Erroneous ribosomal RNAs promote the generation of antisense ribosomal siRNA
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA454449 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7088700.fastq.gz | Fastqsanger.gz | |||
| SRR7088695.fastq.gz | Fastqsanger.gz | |||
| SRR7088696.fastq.gz | Fastqsanger.gz | |||
| SRR7088697.fastq.gz | Fastqsanger.gz | |||
| SRR7088698.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Ribosome biogenesis is a multi-step process, during which mistakes could take place at any step of pre-rRNA processing, modification, and assembly of ribosomes. Misprocessed rRNAs are usually detected and degraded by surveillance machineries. Recently, we identified a class of antisense ribosomal siRNAs (risiRNAs) that downregulate pre-rRNAs through the nuclear RNAi pathway. To further understand the biological roles of risiRNA, we conducted both forward and reverse genetic screenings to search for more susi mutants. We isolated a number of genes that are broadly conserved from yeast to humans and are involved in pre-rRNA modification and processing. Among them, SUSI-2(ceRRP8) is homologous to human RRP8 and engages in m1A methylation of 26S rRNA. C27F2.4(ceBUD23) is a m7G methyltransferase of 18S rRNA. E02H1.1(ceDIMT1L) is a predicted m6(2)Am6(2)A methyltransferase of 18S rRNA . Mutation of these genes led to modification deficiency of rRNAs and elicited accumulation of risiRNAs, which further triggered the cytoplasm to nuclear and nucleolar translocation of an Argonaute protein NRDE-3. The processing deficiency of rRNAs resulted in the accumulation of risiRNAs as well. We isolated SUSI-3(RIOK-1) which is similar to human RIOK1 that cleaves 20S to 18S rRNA. We further utilized RNAi and CRISPR/Cas9 technologies to perform candidate-based reverse genetic screening and identified additional pre-rRNA processing factors that suppressed risiRNA production. Therefore, we concluded that erroneous rRNAs can trigger risiRNA generation and subsequently turn on the nuclear RNAi-mediated gene silencing pathway to inhibit pre-rRNA expression, which may provide a quality control mechanism to maintain the homeostasis of rRNAs.
2018-05-02 | GSE113905 | GEO
Project description:Ribosome biogenesis is a multistep process, during which mistakes can occur at any step of pre-rRNA processing, modification, and ribosome assembly. Misprocessed rRNAs are usually detected and degraded by surveillance machineries. Recently, we identified a class of antisense ribosomal siRNAs (risiRNAs) that down-regulate pre-rRNAs through the nuclear RNAi pathway. To further understand the biological roles of risiRNAs, we conducted both forward and reverse genetic screens to search for more suppressor of siRNA (susi) mutants. We isolated a number of genes that are broadly conserved from yeast to humans and are involved in pre-rRNA modification and processing. Among them, SUSI-2(ceRRP8) is homologous to human RRP8 and engages in m1A methylation of the 26S rRNA. C27F2.4(ceBUD23) is an m7G-methyltransferase of the 18S rRNA. E02H1.1(ceDIMT1L) is a predicted m6(2)Am6(2)A-methyltransferase of the 18S rRNA. Mutation of these genes led to a deficiency in modification of rRNAs and elicited accumulation of risiRNAs, which further triggered the cytoplasmic-to-nuclear and cytoplasmic-to-nucleolar translocations of the Argonaute protein NRDE-3. The rRNA processing deficiency also resulted in accumulation of risiRNAs. We also isolated SUSI-3(RIOK-1), which is similar to human RIOK1, that cleaves the 20S rRNA to 18S. We further utilized RNAi and CRISPR-Cas9 technologies to perform candidate-based reverse genetic screens and identified additional pre-rRNA processing factors that suppressed risiRNA production. Therefore, we concluded that erroneous rRNAs can trigger risiRNA generation and subsequently, turn on the nuclear RNAi-mediated gene silencing pathway to inhibit pre-rRNA expression, which may provide a quality control mechanism to maintain homeostasis of rRNAs.
