Ontology highlight
ABSTRACT:
PROVIDER: PRJNA222288 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1004785.fastq.gz | Fastqsanger.gz | |||
| SRR1004786.fastq.gz | Fastqsanger.gz | |||
| SRR1004787.fastq.gz | Fastqsanger.gz | |||
| SRR1004788.fastq.gz | Fastqsanger.gz | |||
| SRR1004789.fastq.gz | Fastqsanger.gz |
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Project description:De Novo Purine Synthesis Mediates Circadian Control of Cell Cycle in Zebrafish (array)
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Project description:De Novo Purine Synthesis Mediates Circadian Control of Cell Cycle in Zebrafish (HTS)
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Project description:Cell cycle and metabolism are two major outputs controlled by circadian rhythm in many organisms. Here we show that the three processes were linked through inosine 5'-phosphate dehydrogenase (impdh), a rate-limiting enzyme in de novo purine synthesis. We using adult zebrafish as a model system,we applied a genome-wide transcriptome approach that allowed us to investigate circadian gene expression. The whole-genome transcriptome profiles of adult brain in time-series were assayed on Agilent zebrafish microarrays. We used a similar statistical method to identify zebrafish circadian genes (ZCOG) as our previous study in larval zebrafish. Three isoforms of impdh show strong circadian oscillations in different tissues of zebrafish. impdh1a contributes to the ocular development and pigment synthesis, impdh2 promotes and impdh1b delays the development. By limiting the GTP required by DNA synthesis, impdh2 contributes to the daily rhythm of S phase in cell cycle. Multiple enzymes in the de novo purine synthesis pathway show the same circadian oscillations with peaks similar to impdh2. The circadian expression of this pathway is conserved in mouse liver. In summary, we show that the circadian regulation of de novo purine synthesis that supplies crucial building blocks for DNA replication is critical for gating cell cycle in circadian rhythm. Adult zebrafish were sacrificed and dissected at 4h intervals starting at CT0 in both LD and DD conditions for 12 time points. Total RNA of individual zebrafish brain was extracted using Trizol (Invitrogen, Carlsbad, CA) according to the manufacturerM-bM-^@M-^Ys instruction. Microarrays were manufactured by Agilent Technologies (Agilent Technologies, Palo Alto, CA), containing 43,603 probes for zebrafish whole-genome transcriptional profiling.
2013-10-01 | E-GEOD-51277 | biostudies-arrayexpress
Project description:Cell cycle and metabolism are two major outputs controlled by circadian rhythm in many organisms. Here we show that the three processes were linked through inosine 5'-phosphate dehydrogenase (impdh), a rate-limiting enzyme in de novo purine synthesis. We using adult zebrafish as a model system,we applied a genome-wide transcriptome approach that allowed us to investigate circadian gene expression. The whole-genome transcriptome profiles of adult brain in time-series were assayed on Agilent zebrafish microarrays. We used a similar statistical method to identify zebrafish circadian genes (ZCOG) as our previous study in larval zebrafish. Three isoforms of impdh show strong circadian oscillations in different tissues of zebrafish. impdh1a contributes to the ocular development and pigment synthesis, impdh2 promotes and impdh1b delays the development. By limiting the GTP required by DNA synthesis, impdh2 contributes to the daily rhythm of S phase in cell cycle. Multiple enzymes in the de novo purine synthesis pathway show the same circadian oscillations with peaks similar to impdh2. The circadian expression of this pathway is conserved in mouse liver. In summary, we show that the circadian regulation of de novo purine synthesis that supplies crucial building blocks for DNA replication is critical for gating cell cycle in circadian rhythm.
2013-10-01 | GSE51277 | GEO
Project description:Reactivating cell cycle re-entry in adult cardiomyocytes improves cardiac function after myocardial infarction (MI). De novo purine synthesis is a critical source of nucleotides and is involved in modulating cell proliferation. Here, using gain-of-function genetic tools, we explored the role of the de novo purine synthesis enzyme Adssl1 in cardiac regeneration. RNA sequencing analysis suggested that Adssl1 overexpression induced strong dedifferentiation and cell cycle entry.
