report a requirement for association of Musashi1 with the embryonic poly(A) binding protein (ePABP) or the canonical somatic cell poly(A) binding protein PABPC1 for activation of Musashi target mRNA translation. Co-immunoprecipitation studies demonstrated an increased Musashi1 interaction with ePABP during oocyte maturation. Attenuation of endogenous ePABP activity severely compromised Musashi function, preventing downstream signaling and blocking oocyte maturation. Recovery of Musashi-dependent mRNA translational activation and maturation of ePABP attenuated oocytes was achieved through ectopic expression of either ePABP or PABPC1. Consistent with the findings in Xenopus oocytes, PABPC1 remained associated with Musashi under conditions of Musashi target mRNA de-repression and translation during mammalian stem cell differentiation. Since association of Musashi1 with poly(A) binding proteins has previously only been implicated in repression of Musashi target mRNAs, our findings reveal distinct context-dependent roles for the interaction of Musashi with poly[A] binding protein family members in response to extracellular cues that control cell fate.

2019-05-31 | PXD013585 | Pride

Insight into integrated control of pituitary function revealed through analysis of Musashi target mRNAs

Project description:The anterior pituitary is comprised of distinct cell types that each secrete specific hormones to control a variety of biological processes including growth, metabolism, reproduction and stress responses. The anterior pituitary shows a remarkable level of cell type plasticity that allows shifts in hormone producing populations to meet organismal demands. Pituitary cell plasticity is tightly regulated and both deficiency in cell plasticity and excessive cell plasticity are associated with common pituitary pathologies. The molecular mechanisms underlying this plasticity are not well characterized but recent work has implicated the stem cell determinants and sequence-specific mRNA binding proteins of the Musashi family as regulators of adult pituitary hormone production. In this study we have sought to identify the full range of Musashi target mRNAs in the adult mouse pituitary. Using Musashi RNA immunoprecipitation we identify a cohort of 1192 mRNAs that show specific Musashi binding. These include mRNAs restricted to discrete hormone-producing cell lineages as well as mRNAs associated with stem and progenitor cells. The processes influenced by the proteins encoded by the Musashi-associated mRNAs include cellular homeostasis, protein trafficking and secretion, unfolded protein response, endocrine processes and female pregnancy. Functional analysis of validated mRNA regulatory 3' untranslated regions (3’ UTRs) reveals UTR-specific positive or negative control by the Musashi proteins within the same cellular context. Together, our findings indicate a broad role for Musashi proteins in the control of pituitary function.

2023-07-31 | GSE199098 | GEO

Musashi proteins are post-transcriptional regulators of the epithelial-luminal cell state

Project description:mRNA-seq and ribosome profiling of neural stem cells overexpressing or knocked out for Musashi RNA-binding proteins Study of the global effects of Musashi (Msi) proteins on the transcriptome of embryonic neural stem cells. Neural stem cells were derived from brains of E12.5 or E13.5 embryos engineered to have inducible Msi1 or Msi2 genes, or from embryos with double floxed alleles of Msi1 and Msi2 carrying a Tamoxifen-induclble Cre (CreER). The overexpression mice were made using the Flp-in system (OpenBioSystems), where a cDNA of interest (in this case Msi1 or Msi2) is knocked into the Collagen (Col1A1) locus. The expression of the cDNA of interest is driven by m2rTTA that is knocked into the Rosa26 locus (R26). KH2 describes a strain containing the R26-m2rTTA but lacking Msi1 or Msi2 cDNA. MSI1 describes a strain containing R26-m2rTTA and Msi1 cDNA in Col1A1. MSI2 describes a strain containing R26-m2rTTA and Msi2 cDNA in Col1A1. C1 describes a strain lacking the CreER allele but containing double floxed alleles of Msi1/Msi2 (used as Tamoxifen control). C4 describes a strain carrying the CreER allele and double floxed alleles of Msi1/Msi2.

2014-06-13 | E-GEOD-58423 | biostudies-arrayexpress

Musashi-type translational regulator controls the buildup of secondary cell wall in Arabidopsis

Project description:Deciphering the mechanism of secondary cell wall/SCW formation in vascular plants is key to understanding their development and the molecular basis of biomass recalcitrance. Although a sophisticated network of transcription factors has been implicated in SCW synthesis in plants, little is known about the implication of RNA-binding proteins in this process. Here we report that two RNA-binding proteins homologous to the animal translational regulator Musashi, Musashi-Like2/MSIL2 and Musashi-Like4/MSIL4, function redundantly to control SCW formation in interfascicular fibers and the setting of biomass recalcitrance. We show that the disruption of MSIL2/4 (msil2-4 mutant) decreases the abundance of lignin in fibers and triggers an hypermethylation of glucuronoxylan that is linked to an over-accumulation of GlucuronoXylan Methyltransferase1/3 (GXM1/3) proteins.

2023-09-28 | PXD040020 | Pride

Musashi proteins are post-transcriptional regulators of the epithelial-luminal cell state

Project description:mRNA-seq and ribosome profiling of neural stem cells overexpressing or knocked out for Musashi RNA-binding proteins

2014-06-13 | GSE58423 | GEO

Musashi-1 is a master regulator of aberrant translation in Group 3 medulloblastoma

Project description:Transcripts regulated by Musashi-1 (MSI1) are explored through shRNA-mediated knockdown of MSI1 in SU_MB002 medulloblastoma cells.

2020-02-01 | GSE126337 | GEO

Musashi-1 is a master regulator of aberrant translation in Group 3 medulloblastoma

Project description:Transcripts bound to Musashi-1 (MSI1) are explored in Group 3 medulloblastoma (G3 MB) and neural stem cells harvested from the cerebellar portion of a embryonal brain

2022-10-28 | GSE126263 | GEO

Control of the anterior pituitary cell lineage regulator POU1F1 by the stem cell determinant Musashi

Project description:The high energetic cost of reproduction requires that female fertility be closely linked to metabolic status. However, the mechanisms by which the metabolic and reproductive systems communicate is still largely undefined. We have previously reported that signaling through the major metabolic cytokine leptin controls levels of the pituitary maturation determinant POU1F1 (also referred to as Pit1) that is required for optimal reproductive function. These studies further indicated that leptin increases POU1F1levels in females by promoting Pou1f1 mRNA translation, although the mechanism ofPou1f1 mRNA translation control is unknown. In this study, we report that the stem cell marker and mRNA translational control protein, Musashi, represses translation of the Pou1f1 mRNA. In FACS-sorted purified female somatotropes, Msi1 mRNA and Musashi protein levels are increased in the mouse model that lacks leptin signaling (Gh-CRE leprLepr-null), coincident with the observed attenuation of Pou1f1 mRNA translation. Single-cell RNA sequencing of pituitary cells from control female animals indicates that Msi1 and Pou1f1 mRNAs are co-expressed in Gh-expressing cells and immunocytochemistry analyses of these cells confirms that Musashi protein is present in the GH-containing somatotrope population. We demonstrate that Musashi interacts directly with the Pou1f1 mRNA 3’ UTR and exerts translational repression of a Pou1f1 mRNA translation reporter in vitro, and interacts with the Pou1f1 mRNA in vivo. These findings indicate a critical role for Musashi-mediated mRNA translational regulation in the coordination between metabolic status and the maturation of pituitary somatotropes that is required for optimized reproductive function .

2021-01-11 | GSE153045 | GEO

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