| S-EPMC6176571 | biostudies-literature
Project description:Cis-encoded antisense RNAs (asRNAs) are widespread along bacterial transcriptomes. However, the role of the vast majority of these RNAs remains unknown, and there is an ongoing discussion as to what extent these transcripts are the result of transcriptional noise. We show, by comparative transcriptomics of 20 bacterial species and one chloroplast, that the number of asRNAs is exponentially dependent on the genomic AT content, and that expression of asRNA at low levels exerts little impact in terms of energy consumption. A transcription model simulating mRNA and asRNA production indicates that the asRNA regulatory effect is only observed above certain expression thresholds, substantially higher than physiological transcript levels. These predictions were verified experimentally by overexpressing 9 different asRNAs in M. pneumoniae. Our results suggest that most of the antisense transcripts found in bacteria are the consequence of transcriptional noise, arising at spurious promoters throughout the genome.
2018-10-25 | PXD003231 | Pride
Project description:Eukaryotic cells express a wide variety of endogenous small regulatory RNAs that function in the nucleus. We previously found that erroneous rRNAs induce the generation of antisense ribosomal siRNAs (risiRNAs) which silence the expression of rRNAs via the nuclear RNAi defective (Nrde) pathway. To further understand the biological roles and mechanisms of this class of small regulatory RNAs, we conducted forward genetic screening to identify factors involved in risiRNA generation in Caenorhabditis elegans. We found that risiRNAs accumulated in the RNA exosome mutants. risiRNAs directed a NRDE-dependent silencing of pre-rRNAs in the nucleolus. In the presence of risiRNAs, NRDE-2 accumulated in the nucleolus and colocalized with RNA polymerase I. risiRNAs inhibited the transcription elongation of RNA polymerase I by decreasing RNAP I occupancy downstream of the RNAi-targeted site. Meanwhile, exosomes mislocalized from the nucleolus to nucleoplasm in suppressor of siRNA (susi) mutants, in which erroneous rRNAs accumulated. These results established a novel model of rRNA surveillance by combining ribonuclease-mediated RNA degradation with small RNA-directed nucleolar RNAi system.
2021-01-20 | GSE165078 | GEO
Project description:LlorénsRico2016 - Effects of cis-Encoded antisense RNAs (asRNAs) - Case1
Three
putative effects of the asRNAs were considered in this study: in
case 1
(this
model)
,
the binding of the asRNA to the corresponding mRNA induces
degradation of the duplex. In case 2, the binding of the asRNA to
the mRNA induces degradation of the mRNA, but not of the asRNA.
In case 3, the mRNA and the asRNA bind reversibly to form a
stable duplex, preventing translation of the mRNA. In all the
three cases, binding to the ribosome protects the mRNA from the
effect of the asRNA.
This model is described in the article:
Bacterial antisense RNAs are
mainly the product of transcriptional noise.
Lloréns-Rico V, Cano J,
Kamminga T, Gil R, Latorre A, Chen WH, Bork P, Glass JI, Serrano
L, Lluch-Senar M.
Sci Adv 2016 Mar; 2(3): e1501363
Abstract:
cis-Encoded antisense RNAs (asRNAs) are widespread along
bacterial transcriptomes. However, the role of most of these
RNAs remains unknown, and there is an ongoing discussion as to
what extent these transcripts are the result of transcriptional
noise. We show, by comparative transcriptomics of 20 bacterial
species and one chloroplast, that the number of asRNAs is
exponentially dependent on the genomic AT content and that
expression of asRNA at low levels exerts little impact in terms
of energy consumption. A transcription model simulating mRNA
and asRNA production indicates that the asRNA regulatory effect
is only observed above certain expression thresholds,
substantially higher than physiological transcript levels.
These predictions were verified experimentally by
overexpressing nine different asRNAs in Mycoplasma pneumoniae.
Our results suggest that most of the antisense transcripts
found in bacteria are the consequence of transcriptional noise,
arising at spurious promoters throughout the genome.
This model is hosted on
BioModels Database
and identified by:
MODEL1511170000.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-05-18 | MODEL1511170000 | BioModels
Project description:LlorénsRico2016 - Effects of cis-Encoded
antisense RNAs (asRNAs) - Case3
Three putative
effects of the asRNAs were considered in this study: in case 1,
the binding of the asRNA to the corresponding mRNA induces
degradation of the duplex. In case 2, the binding of the asRNA
to the mRNA induces degradation of the mRNA, but not of the
asRNA. In case 3 (this model), the mRNA and the asRNA bind
reversibly to form a stable duplex, preventing translation of
the mRNA. In all the three cases, binding to the ribosome
protects the mRNA from the effect of the asRNA.
