ABSTRACT: BioID data (DIA files) associated with the manuscript by Roth et al. 2023 describing the identification and characterization of neural alternative splicing events and associated PPI changes for 17 gene regulatory factors. BioID experiments were performed for two isoforms of Chtop and Sap30bp with/without a neural-regulated exon. For Chtop, cells were also treated with MS023, an arginine methyltransferase inhibitor, at 3 concentrations (DMSO, 1uM and 4uM).
Project description:BioID data (DDA files) associated with the manuscript by Roth et al. 2023 describing the identification and characterization of neural alternative splicing events and associated PPI changes for 17 gene regulatory factors. BioID experiments were performed for two isoforms of Chtop and Sap30bp with/without inclusion of a neural-regulated exon. For Chtop, cells were also treated with MS023, an arginine methyltransferase inhibitor, at 3 concentrations (DMSO, 1uM and 4uM).
Project description:FLAG AP-MS data (DIA) associated with the manuscript by Roth et al. 2023 describing the identification and characterization of neural alternative splicing events and associated PPI changes for 17 gene regulatory factors. This dataset includes Chtop AP-MS data from N2a cells treated with and without the arginine methyltransferase inhibitor MS023.
Project description:FLAG AP-MS data (DDA) associated with the manuscript by Roth et al. 2023 describing the identification and characterization of neural alternative splicing events and associated PPI changes for 17 gene regulatory factors. This dataset includes Chtop AP-MS data from N2a cells treated with and without the arginine methyltransferase inhibitor MS023.
Project description:FLAG AP-MS data (DDA) associated with the manuscript by Roth et al. 2023 describing the identification and characterization of neural alternative splicing events and associated PPI changes for 17 gene regulatory factors.
Project description:FLAG AP-MS data (DIA) associated with the manuscript by Roth et al. 2023 describing the identification and characterization of neural alternative splicing events and associated PPI changes for 17 gene regulatory factors.
Project description:The use of proximity-dependent biotinylation assays coupled to mass spectrometry (PDB-MS) has changed the field of protein-protein interactions (PPI) studies. Yet, despite the recurrent and successful use of BioID-based PPI screening in mammalian cells, the implementation of PDB-MS in yeast has not been effective. Here we report a simple and rapid approach in yeast to effectively screen for proximal and interacting proteins in their natural cellular environment by using TurboID, a recently described version of the BirA biotin ligase. Using the protein arginine methyltransferase Rmt3 and the RNA exosome subunits, Rrp6 and Dis3, the application of PDB-MS in yeast by using TurboID was able to recover protein-protein interactions previously identified using other biochemical approaches and provided complementary information for a given protein bait. The development of a rapid and effective PDB assay that can systematically analyze PPIs in living yeast cells opens the way for large-scale proteomics studies in this powerful model organism.
Project description:There are hundreds of risk genes for autism spectrum disorder (ASD), but signaling networks at the protein level remain unexplored. We used neuron-specific proximity-labeling proteomics (BioID) to identify protein-protein interaction (PPI) networks for 41 ASD-risk genes. Neuron-specific PPI networks included synaptic transmission proteins, which are disrupted by de novo missense variants. The PPI network map revealed convergent pathways including mitochondrial/metabolic processes, Wnt signaling, ion channel activity and MAPK signaling. CRISPR knockout validations revealed an association between mitochondrial activity and ASD-risk genes. The PPI network showed an enrichment of 112 additional ASD-risk genes and differentially expressed genes from post-mortem ASD patients. Clustering of risk genes based on PPI networks identified gene groups corresponding to clinical behavior score severity. Our data reveal that cell type-specific PPI networks can identify previously unknown individual and convergent ASD signaling networks, provide a method to assess patient variants, and reveal biological insight into disease mechanisms and sub-cohorts of ASD.
Project description:Coactivator associated arginine methyltransferase I (CARM1, also known as Protein aRginine MethylTransferase 4, or PRMT4) regulates gene expression by multiple mechanisms including methylation of histones and coactivation of steroid receptor transcription. Mice lacking CARM1 are smaller than their littermates, fail to breath, and die shortly after birth, demonstrating the critical role of CARM1 in development.We performed gene expression analysis to identify genes that are responsible for hyperproliferaion in CARM1 knockout lung. RNA extracted from murine lung at E18.5 with carm1 knockouts and wild type controls was hybridised to Affymetrix mouse430.2 GeneChips to identify differentially expressed genes in the disease state.
Project description:Somatic mutations in DNA Methyltransferase 3A (DNMT3A) with a hotspot in exon 23 at Arginine 882 (DNMT3AR882mut) are the most frequent single mutations in clonal hematopoiesis. Here we analyze the expression of genes and endogenous retrovirus (ERV) sequences in a murine model carrying human DNMT3A-R882H mutation in one allele of the endogenous DNMT3A with respect to normal condition and azacitidine treatment.
Project description:Formerly we found that cancer-promoting factors, such as some typical epigenetic modification factors, are neural specific or enriched in embryonic neural cells, and play a key role in conferring the property of nerual stemness to cancer cells or in maintaining neural stemness in neural stem/progenitor cells. Our recent study demonstrated that PRMT1, a protein arginine methyltransferase, serves also to maintain neural stemness in either neural stem/progenitor cells or cancer cells. We used microarray to analyze global gene expression change in A549 cells after PRMT1 knockdown.