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PiRNA pathway targets active LINE1 elements to establish repressive H3K9me3 mark in germ cells

ABSTRACT: Transposable elements (TEs) occupy large fraction of metazoan genomes and pose constant threat to genomic integrity. This threat is particularly critical in germ cells, as changes in the genome that are induced by TEs will be transmitted to the next generation. Small non-coding piwi interacting (pi)RNAs recognize and silence a diverse set of TEs in germ cells. In mice, piRNA-guided transposon repression correlates with establishment of CpG DNA methylation on their sequences, yet the mechanism and the spectrum of genomic targets of piRNA silencing are unknown. Here we show that in addition to DNA methylation, the piRNA pathway is required to maintain a high level of the repressive H3K9me3 histone modification on long interspersed nuclear elements (LINEs) in germ cells. piRNA-dependent chromatin repression targets exclusively full-length elements of actively transposing LINE families, demonstrating the remarkable ability of the piRNA pathway to recognize active elements among the large number of genomic transposon fragments.

ORGANISM(S): Mus musculus

PROVIDER: GSE58332 | GEO | 2014/06/13

SECONDARY ACCESSION(S): PRJNA252565

REPOSITORIES: GEO

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piRNA pathway targets active LINE1 elements to establish repressive H3K9me3 mark in germ cells

Project description:Transposable elements (TEs) occupy large fraction of metazoan genomes and pose constant threat to genomic integrity. This threat is particularly critical in germ cells, as changes in the genome that are induced by TEs will be transmitted to the next generation. Small non-coding piwi interacting (pi)RNAs recognize and silence a diverse set of TEs in germ cells. In mice, piRNA-guided transposon repression correlates with establishment of CpG DNA methylation on their sequences, yet the mechanism and the spectrum of genomic targets of piRNA silencing are unknown. Here we show that in addition to DNA methylation, the piRNA pathway is required to maintain a high level of the repressive H3K9me3 histone modification on long interspersed nuclear elements (LINEs) in germ cells. piRNA-dependent chromatin repression targets exclusively full-length elements of actively transposing LINE families, demonstrating the remarkable ability of the piRNA pathway to recognize active elements among the large number of genomic transposon fragments. Total of 34 libraries were analyzed. In case of ChIP libraries, every 'input' sample was used for normalization of the respective ChIP (H3K9me3 or H3) sample; the input libraries preceed ChIP libraries in the list below. There are four replicates (input-ChIP pairs) for H3K9me3 ChIP on liver cells, two for ChIP on testicular somatic cells for each genotype (Miwi2 Het and KO); and four for ChIP on male germ cells for each genotype (one from FACS-sorted germ cells, and three from MACS-sorted germ cells). Each replicate has a Het/KO pair, and the respective libraries were cloned from the material isolated from littermates. One H3 ChIP for each genotype is included, with respective inputs.

2014-06-13 | E-GEOD-58332 | biostudies-arrayexpress

Germline piRNAs counteract endogenous retrovirus invasion from somatic cells - Total genomic DNA

Project description:In metazoan gonads, transposable elements (TEs) mobilization is limited by PIWI-interacting RNAs (piRNAs). These small RNAs originate from specific source loci, the piRNA clusters. piRNAs are known to silence TEs in the cells where they are produced. Endogenous retroviruses (ERVs), a subclass of TEs, pose a particular threat because they are capable of transiting from cell to cell. In this study, we reveal that piRNAs produced locally in germ cells counteract invasion by ERVs arriving from adjacent somatic cells. We reactivated the Drosophila ERV ZAM in somatic gonadal cells by deleting, using CRISPR-Cas9 genome editing, its single copy in the somatic flamenco piRNA cluster, while keeping the piRNA pathway fully functional. Upon reactivation, ZAM invaded the oocytes, resulting in transposition and severe fertility defects. We show that once ZAM-piRNAs are produced in germ cells they counter the invasion. Our study sheds new light on the mechanisms of recognition and regulation of invasive genetic elements, which is essential for the maintenance of genome integrity.

