scholarly journals Non-canonical circadian oscillations in Drosophila S2 cells drive gene-expression cycles coupled to metabolic oscillations

2017 ◽  
Author(s):  
Guillaume Rey ◽  
Nikolay B. Milev ◽  
Utham K. Valekunja ◽  
Ratnasekhar Ch ◽  
Sandipan Ray ◽  
...  
Keyword(s):  
Central Carbon Metabolism ◽  
S2 Cells ◽  
Principal Mechanism ◽  
Genome Wide ◽  
Drive Gene Expression ◽  
Drosophila S2 Cells ◽  
Metabolic Oscillations ◽  
Drive Gene ◽  
Surprising Discovery ◽  
Transcriptional Feedback

ABSTRACTCircadian rhythms are cell-autonomous biological oscillations with a period of about 24 hours. Current models propose that transcriptional feedback loops are the principal mechanism for the generation of circadian oscillations. In these models, Drosophila S2 cells are generally regarded as ‘non-rhythmic’ cells, as they do not express several canonical circadian components. Using an unbiased multi-omics approach, we made the surprising discovery that Drosophila S2 cells do in fact display widespread daily rhythms. Transcriptomics and proteomics analyses revealed that hundreds of genes and their products are rhythmically expressed in a 24-hour cycle. Metabolomics analyses extended these findings and illustrated that central carbon metabolism and amino acid metabolism are the main pathways regulated in a rhythmic fashion. We thus demonstrate that daily genome-wide oscillations, coupled to metabolic cycles, take place in eukaryotic cells without the contribution of known circadian regulators.

Analysis of genome-wide contacts of forum terminus in Drosophila S2 cells

2013 ◽  
Vol 452 (1) ◽  
pp. 259-263 ◽  
Author(s):  
D. V. Sosin ◽  
O. V. Kretova ◽  
Y. V. Kravatsky ◽  
N. A. Tchurikov
Keyword(s):  
S2 Cells ◽  
Genome Wide ◽  
Drosophila S2 Cells

scholarly journals Metabolomic Analysis of Cricket paralysis virus Infection in Drosophila S2 Cells Reveals Divergent Effects on Central Carbon Metabolism as Compared with Silkworm Bm5 Cells

Viruses ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 393 ◽  
Author(s):  
Luo-Luo Wang ◽  
Luc Swevers ◽  
Lieven Van Meulebroek ◽  
Ivan Meeus ◽  
Lynn Vanhaecke ◽  
...  
Keyword(s):  
Virus Infection ◽  
Acute Infection ◽  
Central Carbon Metabolism ◽  
S2 Cells ◽  
Metabolomic Analysis ◽  
Virus Infections ◽  
Opposite Pattern ◽  
Central Carbon ◽  
Drosophila S2 Cells ◽  
Paralysis Virus

High-throughput approaches have opened new opportunities for understanding biological processes such as persistent virus infections, which are widespread. However, the potential of persistent infections to develop towards pathogenesis remains to be investigated, particularly with respect to the role of host metabolism. To explore the interactions between cellular metabolism and persistent/pathogenic virus infection, we performed untargeted and targeted metabolomic analysis to examine the effects of Cricket paralysis virus (CrPV, Dicistroviridae) in persistently infected silkworm Bm5 cells and acutely infected Drosophila S2 cells. Our previous study (Viruses 2019, 11, 861) established that both glucose and glutamine levels significantly increased during the persistent period of CrPV infection of Bm5 cells, while they decreased steeply during the pathogenic stages. Strikingly, in this study, an almost opposite pattern in change of metabolites was observed during different stages of acute infection of S2 cells. More specifically, a significant decrease in amino acids and carbohydrates was observed prior to pathogenesis, while their abundance significantly increased again during pathogenesis. Our study illustrates the occurrence of diametrically opposite changes in central carbon mechanisms during CrPV infection of S2 and Bm5 cells that is possibly related to the type of infection (acute or persistent) that is triggered by the virus.

scholarly journals A Genome-wide RNAi Screen for Microtubule Bundle Formation and Lysosome Motility Regulation in Drosophila S2 Cells

