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Endogenous RNAi pathway evolutionarily shapes the destiny of the antisense lncRNA transcriptome

ABSTRACT: Endogenous RNAi pathway evolutionarily shapes the destiny of the antisense lncRNA transcriptome

PROVIDER: PRJNA530561 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8838460_1.fastq.gz	Fastqsanger.gz
	SRR8838460_2.fastq.gz	Fastqsanger.gz
	SRR8838461_1.fastq.gz	Fastqsanger.gz
	SRR8838461_2.fastq.gz	Fastqsanger.gz
	SRR8838454_1.fastq.gz	Fastqsanger.gz

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Endogenous RNAi pathway evolutionarily shapes the destiny of the antisense lncRNAs transcriptome.

Project description:Antisense long noncoding (aslnc)RNAs are extensively degraded by the nuclear exosome and the cytoplasmic exoribonuclease Xrn1 in the budding yeast Saccharomyces cerevisiae, lacking RNAi. Whether the ribonuclease III Dicer affects aslncRNAs in close RNAi-capable relatives remains unknown. Using genome-wide RNA profiling, here we show that aslncRNAs are primarily targeted by the exosome and Xrn1 in the RNAi-capable budding yeast Naumovozyma castellii, Dicer only affecting Xrn1-sensitive aslncRNAs levels in Xrn1-deficient cells. The dcr1 and xrn1 mutants display synergic growth defects, indicating that Dicer becomes critical in the absence of Xrn1. Small RNA sequencing showed that Dicer processes aslncRNAs into small RNAs, with a preference for Xrn1-sensitive aslncRNAs. Consistently, Dicer localizes into the cytoplasm. Finally, we observed an expansion of the exosome-sensitive antisense transcriptome in N. castellii compared with S. cerevisiae, suggesting that the presence of cytoplasmic RNAi has reinforced the nuclear RNA surveillance machinery to temper aslncRNAs expression. Our data provide fundamental insights into aslncRNAs metabolism and open perspectives into the possible evolutionary contribution of RNAi in shaping the aslncRNAs transcriptome.

| S-EPMC6713810 | biostudies-literature

Endogenous RNAi pathway evolutionarily shapes the destiny of the antisense lncRNA transcriptome

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-08-21 | GSE129233 | GEO

Nucleosome Positioning Shapes Cryptic Antisense Transcription

Project description:Nucleosome Positioning Shapes Cryptic Antisense Transcription

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Nucleosome Positioning Shapes Cryptic Antisense Transcription [Mnase-seq]

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Nucleosome Positioning Shapes Cryptic Antisense Transcription [ChIP-seq]

Project description:Nucleosome Positioning Shapes Cryptic Antisense Transcription [ChIP-seq]

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Nucleosome Positioning Shapes Cryptic Antisense Transcription [RNA-seq]

Project description:Nucleosome Positioning Shapes Cryptic Antisense Transcription [RNA-seq]

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An evolutionarily conserved DNA-encoded logic shapes CpG island formation

Project description:An evolutionarily conserved DNA-encoded logic shapes CpG island formation

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An evolutionarily conserved DNA-encoded logic shapes CpG island formation

Project description:DNA methylation is an epigenetic modification of the vertebrate genome that contributes to transcriptional repression, imprinting, and X-chromosome inactivation. While the majority of the genome is blanketed in DNA methylation, regions known as CpG islands (CGIs) remain remarkably refractory to this modification. CpG islands are associated with roughly two thirds of gene promoters, are evolutionarily conserved, and play central roles in gene regulation, yet how they are protected from DNA methylation remains enigmatic. Based on the conserved nature of CpG islands, we have exploited genomic approaches and a transchromosomic model system to ask if DNA sequence is sufficient to specify the hypomethylated state at CpG islands when a human chromosome is newly introduced into mouse. Interestingly, this approach revealed that promoter-associated CGIs remain immensely refractory to DNA methylation regardless of the host species, in fitting with their conservation across vertebrate species and revealing that DNA sequence is a central driver in this outcome. In contrast, the methylation state of distal elements is highly variable between species and is host nucleus dependent. These alterations in methylation state at distal elements are defined by DNA nucleotide frequency and occupancy of DNA binding transcription factors, uncovering a widespread role for these features in defining the how this aspect of the epigenome forms away from gene promoters. These central principles are further supported by transplantation of mouse DNA sequences into the evolutionarily distant zebrafish genome, revealing the existence of a highly conserved and DNA encoded logic that shapes the vertebrate epigenome.

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Project description:This SuperSeries is composed of the following subset Series: GSE14372: Novel endogenous antisense transcripts (data for the mouse normal tissues) GSE14557: Novel endogenous antisense transcripts (data for the mouse mammary tumors) Refer to individual Series Unpublished data has been masked in the supplementary feature extraction files.

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Nucleosome Positioning Shapes Cryptic Antisense Transcription

Project description:Maintaining transcriptional fidelity is essential for precise gene regulation and genome stability. Despite this, cryptic antisense transcription, occurring opposite to canonical coding sequences, is a pervasive feature across all domains of life. How such potentially harmful cryptic sites are regulated remains incompletely understood. Here, we show that nucleosome arrays within gene bodies play a key role in suppressing cryptic transcription. Using the fission yeast Schizosaccharomyces pombe as a model, we demonstrate that CHD1-family chromatin remodelers coordinate with the transcription elongation machinery, specifically the PAF complex, to position nucleosomes at sites of cryptic transcription initiation within gene bodies. In the absence of CHD1, AT-rich sequences within gene bodies lose nucleosome occupancy, exposing promoter-like sequences that drive cryptic initiation. While cryptic transcription is generally detrimental, we identify a subset of antisense transcripts that encode critical meiotic genes, suggesting that cryptic transcription can also serve as a source of regulatory innovation. These findings underscore the essential role of nucleosome remodelers in maintaining transcriptional fidelity and reveal their broader contributions to cellular homeostasis and evolutionary adaptability.

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