This model is described in the article:
Bacterial antisense RNAs are
mainly the product of transcriptional noise.
Lloréns-Rico V, Cano J,
Kamminga T, Gil R, Latorre A, Chen WH, Bork P, Glass JI, Serrano
L, Lluch-Senar M.
Sci Adv 2016 Mar; 2(3): e1501363
Abstract:
cis-Encoded antisense RNAs (asRNAs) are widespread along
bacterial transcriptomes. However, the role of most of these
RNAs remains unknown, and there is an ongoing discussion as to
what extent these transcripts are the result of transcriptional
noise. We show, by comparative transcriptomics of 20 bacterial
species and one chloroplast, that the number of asRNAs is
exponentially dependent on the genomic AT content and that
expression of asRNA at low levels exerts little impact in terms
of energy consumption. A transcription model simulating mRNA
and asRNA production indicates that the asRNA regulatory effect
is only observed above certain expression thresholds,
substantially higher than physiological transcript levels.
These predictions were verified experimentally by
overexpressing nine different asRNAs in Mycoplasma pneumoniae.
Our results suggest that most of the antisense transcripts
found in bacteria are the consequence of transcriptional noise,
arising at spurious promoters throughout the genome.
This model is hosted on
BioModels Database
and identified by:
MODEL1511170002.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-05-18 | MODEL1511170002 | BioModels
Project description:LlorénsRico2016 - Effects of cis-Encoded
antisense RNAs (asRNAs) - Case1
Three
putative effects of the asRNAs were considered in this study: in
case 1
,
the binding of the asRNA to the corresponding mRNA induces
degradation of the duplex. In case 2
(this
model)
the binding of the asRNA to the mRNA induces degradation of the
mRNA, but not of the asRNA. In case 3, the mRNA and the asRNA
bind reversibly to form a stable duplex, preventing translation
of the mRNA. In all the three cases, binding to the ribosome
protects the mRNA from the effect of the asRNA.
This model is described in the article:
Bacterial antisense RNAs are
mainly the product of transcriptional noise.
Lloréns-Rico V, Cano J,
Kamminga T, Gil R, Latorre A, Chen WH, Bork P, Glass JI, Serrano
L, Lluch-Senar M.
Sci Adv 2016 Mar; 2(3): e1501363
Abstract:
cis-Encoded antisense RNAs (asRNAs) are widespread along
bacterial transcriptomes. However, the role of most of these
RNAs remains unknown, and there is an ongoing discussion as to
what extent these transcripts are the result of transcriptional
noise. We show, by comparative transcriptomics of 20 bacterial
species and one chloroplast, that the number of asRNAs is
exponentially dependent on the genomic AT content and that
expression of asRNA at low levels exerts little impact in terms
of energy consumption. A transcription model simulating mRNA
and asRNA production indicates that the asRNA regulatory effect
is only observed above certain expression thresholds,
substantially higher than physiological transcript levels.
These predictions were verified experimentally by
overexpressing nine different asRNAs in Mycoplasma pneumoniae.
Our results suggest that most of the antisense transcripts
found in bacteria are the consequence of transcriptional noise,
arising at spurious promoters throughout the genome.
This model is hosted on
BioModels Database
and identified by:
MODEL1511170001.
To cite BioModels Database, please use:
BioModels Database:
An enhanced, curated and annotated resource for published
quantitative kinetic models.
To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
CC0
Public Domain Dedication for more information.
