Ontology highlight
ABSTRACT:
PROVIDER: PRJNA769620 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16250903.fastq.gz | Fastqsanger.gz | |||
| SRR16250904.fastq.gz | Fastqsanger.gz | |||
| SRR16250905.fastq.gz | Fastqsanger.gz | |||
| SRR16250906.fastq.gz | Fastqsanger.gz | |||
| SRR16250907.fastq.gz | Fastqsanger.gz |
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Project description:While a plethora of small regulatory RNAs (sRNAs) have been identified in the human pathogen Staphylococcus aureus, the physiological function of most of them remains unknown. We report the characterization of SprY, a sRNA from S. aureus expressed from a pathogenicity island. RNAIII, a major regulator of S. aureus virulence, was discovered as a potential SprY target by an MS2-affinity purification assay. In silico interaction studies suggest a RNA-RNA pairing between the SprY 5’end and the 13rd stem-loop of RNAIII. Overproduction of SprY leads to a 1.5-fold reduction of RNAIII amount. By affecting the rnaIII expression, SprY affects the amount of RNAIII known targets. Indeed, SprY downregulates hla mRNA translation, but also upregulates other secreted factors such as Ecb and Rot. Furthermore, SprY decreases the hemolytic activity and virulence of S. aureus. Our results lead to propose that SprY is involved in S. aureus virulence through a post-transcriptional regulation of RNAIII.
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Project description:Pathogenic variants in MYBPC3 (myosin-binding protein C3) are the leading cause of genetic hypertrophic cardiomyopathy (HCM). Currently, there is no specific and effective treatment for this disease. Base editing is an emerging modality for treating monogenic diseases; however, its effect on MYBPC3 cardiomyopathy remains unexplored. Mybpc3-R946X/R946X mice developed early-onset left ventricular hypertrophy, systolic dysfunction, ventricular dilatation, and arrythmias. SpRY-ABEmax inefficiently corrected the Mybpc3-R946X mutation. In contrast, SpRY-ABE8e increased the efficiency by 3.6-fold and retained low level off-target editing. In vivo administration of SpRY-ABE8e efficiently corrected Mybpc3-R946X mutation in cardiomyocytes and prevented heart function decline, hypertrophic cardiomyopathy, and ventricular dysfunction. The therapeutic efficacy of SpRY-ABE8e-mediated gene correction surmounted AAV-mediated Mybpc3 gene replacement.Our study unveiled the immense potential of base editing to treat fatal inherited cardiomyopathies and opened a new avenue for the therapeutic managements of inherited cardiac diseases.
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Project description:Plant and animal centromeres comprise megabases of highly repeated satellite sequences, yet centromere function can be specified epigenetically on single-copy DNA by the presence of nucleosomes containing a centromere-specific variant of histone H3 (cenH3). We determined the positions of cenH3 nucleosomes in rice (Oryza sativa), which has centromeres composed of both the 155-bp CentO repeat and single-copy non-CentO sequences. We find that cenH3 nucleosomes protect 90-100 bp of DNA from micrococcal nuclease digestion, sufficient for only a single wrap of DNA around the cenH3 nucleosome core. cenH3 nucleosomes are translationally phased with 155-bp periodicity on CentO repeats, but not on non-CentO sequences. CentO repeats have a ~10-bp periodicity in WW dinucleotides and in micrococcal nuclease cleavage, providing evidence for rotational phasing of cenH3 nucleosomes on CentO, and suggesting that satellites evolve for translational and rotational stabilization of centromeric nucleosomes.
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