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RNA expression in P1 sciatic nerves

ABSTRACT: RNA seq was performed comparing SC-specific Dicer mutants with SC-specific Lin28B transgenics to obtain an unbiased list of potentially de-regulated miRNA target candidates.

ORGANISM(S): Mus musculus

PROVIDER: GSE64559 | GEO | 2015/10/12

SECONDARY ACCESSION(S): PRJNA271298

REPOSITORIES: GEO

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Transcriptome analyses of miRNA pathway mutants and injury response in developing and adult sciatic nerves

Project description:We addressed the requirement of DGCR8, DROSHA and DICER functions in developing and adult Schwann cells (SCs) using mouse mutants. We found that the microprocessor components DGCR8 and DROSHA are crucial for axonal radial sorting and to establish correct SC numbers upon myelination. Transcriptome analysis revealed that the microprocessor is essential to prevent aberrant accumulation and de novo expression of injury-response genes. Those genes are predicted targets of stage-specifically enriched miRNAs. In agreement, DGCR8 and DICER are required for proper maintenance of the myelinated SC state. We conclude that the miRNA pathway is crucial for preventing inappropriate activity of injury response genes in developing and adult SCs.

2018-10-08 | GSE109075 | GEO

RNA sequencing analysis of PINCH mutant sciatic nerves

Project description:During peripheral nervous system (PNS) development, Schwann cells (SC) depend on interactions between extracellular matrix proteins, integrins and growth factor signal transduction pathways for survival, sorting and wrapping of axon segments to form myelin. Together with integrin-linked-kinase and parvins, PINCH (Particularly-interesting-new-cystidin-hystidin-rich protein) forms a heterotrimeric complex referred to as the IPP complex, which functions as a signaling hub connecting integrins with various signaling pathways. Using SC-specific conditional gene targeting in mice, gene expression profiling by RNAseq, and other methodologies, we demonstrate distinct functional roles for PINCH1 and PINCH2 in SC.

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Project description:We report RNA sequencing data from induced Schwann cell specific knockouts for DICER and DGCR8 as well as crush injured wild type animals. Induced deletion of DICER and DGCR8 results in expression of numerous injury response genes suggesting a requirement of those proteins in maintaining the myelinated Schwann cell fate.

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Expression data for 2-month-old wild type and Tfam-SCKO (MPZ-Tfam KO) sciatic nerves

Project description:Gene expression analysis of 2-month-old Ctrl and Tfam-SCKO mice. At this age mitochondrial function is disrupted in the Schwann cells of Tfam-SCKO mice ,but their nerves display only very limited pathology. Mitochondrial dysfunction is a common cause of peripheral neuropathy. Much effort has been devoted to examining the role played by neuronal/axonal mitochondria, but how mitochondrial deficits in peripheral nerve glia (Schwann cells, SCs) contribute to peripheral nerve diseases remains unclear. Here, we investigate a mouse model of peripheral neuropathy secondary to SC mitochondrial dysfunction (Tfam-SCKOs). We show that disruption of SC mitochondria activates a maladaptive integrated stress response through actions of heme-regulated inhibitor kinase (HRI), and causes a shift in lipid metabolism away from fatty acid synthesis toward oxidation. These alterations in SC lipid metabolism result in depletion of important myelin lipid components as well as in accumulation of acylcarnitines, an intermediate of fatty acid b-oxidation. Importantly, we show that acylcarnitines are released from SCs and induce axonal degeneration. A maladaptive integrated stress response as well as altered SC lipid metabolism are thus underlying pathological mechanisms in mitochondria-related peripheral neuropathies. Total RNA samples were prepared by isolating and pooling RNA from three different 2-month-old MPZ-Tfam KO and Ctrl mice. 2 replicates per genotype were used in this experiment and they were prepared entirely independently.

2013-03-13 | E-GEOD-44605 | biostudies-arrayexpress

Expression data for 2-month-old wild type and Tfam-SCKO (MPZ-Tfam KO) sciatic nerves

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Biodegradable magnesium wire promotes regeneration of compressed sciatic nerves.

Project description: Not available

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RNA expression in mutants of the miRNA pathway during myelination

Project description:RNA sequencing was performed comparing sciatic nerves of Schwann cell specific DICER mutants with SC-specific DGCR8 and DROSHA mutants.

2018-10-08 | GSE64880 | GEO

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Follistatin promotes LIN28B mediated supporting cell reprogramming and hair cell regeneration in the murine cochlea

Project description:Purpose: To identify how follistatin (FST) and LIN28B re-activation augments the regenerative competence of cochlear supporting cells (SCs), we used bulk-RNA sequencing to analyze the transcriptome of SC-containing control, FST, LIN28B and FST+LIN28B overexpressing organoids after 7 days of culture. The 7 day time point was chosen as it correlates with the peak of SC proliferation and presumed SC reprogramming. Methods: Samples were processed using Illumina's TruSeq stranded Total RNA kit, using the UDI indexes. The samples were sequenced on the NovaSeq 6000, paired end, 2x50 base pair reads.We used kallisto (v0.46.1) to pseudo-align reads to the reference mouse transcriptome Ensembl Mus musculus v96 and to quantify transcript abundance. The companion tool sleuth was used to determine differentially expressed genes (DEGs) comparing control to LIN28B and or FST overexpressing conditions. Results: Applying Wald test we identified 423DEGs for FST+LIN28B(q-value< 0.01), 764 DEGs for LIN28B (q-value< 0.01) and 37 DEGs for FST (q-value< 0.05). The list of downregulated genes included structural genes (Tecta, Col2a1, Col11a2, Col9a3) as well as transcription factor known to promote neuronal/glial cell differentiation (Zbtb20,Nfix, Nfib) and cochlear maturation (Thrb).The list of upregulated genes contained a large number of let-7 target genes known to promote in stemness (e.g., Hmga2, Arid3a, Trim71,Igf2bp1), and to regulate stem cell metabolism (e.g.,Hk2),as well as genes involved in cell cycle regulation (e.g.,Ccnd2,Ccnd3, Cdkn1a, Cdkn2a) and cell fate specification (e.g. Sox11).

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