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Global transcriptome analysis indicates that depletion of rps13 and ribosomes leads to cell cycle arrest in G1

ABSTRACT: Affymetrix Toxoplasma microarray data was analyzed to determine whether there was an association with a G1 transcript profile. Four hundred seventy-five genes with significant gene expression differences (Welch T-test, P = 0.01) between ±ATc samples were identified. Genes were clustered into those increased (153) or decreased (322) -ATc. There are a number of genes with diminished expression and pronounced over expression -ATc including LDH1, 4 zinc finger proteins, leucine-rich protein, and ABC transporter-like molecules, myosin-related molecules with many fold increases and one AP2 protein with a small increase. These gene sets have a large overlap with G1 genes defined in an ongoing cell cycle expression study in T. gondii (Behnke, White). Over 60% of those genes that have diminished expression -ATc overlap with genes that are diminished at G1, and over 40% of genes with increased expression -ATc overlap with genes that are up regulated at G1. A hypergeometric distribution of this association suggests that the probability of this happening by chance is essentially zero. Thus, by both methods, FACS and arrays, parasites -ATc display a G1 profile. To determine the global transcriptional differences of the RSP13 conditional mutant with and without anhydrotetracycline (ATc). Four replicates each.

ORGANISM(S): Toxoplasma gondii

SUBMITTER: Michael Behnke

PROVIDER: E-GEOD-20616 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Global transcriptome analysis indicates that depletion of rps13 and ribosomes leads to cell cycle arrest in G1

Project description:Affymetrix Toxoplasma microarray data was analyzed to determine whether there was an association with a G1 transcript profile. Four hundred seventy-five genes with significant gene expression differences (Welch T-test, P = 0.01) between ±ATc samples were identified. Genes were clustered into those increased (153) or decreased (322) -ATc. There are a number of genes with diminished expression and pronounced over expression -ATc including LDH1, 4 zinc finger proteins, leucine-rich protein, and ABC transporter-like molecules, myosin-related molecules with many fold increases and one AP2 protein with a small increase. These gene sets have a large overlap with G1 genes defined in an ongoing cell cycle expression study in T. gondii (Behnke, White). Over 60% of those genes that have diminished expression -ATc overlap with genes that are diminished at G1, and over 40% of genes with increased expression -ATc overlap with genes that are up regulated at G1. A hypergeometric distribution of this association suggests that the probability of this happening by chance is essentially zero. Thus, by both methods, FACS and arrays, parasites -ATc display a G1 profile.

2010-11-29 | GSE20616 | GEO

Transcriptomes of Chlamydia trachomatis L2 with Conditional GrgA deficiency

Project description:To determine the role that GrgA plays in chlamydial physiology, we constructed a Chlamydia trachomatis mutant that we term L/cgad-peig, in which the chromosomal grgA (ctl0766 or ct504) has been disrupted by Targetron mutagenesis, and the plasmid carries an inducible grgA under the control of anhydrotetracycline (ATC). RNA-Seq analysis was performed for L2/cgad-peig grown with and without ATC.

2023-11-29 | GSE234589 | GEO

flagellar regulon studies

Project description:This study examined the genes under the control of FlhDC and sigmaF in E. coli. Keywords: wild-type, deletion and overexepression strains Under defined steady-state growth condition, we used two different genetic approaches to alter the modulator concentration in cells; (1) moderately expressing FlhDC or sigmaF from anhydrotetracycline (aTc) inducible and Tet repressor-controlled PLtet promoter in a plasmid-borne flhDC or fliA gene; (2) disrupting the expression of FlhDC or sigmaF in flhDC or fliA deletion mutant strains. Samples were taken from culture with wild-type or deletion strains at mid log phase (OD=0.2) or from overexpression strains at mid log phase (OD=0.2) before or 5 minutes after moderate induction. Samples were then RNA-stabilized using Qiagen RNAProtect Bacterial Reagent (Qiagen). Total RNA was then isolated using MasterPure kits (Epicentre Technologies). Purified RNA was reverse-transcribed to cDNA, labeled and hybridized to Affymetrix GeneChip E. coli Antisense Genome Arrays as recommended in the technical manual (www.affymetrix.com).

2009-05-01 | E-GEOD-5818 | biostudies-arrayexpress

SPRY4 as a Potential Mediator of the Anti-Tumoral Role of Macrophages in Anaplastic Thyroid Cancer Cells

Project description:Anaplastic thyroid carcinoma (ATC) is the most lethal subtype of thyroid cancer, with high invasive and metastatic potential, not responding to conventional treatments. Its aggressiveness may be influenced by macrophages, which are abundant cells in the tumor microenvironment. To investigate the role of macrophages in ATC aggressiveness, indirect co-cultures were established between ATC cell lines and THP-1-derived macrophages. Macrophages significantly increased both the migration and invasion of T235 cells (p < 0.01; p < 0.01), contrasting with a decrease in C3948 (p < 0.001; p < 0.05), with mild effects in T238 migration (p < 0.01) and C643 invasion (p < 0.05). Flow cytometry showed upregulation of CD80 (pro-inflammatory, anti-tumoral) and downregulation of CD163 (anti-inflammatory, pro-tumoral) in macrophages from co-culture with T235 (p < 0.05) and C3948 (p < 0.05), respectively. Accordingly, we found an upregulation of secreted pro-inflammatory mediators (e.g., GM-CSF, IL-1α; p < 0.05) in C3948–macrophage co-cultures. Proteomic analysis showed the upregulation of SPRY4, an inhibitor of the MAPK pathway, in C3948 cells from co-culture. SPRY4 silencing promoted cancer cell invasion, reverting the reduced invasion of C3948 caused by macrophages. Our findings support that macrophages play a role in ATC cell aggressiveness. SPRY4 is a possible modulator of macrophage–ATC cell communication, with a tumor suppressor role relevant for therapeutic purposes.

