Genes regulated by Yki play roles in the cell cycle, cell migration and cell adhesion in Drosophila
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA766663 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16089461_1.fastq.gz | Fastqsanger.gz | |||
| SRR16089461_2.fastq.gz | Fastqsanger.gz | |||
| SRR16089462_1.fastq.gz | Fastqsanger.gz | |||
| SRR16089462_2.fastq.gz | Fastqsanger.gz | |||
| SRR16089463_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:In order to investigate the underlying molecular mechanism of Yki-regulated tracheal progenitor migration and proliferation, genomic chromatin immunoprecipitation (ChIP-seq) was performed to identify loci bound by Yki in trachea.The peaks we observed included multiple Yki binding sites in the promoter and intronic regions of expanded (ex) and Diap1, which are well-characterized direct target genes of Yki. Other Yki targets are regulators in cell migration, cell cycle, and cell adhesion, and include hnt, which is a regulator of cell cycle in follicle cells.Yki occupancy was also pronounced in the promoter region of two heparan sulfate proteoglycans (HSPGs), Dally and Dally-like protein (Dlp) , which together with Ex and Diap1 belong to the cell migration GO cluster. Significant ChIP-seq peaks were observed in the region of N-cadherin (Ncad), a cell adhesion molecule that promotes cell migration and Matrix metalloproteinase-1 (MMP-1), a component of the extracellular matrix. Together, these results suggest that Yki activates various targets that function in cell cycle, cell migration and cell adhesion.
2022-04-22 | GSE184856 | GEO
Project description:Previously, we suggested a cytosolic role for the histone-methyltransferase Ezh2 in regulating lymphocyte activation, but molecular mechanisms underpinning this extra-nuclear function remained unclear. Here we show that Ezh2 regulates integrin-signaling and adhesion dynamics of neutrophils and dendritic cells. Ezh2 deficiency impaired integrin-dependent transendothelial migration of innate leukocytes and restricted disease progression in an animal model of multiple sclerosis. Direct methylation of talin, a key regulatory molecule in cell migration, by Ezh2 disrupted talin binding to F-actin and thereby promoted adhesion structure turnover. This regulatory effect was abolished by targeted disruption of Ezh2 interactions with Vav1. Our studies reveal a novel extra-nuclear function for Ezh2 in regulating adhesion dynamics with implications for leukocyte migration, immune responses and potentially pathogenic processes. Control and Ezh2-deficient bone marrow derived immature and mature dendritic cells were analyzed in triplicates
2015-03-09 | E-GEOD-60146 | biostudies-arrayexpress
Project description:Pumilio proteins are RNA-binding proteins that control mRNA translation and stability by binding to the 3' UTR of target mRNAs. Mammals have two canonical Pumilio proteins, PUM1 and PUM2, which are known to act in many biological processes, including embryonic development, neurogenesis, cell cycle regulation and genomic stability. Here, we characterized a new role of both PUM1 and PUM2 in regulating cell morphology, migration, and adhesion in T-REx-293 cells, in addition to previously known defects in growth rate. Gene ontology analysis of differentially expressed genes in PUM double knockout (PDKO) cells for both cellular component and biological process showed enrichment in categories related to adhesion and migration. PDKO cells had a collective cell migration rate significantly lower than that of WT cells and displayed changes in actin morphology. In addition, during growth, PDKO cells aggregated into clusters (clumps) due to an inability to escape cell-cell contacts. Addition of extracellular matrix (Matrigel) alleviated the clumping phenotype. Collagen IV (ColIV), a major component of Matrigel, was shown to be the driving force in allowing PDKO cells to monolayer appropriately, however, ColIV protein levels remained unperturbed in PDKO cells. This study characterizes a novel cellular phenotype associated with cellular morphology, migration, and adhesion which can aid in developing better models for PUM function in both developmental processes and disease.
2023-01-01 | GSE207836 | GEO
Project description:Mammalian Pumilio Proteins Control Cellular Morphology, Migration, and Adhesion
| PRJNA857310 | ENA
Project description:The interaction between monocytes and endothelial cells in inflammation is central to chemoattraction, adhesion, and transendothelial migration. Key players such as selectins and their ligands, integrins and other adhesion molecules and their function in these processes are well studied. Toll-like receptor 2 (TLR2), expressed on monocytes, is critical for sensing invading pathogens and initiating a rapid and effective immune response. However, the extended role of TLR2 in monocyte adhesion and migration has only been partially elucidated. To address this question, we performed several functional cell-based assays using monocyte-like wild type (WT), TLR2-knock-out (KO) and, TLR2-knock-in (KI) THP-1 cells. We found that TLR2 promotes faster and stronger adhesion of monocytes to the endothelium and a more intense endothelial barrier disruption after endothelial activation. In addition, we performed quantitative mass-spectrometry, STRING protein analysis, and RT-qPCR, which revealed the association of TLR2 with specific integrins, but also uncovered novel proteins affected by TLR2. In conclusion, we could show that unstimulated TLR2 affects cell adhesion, endothelial barrier disruption, migration, and actin polymerization.
