The Msi1-mTOR pathway drives the pathogenesis of Paget's disease
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ABSTRACT:
PROVIDER: PRJNA591571 | ENA |
REPOSITORIES: ENA
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Project description:The translational reactivation of maternal mRNAs encoding the drivers of vertebrate meiosis is accomplished mainly by cytoplasmic polyadenylation. The Cytoplasmic Polyadenylation Elements (CPEs) present in the 3’ UTR of these transcripts, together with their cognate CPE-binding proteins (CPEBs), define a combinatorial code that determines the timing and extent of translational activation upon meiosis resumption. In addition, the RNA-binding protein Musashi1 (Msi1) regulates the polyadenylation of CPE-containing mRNAs by an as yet undefined CPEB-dependent or -independent mechanism. Here we show that Msi1 alone does not support cytoplasmic polyadenylation, but its binding triggers the remodeling of RNA structure, thereby exposing adjacent CPEs and stimulating polyadenylation. Thus, Msi1 directs the preferential use of specific CPEs, which in turn affects the timing and extent of polyadenylation during meiotic progression. Genome-wide analysis of CPEB1- and Msi-associated mRNAs identified 491 common targets, thus revealing a new layer of CPE-mediated translational control.
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Project description:The translational reactivation of maternal mRNAs encoding the drivers of vertebrate meiosis is accomplished mainly by cytoplasmic polyadenylation. The Cytoplasmic Polyadenylation Elements (CPEs) present in the 3’ UTR of these transcripts, together with their cognate CPE-binding proteins (CPEBs), define a combinatorial code that determines the timing and extent of translational activation upon meiosis resumption. In addition, the RNA-binding protein Musashi1 (Msi1) regulates the polyadenylation of CPE-containing mRNAs by an as yet undefined CPEB-dependent or -independent mechanism. Here we show that Msi1 alone does not support cytoplasmic polyadenylation, but its binding triggers the remodeling of RNA structure, thereby exposing adjacent CPEs and stimulating polyadenylation. Thus, Msi1 directs the preferential use of specific CPEs, which in turn affects the timing and extent of polyadenylation during meiotic progression. Genome-wide analysis of CPEB1- and Msi-associated mRNAs identified 491 common targets, thus revealing a new layer of CPE-mediated translational control.
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Project description:Comparison of gene expression in intestinal epithelial cells in the presence or absence of ectopic induction of Msi1 in vivo Total RNA was isolated from preparations of total intestinal epithelial cells taken from the jejunum from 3 control (R26-M2rtTA +doxycycline for 24 hrs) and 3 experimental (TRE-Msi1::R26-M2rtTA +doxycycline for 24 hrs) animals and subjected to profiling on affymetrix Gene 1.0ST arrays
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Project description:Musashi1 (Msi1) is a highly conserved RNA binding protein that is required during the development of the nervous system. Msi1 has a role in neural stem cells, controlling the balance between self-renewal and differentiation. Msi1 has also been implicated in cancer, being highly expressed in multiple tumor types. In this study, we analyzed Msi1 expression in a large cohort of medulloblastoma samples and showed that Msi1 is highly expressed in tumor tissue compared to normal cerebellum and that high Msi1 expression is associated with a poor prognosis. Using a nude mouse xenograft model, we demonstrate that Msi1 is important for tumor growth. We then used RIP-chip (ribonucleoprotein immunoprecipitation followed by microarray analysis) to identify mRNA targets of Msi1 in medulloblastoma. In conclusion, our results suggest that Msi1 functions as a regulator of multiple processes in medulloblastoma formation and could become an important therapeutic target.
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Project description:Gene expression analysis of the Msi1 overexpression in HEK 293T cells.
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