2023-10-24 | PXD044861 | Pride

Transcriptome of ring-stage parasites responses to stress conditions upon knockdown of PfGCN5

Project description:Purpose: this study is to analyze the change of overal transcriptome after three stress conditions in ring-stage Plasmodium falciparum before and after knockdown of PfGCN5 by TetR-DOZI system. Methods: In this study, the transcriptomes of a parasite line (TetR-PfGCN5::GFP) for knockdown (KD) of PfGCN5 by withdral of anhydrotetracycline (aTc) comparing to its control (TetR-PfGCN5::GFP with aTc) under three stress conditions [HS: heat shock, low-glucose starvation: L-Glu, and low dose of dihydroartemisinin (DHA) treatment] were analyzed at ring stage by RNAseq. Total RNA were harvested from the eary ring stages after 6 h of stress conditions using the Quick-RNA MiniPrep kit (Zymo Research). RNA sequencing libraries were prepared using the KAPA stranded RNA-seq library preparation kit (Roche) with 500 ng RNA from each sample. Illumina adapter sequence removal and quality trimming of reads were performed using Trimmomatic. Only reads that had a minimum length of 50 base pairs were retained. Reads were then mapped to the P. falciparum 3D7 strain reference genome with HISAT2. Results: Using an optimized data analysis workflow, we mapped about 5 million sequence reads per sample to the malaria parasite genome (pf3D7_V3.0.) and identified over 5 thousands transcripts with high mapping rate at the range between 80% and 95. PfGCN5 KD profoundly changed the global transcription pattern upon stress conditions, indicating PfGCN5 is involved in stress responses. Conclusions: Collectively, transcriptomic analysis of PfGCN5-dependent stress responses shows PfPfGCN5 plays important role in gene regulation of stress responses.

2023-02-08 | GSE221211 | GEO

Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer

Project description:Anaplastic thyroid carcinoma (ATC) is one of the most aggressive malignancy and accounts for the majority of thyroid cancer-related deaths. Despite intensive research, there remains no effective treatment for patients with ATC. Here, we identify THZ1, a covalent inhibitor of cyclin-dependent kinase 7 (CDK7), as a potent anti-ATC compound by high-throughput chemical screening. ATC cells, but not papillary thyroid cancer (PTC) cells, are exceptionally sensitive to CDK7 inhibition. Analyzing both gene expression profiles and super enhancer (SE) features reveals that the SE-mediated oncogenic transcriptional amplification renders the vulnerability of ATC cells to THZ1 treatment. Combining this integrative analysis with functional assays discovers a number of novel cancer genes of ATC, including PPP1R15A, SMG9 and KLF2. Inhibition of PPP1R15A with Guanabenz (GBZ) or Sephin1 greatly suppresses ATC growth. Significantly, the expression level of PPP1R15A is correlated with CDK7 expression in ATC tissue samples. Elevated expression of PPP1R15A and CDK7 are both associated with poor clinical prognosis in ATC patients. Importantly, GBZ or THZ1 treatment sensitizes ATC cells to conventional chemotherapy. Taken together, these findings demonstrate transcriptional addiction in ATC pathobiology and identify CDK7 and PPP1R15A as potential biomarkers and therapeutic targets for ATC.

2019-03-01 | GSE120177 | GEO

Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [ChIP-Seq]

2019-03-01 | GSE120175 | GEO

Targeting super-enhancer-driven oncogenic transcription by CDK7 inhibition in anaplastic thyroid cancer [RNA-Seq]

2019-03-01 | GSE120176 | GEO

Expression analysis of mouse thyroid tumors

Project description:Anaplastic thyroid carcinoma (ATC) is the most aggressive form of thyroid cancer, and often derives from pre-existing well-differentiated tumors. We have engineered the first mouse model of ATC by combining in the mouse thyroid follicular cells two molecular hallmarks of human ATC: activation of PI3K (via Pten deletion) and inactivation of p53. By 9 months of age, over 75% of the compound mutant mice develop aggressive, undifferentiated thyroid tumors that evolve from pre-existing follicular hyperplasia and carcinoma. These tumors display all the features of their human counterpart, including pleomorphism, epithelial-mesenchymal transition, aneuploidy, local invasion and distant metastases.

2012-03-14 | GSE30427 | GEO

Targeting CDK12-mediated transcription regulation in anaplastic thyroid carcinoma [RNA-seq]

Project description:Anaplastic thyroid carcinoma (ATC) is the most aggressive type of thyroid cancer, with no effective treatment available. Identification of new anti-ATC drugs represents an urgent need. In this study, we find that ATC cells are highly sensitive to THZ531, a potent inhibitor of the transcriptional cyclin-dependent kinase (CDK), CDK12. Cell-based assays demonstrate that CDK12 inhibition significantly impedes cell cycle progression, induces apoptotic cell death, and impairs colony formation in ATC cells. THZ531 causes a loss of elongating RNA polymerase II and suppresses gene expression in ATC cells. An integrative analysis of gene expression profiles and super-enhancer landscape, combining with functional assays, leads to the discovery of two new ATC cancer genes, ZC3H4 and NEMP1. Furthermore, CDK12 inhibition enhances the sensitivity of ATC cells to doxorubicin-mediated chemotherapy. Thus, these findings indicate that CDK12 is a potential therapeutic target for ATC treatment and its inhibition may help to overcome the chemoresistance in patients with ATC

2022-09-19 | GSE137697 | GEO

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