2023-10-24 | PXD041819 | Pride
Project description:Cell sedimentation in 3D culture environments refers to the vertical migration of cells towards the bottom of the space. This occurs despite the use of hydrogel materials in 3D cell cultures, which would be expected to prevent this behavior. To better understand and explain these experimental observations, we conducted a multiscale experimental and mathematical examination of 3D cancer growth and sedimentation in triple negative breast cancer cells. The migration of cells towards the bottom was examined in the presence and absence of the migrastatic drug Paclitaxel, as well as in a low adhesion environment and the presence of fibroblasts. The observed behaviour was modeled mathematically by hypothesizing self-generated chemotactic gradients. Our results reveal that active migration mechanisms, specifically collective migration regulated by the MAPK and TGF-β pathways, play an important role in sedimentation. The mathematical model was able to describe the experimental data in the absence and presence of Paclitaxel, suggesting the inhibition of random motion and advection mechanism in the latter case. Low adhesion environment and multiple cell type experiments resulted in an inhibition of sedimentation. Overall, our results suggest that cells, initially uniformly distributed in the 3D space, actively migrate towards the bottom due to the presence of signals produced by cells already attached to it, providing mechanistic insights into this unexpected behavior.
2023-02-15 | GSE223350 | GEO
Project description:Previously, we suggested a cytosolic role for the histone-methyltransferase Ezh2 in regulating lymphocyte activation, but molecular mechanisms underpinning this extra-nuclear function remained unclear. Here we show that Ezh2 regulates integrin-signaling and adhesion dynamics of neutrophils and dendritic cells. Ezh2 deficiency impaired integrin-dependent transendothelial migration of innate leukocytes and restricted disease progression in an animal model of multiple sclerosis. Direct methylation of talin, a key regulatory molecule in cell migration, by Ezh2 disrupted talin binding to F-actin and thereby promoted adhesion structure turnover. This regulatory effect was abolished by targeted disruption of Ezh2 interactions with Vav1. Our studies reveal a novel extra-nuclear function for Ezh2 in regulating adhesion dynamics with implications for leukocyte migration, immune responses and potentially pathogenic processes.
2015-03-09 | GSE60146 | GEO
Project description:The AML1/ETO fusion protein found in acute myeloid leukemias functions as a transcriptional regulator by recruiting co-repressor complexes to its DNA binding site. In order to extend the understanding of its role in preleukemia, we expressed AML1/ETO in a murine immortalized pluripotent hematopoietic stem/progenitor cell line, EML C1, and found that genes involved in functions such as cell-to-cell adhesion and cell motility were among the most significantly regulated as determined by RNA sequencing. In functional assays, AML1/ETO-expressing cells showed a decrease in adhesion to stromal cells, an increase of cell migration rate in vitro, and displayed an impairment in homing and engraftment in vivo upon transplantation into recipient mice. Our results suggest that AML1/ETO expression determines a more mobile and less adherent phenotype in preleukemic cells, therefore altering the interaction with the hematopoietic niche, potentially leading to the migration across the bone marrow barrier and to disease progression.
2016-10-07 | GSE77185 | GEO
Project description:The transcription cofactor Yki drives growth and proliferation in part by controlling mitochondrial network formation. To determine if Yki and Sd are directly bound to DNA corresponding to mitochondrial genes, we used chromatin immunoprecipitation and whole genome tiling arrays (ChIP-chip) to identify regions bound by these factors in eye-antenna and wing imaginal discs. The supplementary .bed files contain all Yki or Sd binding sites (called at 5% FDR) in wing or eye-antenna imaginal discs, as well as shared Sd+Yki sites and associated target genes. Wing or eye-antenna imaginal discs ChIPped for Yki or Sd-GFP vs. input DNA from corresponding imaginal discs.
2012-10-03 | E-GEOD-26678 | biostudies-arrayexpress
Project description:Activated leukocyte cell adhesion molecule on human oligodendrocytes mediates Th17 cell adhesion
| PRJNA962726 | ENA