Ontology highlight
ABSTRACT:
PROVIDER: PRJNA530618 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8839731.fastq.gz | Fastqsanger.gz | |||
| SRR8839732.fastq.gz | Fastqsanger.gz | |||
| SRR8839733.fastq.gz | Fastqsanger.gz | |||
| SRR8839734.fastq.gz | Fastqsanger.gz |
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Project description:For establishing the photosynthetic apparatus plant cells must orchestrate the expression of genes encoded in both nucleus and chloroplast. Therefore a crosstalk between the two compartments is necessary. We employed a trivalent gene expression profiling approach in order to elucidate the changes in gene expression that occur during the early steps of light-induced chloroplast biogenesis.
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Project description:The regulator for chloroplast biogenesis (rcb) mutant was identified as a mutant defective in phytochrome-mediated chloroplast biogenesis. The rcb mutant has long hypocotyl and albino phenotypes. RCB initiates chloroplast biogenesis in the nucleus by promoting the degradation of the master repressors for chloroplast biogenesis, the PIFs (Phytochrome Interacting Factors). To understand how RCB regulates the expression of PIF-regulated genes, we performed genome-wide expression analysis of RCB-dependent genes using a rcb-10 null allele.
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Project description:RATIONALE: Studying the genes expressed in samples of tissue from patients with cancer may help doctors identify biomarkers related to cancer.
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Project description:Chromosome loss that results in monosomy has detrimental consequences for human cells, but the underlying molecular mechanisms remain enigmatic. Using p53 deficient monosomic cell lines, we found that chromosome loss impairs proliferation and genomic stability. Transcriptome and proteome analysis revealed a partial compensation of the gene dosage changes that mitigates the effects of chromosome loss. Monosomy triggers global gene expression changes that differ from the effects of trisomy. Strikingly, ribosome biogenesis and translation were commonly downregulated in monosomic cells. Polysome profiling and translation analysis suggest that the defects arise due to haploinsufficiency of ribosomal genes. The ensuing ribosome biogenesis stress triggers the p53 pathway and G1 arrest when TP53 is reintroduced into monosomic cells. Accordingly, impaired ribosome biogenesis and p53 inactivation are associated with monosomy in cancer. Our first systematic study of monosomy in human cells demonstrates that haploinsufficiency of ribosomal genes presents a dominant negative phenotype of monosomy.
2021-06-17 | PXD022927 | Pride
Project description:Chromosome loss that results in monosomy has detrimental consequences for human cells, but the underlying molecular mechanisms remain enigmatic. Using p53 deficient monosomic cell lines, we found that chromosome loss impairs proliferation and genomic stability. Transcriptome and proteome analysis revealed a partial compensation of the gene dosage changes that mitigates the effects of chromosome loss. Monosomy triggers global gene expression changes that differ from the effects of trisomy. Strikingly, ribosome biogenesis and translation were commonly downregulated in monosomic cells. Polysome profiling and translation analysis suggest that the defects arise due to haploinsufficiency of ribosomal genes. The ensuing ribosome biogenesis stress triggers the p53 pathway and G1 arrest when TP53 is reintroduced into monosomic cells. Accordingly, impaired ribosome biogenesis and p53 inactivation are associated with monosomy in cancer. Our first systematic study of monosomy in human cells demonstrates that haploinsufficiency of ribosomal genes presents a dominant negative phenotype of monosomy.
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Project description:We report widespread changes in ribosome biogenesis factor, aerobic respiration and hexose tranporter gene expression. We also identify antisense transcripts to hexose transporter genes in dbp2∆ cells.
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Project description:Photosynthesis requires chloroplasts, where most proteins are nucleus-encoded and produced via cytoplasmic translation. The translation initiation factor eIF5B gates the transition from initiation (I) to elongation (E), and the Kozak motif is associated with translation efficiency, but their relationship is previously unknown. Here, with ribosome profiling, we determined the genome-wide I-E transition efficiencies. We discovered that the most prevalent Kozak motif is associated with high I-E transition efficiency in Arabidopsis, rice, and wheat, thus implicating the Kozak motif in facilitating the I-E transition. Indeed, the effects of most Kozak motifs, including the most effective ones, depend on HOT3/eIF5B1 in Arabidopsis. HOT3 preferentially promotes the translation of photosynthesis-associated nuclear genes in a Kozak motif-dependent manner, which explains the chloroplast defects of hot3 mutants. Our study reveals an evolutionarily-conserved link between the Kozak motif and eIF5B-mediated translational I-E efficiency and elucidates a HOT3-mediated translational control of nuclear photosynthesis genes for chloroplast biogenesis.
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Project description:Photosynthesis requires chloroplasts, where most proteins are nucleus-encoded and produced via cytoplasmic translation. The translation initiation factor eIF5B gates the transition from initiation (I) to elongation (E), and the Kozak motif is associated with translation efficiency, but their relationship is previously unknown. Here, with ribosome profiling, we determined the genome-wide I-E transition efficiencies. We discovered that the most prevalent Kozak motif is associated with high I-E transition efficiency in Arabidopsis, rice, and wheat, thus implicating the Kozak motif in facilitating the I-E transition. Indeed, the effects of most Kozak motifs, including the most effective ones, depend on HOT3/eIF5B1 in Arabidopsis. HOT3 preferentially promotes the translation of photosynthesis-associated nuclear genes in a Kozak motif-dependent manner, which explains the chloroplast defects of hot3 mutants. Our study reveals an evolutionarily-conserved link between the Kozak motif and eIF5B-mediated translational I-E efficiency and elucidates a HOT3-mediated translational control of nuclear photosynthesis genes for chloroplast biogenesis.
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Project description:Chromosome loss that results in monosomy has detrimental consequences for human cells, but the underlying molecular mechanisms remain enigmatic. Using p53 deficient monosomic cell lines, we found that chromosome loss impairs proliferation and genomic stability. Transcriptome and proteome analysis revealed a partial compensation of the gene dosage changes that mitigates the effects of chromosome loss. Monosomy triggers global gene expression changes that differ from the effects of trisomy. Strikingly, ribosome biogenesis and translation were commonly downregulated in monosomic cells. Polysome profiling and translation analysis suggest that the defects arise due to haploinsufficiency of ribosomal genes. The ensuing ribosome biogenesis stress triggers the p53 pathway and G1 arrest when TP53 is reintroduced into monosomic cells. Accordingly, impaired ribosome biogenesis and p53 inactivation are associated with monosomy in cancer. Our first systematic study of monosomy in human cells demonstrates that haploinsufficiency of ribosomal genes presents a dominant negative phenotype of monosomy.
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