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ABSTRACT: PTRF RIP-seq

PROVIDER: PRJNA777377 | ENA |

REPOSITORIES: ENA

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Dataset's files

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			Action	DRS
	SRR17255447.fastq.gz	Fastqsanger.gz
	SRR17255447_1.fastq.gz	Fastqsanger.gz
	SRR17255447_2.fastq.gz	Fastqsanger.gz
	SRR17255448_1.fastq.gz	Fastqsanger.gz
	SRR17255448_2.fastq.gz	Fastqsanger.gz

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Effect of muscular dystrophy caused by PTRF deletion on the transcriptome of skeletal muscles

Project description:Muscular dystrophy is a group of diseases that cause progressive weakness and degeneration of the skeletal muscles that control movement. Lacking the caveolae component polymerase I transcription release factor (PTRF) causes a secondary deficiency of caveolins resulting in muscular dystrophy. To investigate the effect of PTRF deletion on skeletal muscle, we created gene-edited mice with PTRF knockout (KO). We then performed RNA-seq of soleus and quadriceps muscles from soleus and quadriceps muscles of 3 months old WT (n=3) and PTRF KO mice (n=3) and analyzed the data for gene expression profiling. 12933 genes were detected across all 12 libraries. The hierarchy clustering of co-expressed genes revealed a clear split between PTRF KO and WT mice for both skeletal muscles. Differential expression analysis identified 1293 and 705 differentially expressed genes (DEGs) in the soleus and quadriceps, respectively. 971 and 534 DEGs were up-regulated, and 322 and 171 DEGs were down-regulated in the soleus and quadriceps of PTRF KO mice, respectively.

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Project description:MAPK inhibitors (MAPKi) show outstanding clinical response rates in melanoma patients harbouring BRAF mutations, but resistance is common. High-throughput, subcellular proteome analyses at two different MS laboratories and RNA-seq on two panels of primary melanoma cells that were either sensitive or MAPKi resistant, revealed that only fifteen proteins were sufficient to discriminate between resistant and sensitive cells. The two proteins with the highest discriminatory power were PTRF and IGFBP7, both highly upregulated in the resistant cells. They were associated with epithelial-mesenchymal transition (EMT) and are mechanistically linked. Knock-out of PTRF revealed targets involved in lysosomal activation, endocytosis, pH regulation, EMT, TGFbeta signalling and cell migration and adhesion. In addition, immunohistochemistry on patient samples showed that PTRF and IGFBP7 expression levels were significant biomarkers of poor progression free survival under MAPKi treatment. A drug screen of MAPKi resistant cells using a 960-compound kinase modulator library identified two lead compounds that were effective in targeting MAPKi resistant cells.

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Project description:Lungs from newborn cavin-1/PTRF-deficient and wild-type mice were analyzed 6 cavin-1 deficient newborn mice and 6 wild-type mice

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