Intronic miRNA–directed regulation of mitochondrial RNA editing enhances plant stress tolerance in Arabidopsis
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PROVIDER: PRJNA872480 | ENA |
REPOSITORIES: ENA
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Project description:MicroRNAs (miRNAs) have emerged as key regulators in plant development and stress responses. Increasing evidence points to the crucial role of intronic miRNA that derived from the introns of other genes in animals, whereas few reports have explored this topic in plants. We report here an RNA splicing–mediated mechanism involved in stress responses, whereby intronic miR400 modulates mitochondrial RNA editing by targeting the PPR1 mRNA. An intronic miR400 splicing–dependent luciferase transgenic line was generated to monitor the intron splicing events. We determined that luciferase activity decreases upon cadmium (Cd) treatment due to the retention of the intron containing miR400, which inhibits the production of mature miR400. Overexpression of MIR400 rendered plants more sensitive to Cd stress, whereas impaired miR400 expression enhanced their tolerance. Genetic and molecular experiments identified the PENTATRICOPEPTIDE REPEAT PROTEIN 1 (PPR1) as the miR400 target responsible for the plant Cd response. In addition, we demonstrate that PPR1 affects RNA editing of the mitochondrial gene ccb206 to control reactive oxygen species accumulation and improve plant tolerance. Our study illustrates intron splicing as a key step in intronic miR400 regulation and highlights the function of intronic miRNA as a “signal transducer” to enhance plant stress tolerance.
2025-08-19 | GSE211873 | GEO
Project description:Multiprotein bridging factor 1c MBF1c (At3g24500) is a stress-response transcription co-activator. To test the function of MBF1c, we over-expressed it in transgenic Arabidopsis plants using the 35S-CaMV promoter. T4 seeds form 3 independent lines were tested for their tolerance to biotic and abiotic stress conditions. Constitutive expression of MBF1c in Arabidopsis enhanced the tolerance of transgenic plants to bacterial infection, salinity, heat and osmotic stress. Moreover, the enhanced tolerance of transgenic plants to osmotic and heat stress was maintained even when these two stresses were combined. The expression of MBF1c in transgenic plants augmented the accumulation of a number of sugars and defense transcrtipts in response to heat stress. Transcriptome profiling and inhibitor studies suggest that MBF1c expression enhances the tolerance of transgenic plants to heat and osmotic stress by partially activating, or perturbing, the ethylene-response signal transduction pathway. MBF1 proteins could be used to enhance the tolerance of plants to different abiotic stresses. Suzuki et al., 2005 Plant Physiology, submitted. Experimenter name = Ron Mittler; Experimenter phone = 1-775-784-1384; Experimenter fax = 1-775-784-1650; Experimenter department = Dept. of Biochemistry; Experimenter institute = University of Nevada; Experimenter address = MS200; Experimenter address = Reno; Experimenter address = Nevada; Experimenter zip/postal_code = 89557; Experimenter country = USA Experiment Overall Design: 6 samples were used in this experiment
2008-06-13 | E-GEOD-5539 | biostudies-arrayexpress
Project description:Glutamine deprivation enhances directed differentiation of renal organoids
| PRJNA529412 | ENA
Project description:The RNA editing enzyme ADAR chemically modifies adenosine (A) to inosine (I), which is interpreted by the ribosome as a guanosine. Here we assess cotranscriptional A-to-I editing in Drosophila, by isolating nascent RNA from adult fly heads and subjecting samples to high-throughput sequencing. There are a large number of edited sites within nascent exons. Nascent RNA from an ADAR null mutant strain was also sequenced, indicating that almost all A-to-I events require ADAR. Moreover, mRNA editing levels correlate with editing levels within the cognate nascent RNA sequence, indicating that the extent of editing is set cotranscriptionally. Surprisingly, the nascent data also identify an excess of intronic over exonic editing sites. These intronic sites occur preferentially within introns that are poorly spliced cotranscriptionally, suggesting a link between editing and splicing. We conclude that ADAR-mediated editing is more widespread than previously indicated and largely occurs cotranscriptionally. GSM914095: Fly genomic DNA sequencing. Sequenced on the Illumina GA II. GSM914102-GSM914113: Fly head nascent RNA profiles over 6 time points of a 12hr light:dark cycle in duplicate; sequenced on the Illumina GA II. GSM914114-GSM914119: Fly head nascent RNA profiles of yw, FM7, ADAR0 males in duplicate; sequenced on the HiSeq2000. GSM915213-GSM915214: Fly head mRNA profiles over 2 time points of a 12hr light:dark cycle; sequenced on the Illumina GA II. GSM915215-GSM915220: Fly head mRNA profiles over 6 time points of a 12hr light:dark cycle; paired-end sequenced on the Illumina GA II. GSM915221-GSM91526: Fly head mRNA profiles over 6 time points of a 12hr light:dark cycle; sequenced on the Illumina GA II.
