Divergent rRNAs as regulators of gene expression at the ribosome level
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA438895 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8258332.fastq.gz | Fastqsanger.gz | |||
| SRR8258333.fastq.gz | Fastqsanger.gz | |||
| SRR8258334.fastq.gz | Fastqsanger.gz | |||
| SRR8258335.fastq.gz | Fastqsanger.gz | |||
| SRR8258336.fastq.gz | Fastqsanger.gz |
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Project description:It is generally assumed that each organism has evolved to possess a unique ribosomal RNA (rRNA) species optimal for its physiological needs. However, some organisms express divergent rRNAs, the functional roles of which remain unknown. Here, we show that ribosomes containing the most variable rRNAs, encoded by the rrnI operon (herein designated I-ribosomes), direct the preferential translation of a subset of mRNAs in Vibrio vulnificus, enabling the rapid adaptation of bacteria to temperature and nutrient shifts. In addition, genetic and functional analyses of I-ribosomes and target mRNAs suggest that both I-ribosomal subunits are required for the preferential translation of specific mRNAs, the Shine-Dalgarno sequences of which do not play a critical role in I-ribosome binding. This study identifies genome-encoded divergent rRNAs as regulators of gene expression at the ribosome level, providing an additional level of regulation of gene expression in bacteria in response to environmental changes.
2018-11-27 | GSE111991 | GEO
Project description:To achieve maximal growth, cells must manage a massive economy of ribosomal proteins (r-proteins) and RNAs (rRNAs) to produce thousands of ribosomes every minute. Although ribosomes are essential in all cells, natural disruptions to ribosome biogenesis lead to heterogeneous phenotypes. Here, we model these perturbations in Saccharomyces cerevisiae and show that challenges to ribosome biogenesis result in acute loss of proteostasis. Imbalances in the synthesis of r-proteins and rRNAs lead to the rapid aggregation of newly synthesized orphan r-proteins and compromise essential cellular processes, which cells alleviate by activating proteostasis genes. Exogenously bolstering the proteostasis network increases cellular fitness in the face of challenges to ribosome assembly, demonstrating the direct contribution of orphan r-proteins to cellular phenotypes. We propose that ribosome assembly is a key vulnerability of proteostasis maintenance in proliferating cells that may be compromised by diverse genetic, environmental, and xenobiotic perturbations that generate orphan r-proteins.
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Project description:In all domains of life, the rate of protein synthesis is directly linked to the rates of cell growth and proliferation. Consequently, highly proliferative cancer cells are especially sensitive to perturbations in ribosome biogenesis. While ribosome synthesis and cancer have a well-established relationship, only recently has ribosome biogenesis drawn interest as a cancer therapeutic target. Here, we have exploited the relationship between ribosome biogenesis and cancer cell proliferation by using a potent ribosome biogenesis inhibitor: RBI2 (Ribosome Biogenesis Inhibitor 2) to perturb cancer cell growth and viability. We demonstrate that RBI2 significantly decreases cell viability in malignant melanoma cells and breast cancer cell lines. Treatment with RBI2 dramatically and rapidly decreases ribosomal RNA (rRNA) synthesis, without affecting the occupancy of RNA polymerase I (Pol I) on the ribosomal DNA template. Next-generation RNA sequencing (RNA-seq) reveals that RBI2 and previously described ribosome biogenesis inhibitor CX-5461 induce distinct changes in the transcriptome. Investigation of the content of the pre-rRNAs through RT-qPCR reveals an increase in polyadenylation of cellular rRNA after treatment with RBI2, a known pathway by which rRNA degradation occurs. Northern blotting revealed that RBI2 does not appear to impair or alter rRNA processing. Collectively, these data suggest that RBI2 inhibits rRNA synthesis distinctly from other previously described ribosome biogenesis inhibitors, potentially through a novel pathway that upregulates turnover of premature rRNAs.
