Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA348194 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Analysis of eH3.3 occupancy in a ATRX loss-of-function line [ChIP-seq]
| PRJNA348193 | ENA
Project description:RNAseq analysis of NGATHA loss and gain of function alleles
| PRJNA242915 | ENA
Project description:Root hair specific transcriptome analysis of gain-of-function and loss-of-function of GTL1 and DF1
| PRJNA407477 | ENA
Project description:Heterochromatin in the eukaryotic genome is rigorously controlled by the concerted action of protein factors and RNAs. Here, we investigate the RNA binding function of ATRX, a chromatin remodeler with roles in silencing of repetitive regions of the genome and in recruitment of the polycomb repressive complex 2 (PRC2). We identify ATRX RNA binding regions (RBRs) and discover that the major ATRX RBR lies within the N-terminal region of the protein, distinct from its PHD and helicase domains. Deletion of this ATRX RBR (ATRXRBR) compromises ATRX interactions with RNAs in vitro and in vivo and alters its chromatin binding properties. Genome-wide studies reveal that loss of RNA interactions results in a redistribution of ATRX on chromatin. Finally, our studies identify a role for ATRX-RNA interactions in regulating PRC2 localization to a subset of polycomb target genes.
2020-03-09 | PXD017806 | Pride
Project description:RNA-seq analysis of flg22-induced gene expression changes in wild type, asr3-1 mutant and OX9 overexpression line
| PRJNA268383 | ENA
Project description:ngs2021_03_snap33-rna-seq snap33-1 vs wt -What molecular pathways (transcripts) contribute to the phenotype of the snap33 loss-of-function mutant-comparing snap33 mutant to the WT out-segregating line in normal growth conditions at 5 and 12 days (before and after the appearance of the phenotype of the mutant snap33
2024-01-29 | GSE247242 | GEO
Project description:The SWI/SNF-family chromatin remodeling protein ATRX is a tumor suppressor in sarcomas, gliomas and other malignancies. Its loss of function facilitates the alternative lengthening of telomeres (ALT) pathway in tumor cells, while it also affects Polycomb repressive complex 2 (PRC2) silencing of its target genes. To further define the role of inactivating ATRX mutations in carcinogenesis, we knocked out atrx in our previously published p53/nf1-deficient zebrafish line that develops malignant peripheral nerve sheath tumors and gliomas. Complete inactivation of atrx using CRISPR-cas9 was lethal in developing fish and resulted in an alpha-thalassemia-like phenotype including reduced alpha-globin expression. In p53/nf1-deficient zebrafish neither peripheral nerve sheath tumors nor gliomas showed accelerated onset in atrx+/- fish, but these fish developed various tumors that were not observed in their atrx+/+ siblings, including epithelioid sarcoma, angiosarcoma, undifferentiated pleomorphic sarcoma and rare types of carcinoma. Most of these cancer types are included in the AACR Genie database of human tumors associated with mutant ATRX, indicating that our zebrafish model reliably reflects a role for ATRX-loss in the early pathogenesis of these types of human cancers. RNA-seq of p53/nf1- and p53/nf1/atrx-deficient tumors revealed that down-regulation of telomerase accompanied ALT-mediated lengthening of the telomeres in atrx-mutant samples. Moreover, inactivating mutations in atrx disturbed PRC2-target gene silencing, indicating a connection between ATRX loss and PRC2 dysfunction in cancer development.
2019-02-15 | GSE125040 | GEO
Project description:Analysis of gene expression and of H3.3 distribution and abundance in a ATRX loss-of-function line
| PRJNA348185 | ENA
Project description:<p>Many tumors maintain chromosome ends through a telomerase-independent, homologous recombination based mechanism called alternative lengthening of telomeres (ALT). While ALT occurs in only a subset of tumors, it is strongly associated with mutations in the genes encoding components of the histone H3.3 chaperone complex, ATRX and DAXX. To date the mechanistic role of ATRX and particularly DAXX mutations in potentiating ALT remains poorly understood. We identify an osteosarcoma cell line, G292, with a unique chromosomal translocation resulting in loss of DAXX function, while retaining functional ATRX. Using this distinctive resource, we demonstrate that introduction of wild type DAXX suppresses the ALT phenotype and restores localization of the ATRX/DAXX complex to PML bodies. This provides the first direct molecular evidence that ongoing DAXX deficiency is essential for maintenance of the ALT phenotype and highlights the potential for therapeutic targeting of this oncogenic pathway.</p>
| phs001495 | dbGaP
Project description:RNA-seq of genes mis-regulated in WT and the bpc1,2,3,4,6 loss-of-function mutant in response to cytokinin in roots of Arabidopsis thaliana
| PRJNA398488 | ENA