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Drosophila PTB regulates dorso-ventral patterning genes in embryos

ABSTRACT: Drosophila PTB (Polypyrimidine Tract-binding protein dmPTB) regulates dorso-ventral patterning genes in embryos

ORGANISM(S): Drosophila melanogaster

PROVIDER: GSE57517 | GEO | 2014/05/10

SECONDARY ACCESSION(S): PRJNA246579

REPOSITORIES: GEO

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Drosophila PTB regulates dorso-ventral patterning genes in embryos

Project description:Drosophila PTB (Polypyrimidine Tract-binding protein dmPTB) regulates dorso-ventral patterning genes in embryos Comparison of wild type (yw genotype) and PTB mutant (heph03429) drosophila embryos

2014-05-10 | E-GEOD-57517 | biostudies-arrayexpress

PTB CLIP-seq

2009-12-24 | GSE19323 | GEO

Drosophila melanogaster

Project description:Drosophila PTB regulates dorso-ventral patterning genes in embryos

| PRJNA246579 | ENA

PTB CLIP-seq

Project description:Recent transcriptome analysis indicates that >90% of human genes undergoes alternative splicing, underscoring the contribution of differential RNA processing to diverse proteomes in higher eukaryotic cells. The polypyrimidine tract binding protein PTB is a well-characterized splicing repressor, but PTB knockdown causes both exon inclusion and skipping. Genome-wide mapping of PTB-RNA interactions and construction of a functional RNA map now revealed that dominant PTB binding near a competing constitutive splice site generally induces exon inclusion whereas prevalent binding close to an alternative site often causes exon skipping. This positional effect was further demonstrated by disrupting or creating a PTB binding site on minigene constructs and testing their responses to PTB knockdown or overexpression. These findings suggest a mechanism for PTB to modulate splice site competition to produce opposite functional consequences, which may be generally applicable to RNA binding splicing factors to positively or negatively regulate alternative splicing in mammalian cells. Examination of PTB-RNA binding in Hela cells using CLIP-seq (Cross-Linking ImmunoPrecipitation coupled with high-throughput sequencing) method. Peaks: The four alignment files (linked as supplementary files on Sample records) were combined together for peak finding, as we found that most of the monomeric and dimeric tags are similarly distributed in the genome with high pearson correlation coefficient. The method to detect the peaks above gene-specific randomized background was similar to (Yeo et al., 2009) and described in the paper (Xue et al., 2009).

2009-12-24 | E-GEOD-19323 | biostudies-arrayexpress

Transcriptomic analysis of dorso-ventral cell-types of Arabidopsis shoot apical meristem

Project description:Dorso-ventral (DV) patterning at the Shoot Apical meristem (SAM) is essential for organogenesis in Arabidopsis. Dorsal and ventral gene expressed domains are separated by boundaries from where the new organ initiation starts. Here by using cell-types specific transcriptomics approach, we have identified doral, ventral and boundary specific genes in SAM.

2020-04-16 | GSE90169 | GEO

A Non-Canonical Raf Function Is Required for Dorsal-Ventral Patterning in Drosophila Embryogenesis

Project description:Embryonic development requires the establishment of directional axes. In Drosophila, spatially discrete expression of transcription factors determines the anterior to posterior organization of the early embryo, while the Toll and TGF-beta signalling pathways determine the early dorsal to ventral pattern. Embryonic MAPK/ERK signaling contributes to both anterior to posterior patterning in the terminal regions and to dorsal to ventral patterning during oogenesis and embryonic stages. Here we describe a novel loss of function mutation in the Raf kinase gene, which leads to loss of ventral cell fates as seen through the loss of the ventral furrow, the absence of Dorsal/NF-kB nuclear localization, the absence of mesoderm determinants Twist and Snail, and the expansion of TGF-beta. Gene expression analysis showed cells adopting ectodermal fates similar to loss of Toll signaling. Our results combine novel mutants, live imaging, optogenetics and transcriptomics to establish a novel role for Raf, that appears to be independent of the MAPK cascade, in embryonic patterning.

2021-08-03 | GSE178187 | GEO

Micro-C of Drosophila embryos to investigate chromatin conformation during dorsal-ventral patterning

Project description:Micro-C of Drosophila embryos to investigate chromatin conformation during dorsal-ventral patterning

| PRJEB41445 | ENA

ChIP-seq of Drosophila embryos to investigate chromatin state during dorsal-ventral patterning

Project description:ChIP-seq of Drosophila embryos to investigate chromatin state during dorsal-ventral patterning

| PRJEB39232 | ENA

Hi-C of Drosophila embryos to investigate chromatin conformation during dorsal-ventral patterning

Project description:Hi-C of Drosophila embryos to investigate chromatin conformation during dorsal-ventral patterning

| PRJEB39238 | ENA

Position-dependent alternative splicing activity revealed by global profiling of alternative splicing events regulated by PTB (HJAY)

Project description:To gain global insights into the role of the well-known repressive splicing regulator PTB we analyzed the consequences of PTB knockdown in HeLa cells using high-density oliogonucleotide splice-sensitive microarrays. The major class of identified PTB-regulated splicing event was PTB-repressed cassette exons, but there was also a substantial number of PTB-activated splicing events. PTB repressed and activated exons showed a distinct arrangement of motifs with pyrimidine-rich motif enrichment within and upstream of repressed exons, but downstream of activated exons. The N-terminal half of PTB was sufficient to activate splicing when recruited downstream of a PTB-activated exon. Moreover, insertion of an upstream pyrimidine tract was sufficient to convert a PTBactivated to a PTB-repressed exon. Our results demonstrate that PTB, an archetypal splicing repressor, has variable splicing activity that predictably depends upon its binding location with respect to target exons.

2010-09-01 | GSE23513 | GEO

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