2022-09-30 | GSE213456 | GEO

Germline piRNAs counteract endogenous retrovirus invasion from somatic cells- small RNA

2022-09-30 | GSE213368 | GEO

Domestic chickens activate a piRNA defense against avian leukosis virus

Project description:PIWI-interacting RNAs (piRNAs) protect the germ line by targeting transposable elements (TEs) through base-pair complementarity. We do not know how piRNAs co-evolve with TEs in chickens. Here we reported that all active TEs in the chicken germ line are targeted by piRNAs, and as TEs lose their activity, the corresponding piRNAs erode away. We observed de novo piRNA birth as host responds to a recent retroviral invasion. Avian leukosis virus (ALV) has endogenized prior to chicken domestication, remains infectious, and threatens poultry industry. Domestic fowl produced piRNAs targeting ALV from a genomic locus that was known to render its host ALV resistant. This genomic locus does not produce piRNAs in undomesticated wild chickens. Our findings uncover rapid piRNA evolution reflecting contemporary TE activity, identify a new piRNA acquisition modality by activating a pre-existing genomic locus, and extend piRNA defense roles to include the period when endogenous retroviruses are still infectious.

2017-04-07 | GSE93559 | GEO

Germline piRNAs counteract endogenous retrovirus invasion from somatic cells

Project description:In metazoan gonads, transposable elements (TEs) mobilization is limited by PIWI-interacting RNAs (piRNAs). These small RNAs originate from specific source loci, the piRNA clusters. piRNAs are known to silence TEs in the cells where they are produced. Endogenous retroviruses (ERVs), a subclass of TEs, pose a particular threat because they are capable of transiting from cell to cell. In this study, we reveal that piRNAs produced locally in germ cells counteract invasion by ERVs arriving from adjacent somatic cells. We reactivated the Drosophila ERVZAMin somatic gonadal cells by deleting, using CRISPR-Cas9 genome editing, its single copy in the somaticflamencopiRNA cluster, while keeping the piRNA pathway fully functional. Upon reactivation,ZAMinvaded the oocytes, resulting in transposition and severe fertility defects. We show that onceZAM-piRNAs are produced in germ cells they counter the invasion. Our study sheds new light on the mechanisms of recognition and regulation of invasive genetic elements, which is essential for the maintenance of genome integrity.

2023-08-25 | GSE235966 | GEO

A genome-wide RNAi screen draws a genetic framework for transposon control and primary piRNA biogenesis in Drosophila

Project description:A large fraction of our genome consists of mobile genetic elements. Governing transposons in germ cells is critically important, and failure to do so compromises genome integrity, leading to sterility. In animals, the piRNA pathway is the key to transposon constraint, yet the precise molecular details of how piRNAs are formed and how the pathway represses mobile elements remain poorly understood. In an effort to identify general requirements for transposon control and novel components of the piRNA pathway, we carried out a genome-wide RNAi screen in Drosophila ovarian somatic sheet cells. We identified and validated 87 genes necessary for transposon silencing. Among these were several novel piRNA biogenesis factors. We also found CG3893 (asterix) to be essential for transposon silencing, most likely by contributing to the effector step of transcriptional repression. Asterix loss leads to decreases in H3K9me3 marks on certain transposons but has no effect on piRNA levels. We sequenced small RNAs, RNA-seq and ChIP-seq from either tj-Gal4 driven hpRNA knockdown flies or P-element insertion flies

2013-05-09 | E-GEOD-46009 | biostudies-arrayexpress

A genome-wide RNAi screen draws a genetic framework for transposon control and primary piRNA biogenesis in Drosophila