Cell Reports ◽  
2016 ◽  
Vol 14 (3) ◽  
pp. 611-620 ◽  
Author(s):  
Amber L. Jolly ◽  
Chi-Hao Luan ◽  
Brendon E. Dusel ◽  
Sara F. Dunne ◽  
Michael Winding ◽  
...  
Keyword(s):  
Rnai Screen ◽  
S2 Cells ◽  
Microtubule Bundle ◽  
Genome Wide ◽  
A Genome ◽  
Motility Regulation ◽  
Drosophila S2 Cells

scholarly journals Functional mapping of androgen receptor enhancer activity

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Chia-Chi Flora Huang ◽  
Shreyas Lingadahalli ◽  
Tunc Morova ◽  
Dogancan Ozturan ◽  
Eugene Hu ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Androgen Receptor ◽  
Binding Sites ◽  
Gene Promoters ◽  
Strongly Correlated ◽  
Enhancer Activity ◽  
Drive Gene Expression ◽  
In Vitro Cell Lines ◽  
Drive Gene

Abstract Background Androgen receptor (AR) is critical to the initiation, growth, and progression of prostate cancer. Once activated, the AR binds to cis-regulatory enhancer elements on DNA that drive gene expression. Yet, there are 10–100× more binding sites than differentially expressed genes. It is unclear how or if these excess binding sites impact gene transcription. Results To characterize the regulatory logic of AR-mediated transcription, we generated a locus-specific map of enhancer activity by functionally testing all common clinical AR binding sites with Self-Transcribing Active Regulatory Regions sequencing (STARRseq). Only 7% of AR binding sites displayed androgen-dependent enhancer activity. Instead, the vast majority of AR binding sites were either inactive or constitutively active enhancers. These annotations strongly correlated with enhancer-associated features of both in vitro cell lines and clinical prostate cancer samples. Evaluating the effect of each enhancer class on transcription, we found that AR-regulated enhancers frequently interact with promoters and form central chromosomal loops that are required for transcription. Somatic mutations of these critical AR-regulated enhancers often impact enhancer activity. Conclusions Using a functional map of AR enhancer activity, we demonstrated that AR-regulated enhancers act as a regulatory hub that increases interactions with other AR binding sites and gene promoters.

Suppression of  -N-acetylglucosaminidase in the N-glycosylation pathway for complex glycoprotein formation in Drosophila S2 cells

Glycobiology ◽  
2008 ◽  
Vol 19 (3) ◽  
pp. 301-308 ◽  
Author(s):  
Y. K. Kim ◽  
K. R. Kim ◽  
D. G. Kang ◽  
S. Y. Jang ◽  
Y. H. Kim ◽  
...  
Keyword(s):  
S2 Cells ◽  
Drosophila S2 Cells ◽  
Glycosylation Pathway

scholarly journals Dissection of a Hypoxia-induced, Nitric Oxide–mediated Signaling Cascade

2009 ◽  
Vol 20 (18) ◽  
pp. 4083-4090 ◽  
Author(s):  
Pascale F. Dijkers ◽  
Patrick H. O'Farrell
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Signaling Cascade ◽  
S2 Cells ◽  
Signal Transduction System ◽  
Signaling Systems ◽  
Calcium Dependent ◽  
Drosophila S2 Cells ◽  
Oxide Synthase ◽  
Multiple Signaling

Befitting oxygen's key role in life's processes, hypoxia engages multiple signaling systems that evoke pervasive adaptations. Using surrogate genetics in a powerful biological model, we dissect a poorly understood hypoxia-sensing and signal transduction system. Hypoxia triggers NO-dependent accumulation of cyclic GMP and translocation of cytoplasmic GFP-Relish (an NFκB/Rel transcription factor) to the nucleus in Drosophila S2 cells. An enzyme capable of eliminating NO interrupted signaling specifically when it was targeted to the mitochondria, arguing for a mitochondrial NO signal. Long pretreatment with an inhibitor of nitric oxide synthase (NOS), L-NAME, blocked signaling. However, addition shortly before hypoxia was without effect, suggesting that signaling is supported by the prior action of NOS and is independent of NOS action during hypoxia. We implicated the glutathione adduct, GSNO, as a signaling mediator by showing that overexpression of the cytoplasmic enzyme catalyzing its destruction, GSNOR, blocks signaling, whereas knockdown of this activity caused reporter translocation in the absence of hypoxia. In downstream steps, cGMP accumulated, and calcium-dependent signaling was subsequently activated via cGMP-dependent channels. These findings reveal the use of unconventional steps in an NO pathway involved in sensing hypoxia and initiating signaling.

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