2021-11-08 | GSE188262 | GEO
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Project description:2’-O-methylation (2’-O-me) is one of the most abundant covalent modifications in ribosomal RNAs (rRNAs) vital for the functionality of the ribosome, in particular, translational regulation. Aberrant 2’-O-me causes developmental defects in animals and is associated with human cancer. However, a lack of systematic delineation of 2’-O-me sites significantly impedes our understanding of 2’-O-me in plants. Here we report the global profiling of 2’-O-me in Arabidopsis rRNAs, leading to the identification of 221 2’-O-me sites, including 137 novel ones compared to the Arabidopsis database that documents predicted rRNA 2-O-me sites. We show that 65% of yeast and 53% of human 2’-O-me sites are conserved in Arabidopsis. We discover not only 2’-O-me guided by box C/D snoRNAs, but also unprecedentedly a prevalent snoRNA-independent mechanism in Arabidopsis: 48% of the 2’-O-me sites are devoid of snoRNAs, including some conserved sites where snoRNAs are indispensable in human and yeast. Through HITS-CLIP (high-throughput sequencing of RNAs isolated by cross-linking immunoprecipitation), we show that Fibrillarin (FIB1) and FIB2 predominantly associate with box C/D snoRNAs in vivo and uncover previously unknown snoRNAs. By generating and analyzing mutants in the FIB genes, we demonstrate that they are responsible for the ribose methylation at many rRNA sites regardless of their snoRNA-dependent or independent nature. We report, for the first time, extensive 2’-O-me of chloroplast rRNAs and, intriguingly, the dependence of FIB1/2 at some sites. Our studies reveal the landscape of 2’-O-me in nuclear and chloroplast rRNAs and provide novel insights into the deposition of rRNA 2’-O-me.
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Project description:2’-O-methylation (2’-O-me) is one of the most abundant covalent modifications in ribosomal RNAs (rRNAs) vital for the functionality of the ribosome, in particular, translational regulation. Aberrant 2’-O-me causes developmental defects in animals and is associated with human cancer. However, a lack of systematic delineation of 2’-O-me sites significantly impedes our understanding of 2’-O-me in plants. Here we report the global profiling of 2’-O-me in Arabidopsis rRNAs, leading to the identification of 221 2’-O-me sites, including 137 novel ones compared to the Arabidopsis database that documents predicted rRNA 2-O-me sites. We show that 65% of yeast and 53% of human 2’-O-me sites are conserved in Arabidopsis. We discover not only 2’-O-me guided by box C/D snoRNAs, but also unprecedentedly a prevalent snoRNA-independent mechanism in Arabidopsis: 48% of the 2’-O-me sites are devoid of snoRNAs, including some conserved sites where snoRNAs are indispensable in human and yeast. Through HITS-CLIP (high-throughput sequencing of RNAs isolated by cross-linking immunoprecipitation), we show that Fibrillarin (FIB1) and FIB2 predominantly associate with box C/D snoRNAs in vivo and uncover previously unknown snoRNAs. By generating and analyzing mutants in the FIB genes, we demonstrate that they are responsible for the ribose methylation at many rRNA sites regardless of their snoRNA-dependent or independent nature. We report, for the first time, extensive 2’-O-me of chloroplast rRNAs and, intriguingly, the dependence of FIB1/2 at some sites. Our studies reveal the landscape of 2’-O-me in nuclear and chloroplast rRNAs and provide novel insights into the deposition of rRNA 2’-O-me.
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Project description:Multiomic Analysis of Neurons with Divergent Projection Patterns Identifies Novel Regulators of Axon Pathfinding
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Project description:Ribosome profiling, which is based on deep sequencing of ribosome footprints, has served as a powerful tool for elucidating the regulatory mechanism of protein synthesis. However, the current method has substantial issues: contamination by rRNAs and the lack of appropriate methods to measure ribosome numbers in transcripts. Here, we overcomeovercame these hurdles through the development of “Ribo-FilterOut”, which is based on the separation of footprints from ribosome subunits by ultrafiltration, and “Ribo-Calibration”, which relies on external spike-ins of stoichiometrically defined mRNA-ribosome complexes. A combination of these approaches estimates the number of ribosomes on a transcript, the translation initiation rate, and the overall number of translation events before its decay, all in a genome-wide manner. Moreover, our method revealed the allocation of ribosomes under heat shock stress, during aging, and across cell types. Our strategy of modified ribosome profiling measures kinetic and stoichiometric parameters of cellular translation across the transcriptome.
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Project description:In general, RNA-binding proteins act to modulate gene expression at transcript level through degradation or at protein level through translation. To elucidate the effect of Whi3, a yeast RNA binding protein, on gene expression, we performed ribosome profiling experiment on whi3 mutant and wildtype cells. Comparison ribosome profiling and RNA-seq data between whi3 mutant and wildtype cells
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Project description:Genome-wide reporter screen for transcriptional regulators of ribosome biogenesis genes and ribosomal protein genes
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