2017-05-18 | MODEL1511170001 | BioModels
Project description:Background: Eukaryotic cells express a complex layer of noncoding RNAs. An intriguing family of regulatory RNAs includes transcripts from the opposite strand of protein coding genes, so called natural antisense transcripts (NATs). Here, we test the hypothesis that antisense transcription triggers RNA interference and gives rise to endogenous short RNAs (endo-siRNAs). Methods/Results: We used cloned human embryonic kidney cells (HEK293) followed by short RNAseq to investigate the small genic RNA transcriptome. 378 genes gave rise to short RNA reads that mapped to exons of RefSeq genes. The length profile of short RNAs showed a broad peak of 20-24 nucleotides, indicative of endo-siRNAs. Collapsed reads mapped predominantly to the first and the last exon of genes (74%). RNAs reads were intersected with sequences occupied by RNAPolII or bound to Argonaute (AGO1 by crosslinking, ligation, and sequencing of hybrids, CLASH). In the first exon, 94% of the reads correlated with PolII occupancy with an average density of 130 (relative units); this decreased to 65%/20 in middle exons and 54%/12 in the last exon. CLASH reads mapping to multi-exon genes showed little distribution bias with an average of about 5 CLASH reads overlapping with 60% of the endo-siRNA reads. However, endo-siRNAs (21-25 nt) intersecting with CLASH reads were enriched at the 5'end and decreased towards the 3'end. We then investigated the 378 genes with particular focus on features indicative for short RNA production; however, found that endo-siRNA numbers did not correlate with gene structures that favor convergent transcription. In contrast, our gene set was found notably over-represented in the NATsDB sense/antisense group as compared to non-overlapping and non-bidirectional groups. Moreover, read counts showed no correlation with the steady-state levels of the related mRNAs and the pattern of endo-siRNAs proved reproducible after an induced mutagenic insult. Conclusions: Our results suggest that antisense transcripts contribute to low levels of endo-siRNAs in fully differentiated human cells. A characteristic endo-siRNA footprint is being produced at sites of RNAPolII transcription which is also related to AGO1. This endo-siRNA signature represents an intriguing finding and its reproducibility suggests that the production of endo-siRNAs is a regulated process with potential homoeostatic impact.
2014-02-28 | GSE52996 | GEO
Project description:lncRNA TINCR antisense pulldown of interacting RNAs
| PRJNA517674 | ENA
Project description:Background: Eukaryotic cells express a complex layer of noncoding RNAs. An intriguing family of regulatory RNAs includes transcripts from the opposite strand of protein coding genes, so called natural antisense transcripts (NATs). Here, we test the hypothesis that antisense transcription triggers RNA interference and gives rise to endogenous short RNAs (endo-siRNAs). Methods/Results: We used cloned human embryonic kidney cells (HEK293) followed by short RNAseq to investigate the small genic RNA transcriptome. 378 genes gave rise to short RNA reads that mapped to exons of RefSeq genes. The length profile of short RNAs showed a broad peak of 20-24 nucleotides, indicative of endo-siRNAs. Collapsed reads mapped predominantly to the first and the last exon of genes (74%). RNAs reads were intersected with sequences occupied by RNAPolII or bound to Argonaute (AGO1 by crosslinking, ligation, and sequencing of hybrids, CLASH). In the first exon, 94% of the reads correlated with PolII occupancy with an average density of 130 (relative units); this decreased to 65%/20 in middle exons and 54%/12 in the last exon. CLASH reads mapping to multi-exon genes showed little distribution bias with an average of about 5 CLASH reads overlapping with 60% of the endo-siRNA reads. However, endo-siRNAs (21-25 nt) intersecting with CLASH reads were enriched at the 5'end and decreased towards the 3'end. We then investigated the 378 genes with particular focus on features indicative for short RNA production; however, found that endo-siRNA numbers did not correlate with gene structures that favor convergent transcription. In contrast, our gene set was found notably over-represented in the NATsDB sense/antisense group as compared to non-overlapping and non-bidirectional groups. Moreover, read counts showed no correlation with the steady-state levels of the related mRNAs and the pattern of endo-siRNAs proved reproducible after an induced mutagenic insult. Conclusions: Our results suggest that antisense transcripts contribute to low levels of endo-siRNAs in fully differentiated human cells. A characteristic endo-siRNA footprint is being produced at sites of RNAPolII transcription which is also related to AGO1. This endo-siRNA signature represents an intriguing finding and its reproducibility suggests that the production of endo-siRNAs is a regulated process with potential homoeostatic impact. Size selected RNASeq of 3 human embryonic kidney cell (HEK293) samples. 1 control and 2 samples exposed to 100 μg/ml ethyl methanesulfonate for 24 hrs.
2014-02-28 | E-GEOD-52996 | biostudies-arrayexpress