2012-05-31 | E-GEOD-37232 | biostudies-arrayexpress
Project description:DNA epigenome editing using CRISPR-Cas SunTag-directed DNMT3A
| PRJNA382980 | ENA
Project description:Gene disruption by CRISPR/Cas9 is highly efficient and relies on the error-prone non-homologous end-joining (NHEJ) pathway. Conversely, precise gene editing requires homology-directed repair (HDR), which occurs at a lower frequency than NHEJ in mammalian cells. Here, by testing whether manipulation of DNA repair factors would improve HDR efficacy, we show that transient ectopic co-expression of RAD52 and a dominant-negative 53BP1 (dn53BP1) synergize to enable efficient HDR using a single-stranded oligonucleotide DNA donor template at multiple loci in human cells, including patient-derived induced pluripotent stem (iPS) cells. Co-expression of RAD52 and dn53BP1 improves multiplexed HDR-mediated editing, whereas expression of RAD52 alone enhances HDR with Cas9 nickase. Our data show that the frequency of NHEJ-mediated DSB repair in the presence of these two factors is not suppressed, and suggest that dn53BP1 competitively antagonizes 53BP1 to augment HDR in combination with RAD52. Importantly, co-expression of RAD52 and dn53BP1 does not alter Cas9 off-target activity. These findings support the use of RAD52 and dn53BP1 co-expression to overcome bottlenecks that limit HDR in precision genome editing.
2017-11-23 | GSE103241 | GEO
Project description:Ethanol Treatment Enhances Drought Stress Tolerance in Plants
| PRJNA832309 | ENA
Project description:Repair of double-strand DNA breaks generated by site-directed endonucleases, like Cas9, is the hallmark of gene editing based on homology-directed repair (HDR). HDR uses an exogenous DNA template to restore the cleaved DNA sequence and can facilitate specific gene corrections as well as insertion of genes or partial cDNA sequences. For CRISPR/Cas-directed gene editing, co-administration of the Cas9/single guide RNA (sgRNA) ribonucleoprotein (RNP) complex and a DNA template typically involves two different delivery strategies or different types of vehicles. This requires exquisite timing of delivery and may potentially challenge safety and therapeutic applicability. There is a need therefore for technologies that can ferry complete editing tool kits into cells. Here, we demonstrate the use of lentivirus-derived nanoparticles (LVNPs) to transport both RNP complexes and vector RNA, which upon reverse transcription serves as donor for HDR-directed repair. These ‘all-in-one’ LVNPs support targeted gene insertion with reduced off-target effects relative to nucleofection procedures. We show potent editing in the HBB gene in human erythroid progenitor cells as well as HDR-directed editing in hematopoietic stem and progenitor cells. Our findings mark a first step toward using a single virus-derived vehicle for delivering a full HDR gene editing kit.
2025-08-14 | GSE283171 | GEO
Project description:Approximately half of all microRNAs reside within intronic regions and are often co-transcribed with their host genes. However, most studies on intronic microRNAs focus on individual microRNAs, and conversely most studies on protein-coding and non-coding genes frequently ignore any intron-derived microRNAs. We hypothesize that the individual components of such multi-genic loci may play cooperative or competing roles in driving disease progression, and that examining the combinatorial effect of these components would uncover deeper insights into their functional importance. To address this, we perform systematic analyses of intronic microRNA:host loci in colon cancer. We observe that the FTX locus, comprising of a long non-coding RNA FTX and multiple intronic microRNAs, is highly upregulated in cancer and demonstrate that cooperativity within this multi-component locus promotes cancer growth. In addition, we show that FTX interacts with DHX9 and DICER and delineate its novel roles in regulating A-to-I RNA editing and microRNA expression. These results show for the first time that a long non-coding RNA can regulate A-to-I RNA editing, further expanding the functional repertoire of long non-coding RNAs. We further demonstrate the inhibitory effects of intronic miR-374b and -545 on the tumor suppressors PTEN and RIG-I to enhance the proto-oncogenic PI3K-AKT signaling. Finally, we show that intronic miR-421 may exert an autoregulatory effect on miR-374b and -545. Taken together, our data unveil the intricate interplay between intronic microRNAs and their host transcripts in the modulation of key signaling pathways and disease progression, adding new perspectives to the functional landscape of multi-genic loci.
2021-01-05 | PXD021823 | Pride
Project description:Glutamine deprivation enhances metabolic reprogramming during kidney organoid directed differentiation
| PRJNA523040 | ENA