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Antagonistic conflict between transposon-encoded introns and guide RNAs (RIP-Seq)

ABSTRACT: Antagonistic conflict between transposon-encoded introns and guide RNAs (RIP-Seq)

PROVIDER: PRJNA1086529 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28292648_1.fastq.gz	Fastqsanger.gz
	SRR28292648_2.fastq.gz	Fastqsanger.gz
	SRR28292649_1.fastq.gz	Fastqsanger.gz
	SRR28292649_2.fastq.gz	Fastqsanger.gz
	SRR28292650_1.fastq.gz	Fastqsanger.gz

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Antagonistic conflict between transposon-encoded introns and guide RNAs

Project description:Antagonistic conflict between transposon-encoded introns and guide RNAs

| PRJNA1086522 | ENA

Antagonistic conflict between transposon-encoded introns and guide RNAs (RNA-Seq)

Project description:Antagonistic conflict between transposon-encoded introns and guide RNAs (RNA-Seq)

| PRJNA1086528 | ENA

Antagonistic conflict between transposon-encoded introns and guide RNAs (RNA-Seq)

Project description:TnpB nucleases represent the evolutionary precursors to CRISPR-Cas12 and are widespread in all domains of life. IS605-family TnpB homologs function in bacteria as programmable RNA-guided homing endonucleases driving transposon maintenance through DSB-stimulated homologous recombination. Here we uncover molecular mechanisms of transposition lifecycle of IS607-family elements that, remarkably, also encode group I introns. We discover molecular features for a candidate ‘IStron’ from Clostridium botulinum that allow the element to carefully control the relative levels of spliced products versus functional guide RNAs. Our results suggest that IStron transcripts have evolved a sensitive equilibrium to balance competing and mutually exclusive activities that promote transposon maintenance while limiting adverse fitness costs on the host. Collectively, this work highlights molecular innovation in the multi-functional utility of transposon-encoded noncoding RNAs.

2024-05-06 | GSE261343 | GEO

Antagonistic conflict between transposon-encoded introns and guide RNAs (RIP-Seq)

2024-05-06 | GSE261342 | GEO

Antagonistic conflict between transposon-encoded introns and guide RNAs.

Project description:TnpB nucleases represent the evolutionary precursors to CRISPR-Cas12 and are widespread in all domains of life. IS605-family TnpB homologs function as programmable RNA-guided homing endonucleases in bacteria, driving transposon maintenance through DNA double-strand break-stimulated homologous recombination. In this work, we uncovered molecular mechanisms of the transposition life cycle of IS607-family elements that, notably, also encode group I introns. We identified specific features for a candidate "IStron" from Clostridium botulinum that allow the element to carefully control the relative levels of spliced products versus functional guide RNAs. Our results suggest that IStron transcripts evolved an ability to balance competing and mutually exclusive activities that promote selfish transposon spread while limiting adverse fitness costs on the host. Collectively, this work highlights molecular innovation in the multifunctional utility of transposon-encoded noncoding RNAs.

| S-EPMC11758368 | biostudies-literature

Antagonistic conflict between transposon-encoded introns and guide RNAs.

Project description:TnpB nucleases represent the evolutionary precursors to CRISPR-Cas12 and are widespread in all domains of life, presumably due to the critical roles they play in transposon proliferation. IS605family TnpB homologs function in bacteria as programmable homing endonucleases by exploiting transposon-encoded guide RNAs to cleave vacant genomic sites, thereby driving transposon maintenance through DSB-stimulated homologous recombination. Whether this pathway is conserved in other genetic contexts, and in association with other transposases, is unknown. Here we uncover molecular mechanisms of transposition and RNA-guided DNA cleavage by IS607-family elements that, remarkably, also encode catalytic, self-splicing group I introns. After reconstituting and systematically investigating each of these biochemical activities for a candidate 'IStron' derived from Clostridium botulinum, we discovered sequence and structural features of the transposon-encoded RNA that satisfy molecular requirements of a group I intron and TnpB guide RNA, while still retaining the ability to be faithfully mobilized at the DNA level by the TnpA transposase. Strikingly, intron splicing was strongly repressed not only by TnpB, but also by the secondary structure of ωRNA alone, allowing the element to carefully control the relative levels of spliced products versus functional guide RNAs. Our results suggest that IStron transcripts have evolved a sensitive equilibrium to balance competing and mutually exclusive activities that promote transposon maintenance while limiting adverse fitness costs on the host. Collectively, this work explains how diverse enzymatic activities emerged during the selfish spread of IS607-family elements and highlights molecular innovation in the multi-functional utility of transposon-encoded noncoding RNAs.

| S-EPMC10690162 | biostudies-literature

Antagonistic conflict between transposon-encoded introns and guide RNAs

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

2024-05-06 | GSE261344 | GEO

Project description:Antagonistic conflict between transposon-encoded introns and guide RNAs

| PRJNA1107998 | ENA

Transposon-encoded nucleases use guide RNAs to selfishly bias their inheritance

Project description:Transposon-encoded nucleases use guide RNAs to selfishly bias their inheritance

| PRJNA925099 | ENA

Parental conflict driven regulation of endosperm cellularization by a family of Auxin Response Factors

Project description:The endosperm is a reproductive tissue supporting embryo development. In most flowering plants, the initial divisions of endosperm nuclei are not succeeded by cellularization; this process occurs only after a specific number of mitotic cycles have taken place. The timing of cellularization significantly influences seed viability and size. Previous research implicated auxin as a key factor in initiating nuclear divisions and determining the timing of cellularization. Here we uncover the involvement of a family of clustered auxin response factors (cARFs) as dosage-sensitive regulators of endosperm cellularization. cARFs, maternally expressed and paternally silenced, are shown to induce cellularization, thereby restricting seed growth. Our findings align with the predictions of the parental conflict theory, suggesting that cARFs represent major molecular targets in this conflict. We further demonstrate a recurring amplification of cARFs in the Brassicaceae, suggesting an evolutionary response to parental conflict by reinforcing maternal control over endosperm cellularization. Our study highlights that antagonistic parental control on endosperm cellularization converges on auxin biosynthesis and signalling.

2024-03-22 | GSE232803 | GEO

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