2013-05-09 | GSE46009 | GEO

piRNA processing by a trimeric Schlafen-domain-containing nuclease

Project description:Transposable elements are genomic parasites that expand within and spread between genomes. Piwi proteins control transposon activity, notably in the germline. These proteins recognize their targets through small RNA co-factors named piRNAs, making piRNA biogenesis a key specificity-determining step in this important genome immunity system. While the processing of piRNA precursors is an essential step in this process, many molecular details of this process remain unknown. We identify a novel endoribonuclease, PUCH, that initiates piRNA processing in the nematode Caenorhabditis elegans. Genetic and biochemical studies show that PUCH, a trimer of Schlafen-like-domain (SLFNL) proteins, executes 5ï‚¢-end piRNA precursor cleavage. PUCH-mediated processing strictly requires an m7G-Cap and a Uracil at position three. We also demonstrate how PUCH interacts with PETISCO, a complex that binds piRNA precursors, and that this interaction enhances piRNA production in vivo. The identification of PUCH completes the C. elegans piRNA biogenesis repertoire and uncovers a novel type of RNA endonuclease formed by three SLFL proteins. Mammalian Slfn genes have been associated with immunity responses, exposing a novel molecular link between immune responses in mammals and deeply conserved RNA-based mechanisms that control transposable elements.

2023-10-24 | PXD039502 | Pride

Two-factor authentication underpins the precision of piRNA-directed LINE1 DNA methylation

Project description:The PIWI-interacting RNA (piRNA) pathway guides the DNA methylation of young active transposons during male mouse germline development. piRNAs tether the PIWI protein MIWI2 (PIWIL4) to the nascent transposon transcript that results in DNA methylation through SPOCD1. Transposon methylation requires exacting precision: all copies need to be methylated yet, at the same time, off-target methylation must be avoided. However, the underlying mechanisms that ensure this precision remain unknown. Here, we show that SPOCD1 directly interacts with SPIN1, a chromatin reader that primarily binds H3K4me3 and this association is augmented by H3K9me3. The prevailing assumption is that all molecular events required for piRNA-directed DNA methylation occur after the engagement of MIWI2. Interestingly, we find that SPIN1 expression precedes that of both SPOCD1 and MIWI2. Furthermore, we demonstrate that young LINE1s, but not old copies are marked by H3K4me3 and H3K9me3 prior to the initiation of piRNA-directed DNA methylation. We generated a Spocd1 separation-of-function allele in the mouse that encodes a SPOCD1 variant that no longer interacts with SPIN1. We found that the SPOCD1-SPIN1 interaction is essential for spermatogenesis and piRNA-directed DNA methylation of young LINE1 elements. We propose that young LINE1 elements require a two-factor authentication process for DNA methylation, the first being the recruitment of SPIN1-SPOCD1 to licence the locus and the second is MIWI2 engagement with the nascent transcript, which is the trigger for methylation. In summary, independent events that licence, and trigger methylation underpin the basis of precision.

2024-09-04 | PXD041214 | Pride

Somatic piRNA pathway prevents transgenerational germline transposition [circularDNA-seq]

Project description:Transposable elements (TEs) are genomic parasite that threat genome integrity. One major strategy organisms evolved to balance TE activity in the germline is the Piwi-interacting RNAs (piRNAs) pathway. It prevents transposition by repressing TE at transcriptional and/or post-transcriptional level. However, evidence that TE derepression caused by piRNA pathway impairment is actually followed by bursts of transposition is still lacking. Here we present a genome-wide TE-analyses of the replicative TE life cycle (their expression, their translation to their transposition in the germline) after piRNA pathway impairment in the somatic follicle cells. We observed a high transposition-rate in the germline, leading to a 10-fold increase in genomic TE-load after 70 successive generations of piRNA pathway impairment. Moreover, we demonstrate that siRNAs co-regulate TE activity at post transcriptional level in follicle cells. These observations demonstrate that the small RNA-mediated TE repression in follicle cells contribute to genome homeostasis.

2018-08-09 | GSE112968 | GEO

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