2024-07-06 | GSE271411 | GEO
Project description:To investigate whether BRD4-chromatin binding is modulated by purine levels, we performed BRD4 ChIP-seq in cells with SLC nucleoside transporters knockout, or cells with de novo purine synthesis inhibitor 6-MP treatment. (+)-JQ1, an inhibitor which disrupts BRD4 and acetylated histone binding, was used as a positive control.
2021-04-17 | GSE167374 | GEO
Project description:In the McSC lineage in zebrafish, Aldh2 activity is an important source of formate through its metabolism of its substrate formaldehyde. This formate is required as input into the folate cycle, in particular de novo purine biosynthesis. This scRNA-seq experiment was conducted to investigate the global effects of Aldh2 inhibition on the transcriptomes of isolated McSCs.
2022-05-09 | GSE183868 | GEO
Project description:Purine biosynthesis and metabolism, conserved in all living organisms, is essential for cellular energy homeostasis and nucleic acids synthesis. The de novo synthesis of purine precursors is under tight negative feedback regulation mediated by adenine and guanine nucleotides. We describe a new early-onset distinct neurodegenerative condition resulting from mutations in the adenosine monophosphate deaminase 2 gene (AMPD2). Patients have characteristic brain imaging features of pontocerebellar hypoplasia (PCH), due to loss of brainstem and cerebellar parenchyma. We found that AMPD2 plays an evolutionary conserved role in the maintenance of cellular guanine nucleotide pools by regulating the feedback inhibition of adenosine derivatives on de novo purine synthesis. AMPD2 deficiency results in defective GTP-dependent initiation of protein translation, which can be rescued by administration of purine precursors. These data suggest AMPD2-related PCH as a new potentially treatable early-onset neurodegenerative disease.
2013-12-01 | GSE46615 | GEO
Project description:Purine biosynthesis and metabolism, conserved in all living organisms, is essential for cellular energy homeostasis and nucleic acids synthesis. The de novo synthesis of purine precursors is under tight negative feedback regulation mediated by adenine and guanine nucleotides. We describe a new early-onset distinct neurodegenerative condition resulting from mutations in the adenosine monophosphate deaminase 2 gene (AMPD2). Patients have characteristic brain imaging features of pontocerebellar hypoplasia (PCH), due to loss of brainstem and cerebellar parenchyma. We found that AMPD2 plays an evolutionary conserved role in the maintenance of cellular guanine nucleotide pools by regulating the feedback inhibition of adenosine derivatives on de novo purine synthesis. AMPD2 deficiency results in defective GTP-dependent initiation of protein translation, which can be rescued by administration of purine precursors. These data suggest AMPD2-related PCH as a new potentially treatable early-onset neurodegenerative disease. An 18 chip study, that compares iPSC derived neural progenitor cells from two individuals: a patient with pontocerebellar hypoplasia and an unaffected parent. Samples are run as either non-treated, treated with Adenosine, or treated with Adenosine and AICAr. Three replicates are included for every individuals in every treatment condition.
2013-12-01 | E-GEOD-46615 | biostudies-arrayexpress
Project description:Although ADSL is an enzyme that is involved in de novo purine synthesis, it was reported that ADSL knockdown did not result in decreases in adenine nucleotides (AMP, ADP, and ATP) or GTP. Then, we hypothesized that decreased cell proliferation, migration and invasion capability by ADSL knockdown in endometrial cancer cells were caused through a mechanism independent of purine synthesis. To elucidate a mechanism, we performed DNA microarray-based gene expression profiling using ADSL knockdown and control HEC1B cells. In the analysis, 940 out of 34,127 probes showed greater than two-fold changes in expression with a significant difference, p value < 0.05.
2018-03-08 | GSE100703 | GEO