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MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE32183 | GEO | 2011/11/30

SECONDARY ACCESSION(S): PRJNA147395

REPOSITORIES: GEO

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MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing

Project description:This SuperSeries is composed of the following subset Series: GSE32180: MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing [microarray] GSE32184: MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing [deep sequencing] Refer to individual Series

2011-11-30 | E-GEOD-32183 | biostudies-arrayexpress

MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing [microarray]

Project description:Here we show that MIWI is a small RNA-guided ribonuclease (Slicer) that requires extensive complementarity for target cleavage in vitro. Disruption of its catalytic activity in mice by a single point mutation results in male infertility and displays increased accumulation of LINE1 transposon transcripts. Round spermatids were purified from adult mouse testes of indicated Miwi genotypes. Total RNA was extracted and subjected to microarray analysis for gene expression profiling.

2011-11-30 | E-GEOD-32180 | biostudies-arrayexpress

MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing [microarray]

2011-11-30 | GSE32180 | GEO

MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing [deep sequencing]

Project description:Here we show that MIWI is a small RNA-guided ribonuclease (Slicer) that requires extensive complementarity for target cleavage in vitro. Disruption of its catalytic activity in mice by a single point mutation results in male infertility and displays increased accumulation of LINE1 transposon transcripts. MIWI-associated piRNAs from different genotypes were sequenced. Total RNA from purified round spermatids were subjected to Ribozero purification and strand-specific RNAseq lib prepared. Global 5' RACE library was prepare from indicated genotypes.

2011-11-30 | E-GEOD-32184 | biostudies-arrayexpress

MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing [deep sequencing]

2011-11-30 | GSE32184 | GEO

MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing

Project description:MIWI catalysis is required for piRNA amplification-independent LINE1 transposon silencing

| PRJNA147395 | ENA

MIWI N-terminal RG motif promotes efficient pachytene piRNA production and spermatogenesis independent of LINE1 transposon silencing.

Project description:PIWI proteins and their associated piRNAs act to silence transposons and promote gametogenesis. Murine PIWI proteins MIWI, MILI, and MIWI2 have multiple arginine and glycine (RG)-rich motifs at their N-terminal domains. Despite being known as docking sites for the TDRD family proteins, the in vivo regulatory roles for these RG motifs in directing PIWI in piRNA biogenesis and spermatogenesis remain elusive. To investigate the functional significance of RG motifs in mammalian PIWI proteins in vivo, we genetically engineered an arginine to lysine (RK) point mutation of a conserved N-terminal RG motif in MIWI in mice. We show that this tiny MIWI RG motif is indispensable for piRNA biogenesis and male fertility. The RK mutation in the RG motif disrupts MIWI-TDRKH interaction and impairs enrichment of MIWI to the intermitochondrial cement (IMC) for efficient piRNA production. Despite significant overall piRNA level reduction, piRNA trimming and maturation are not affected by the RK mutation. Consequently, MiwiRK mutant mice show chromatoid body malformation, spermatogenic arrest, and male sterility. Surprisingly, LINE1 transposons are effectively silenced in MiwiRK mutant mice, indicating a LINE1-independent cause of germ cell arrest distinctive from Miwi knockout mice. These findings reveal a crucial function of the RG motif in directing PIWI proteins to engage in efficient piRNA production critical for germ cell progression and highlight the functional importance of the PIWI N-terminal motifs in regulating male fertility.

| S-EPMC10681313 | biostudies-literature

piRNA-independent transposon silencing by the Drosophila THO complex.

Project description:piRNAs guide Piwi/Panoramix-dependent H3K9me3 chromatin modification and transposon silencing during Drosophila germline development. The THO RNA export complex is composed of Hpr1, Tho2, and Thoc5-7. Null thoc7 mutations, which displace Thoc5 and Thoc6 from a Tho2-Hpr1 subcomplex, reduce expression of a subset of germline piRNAs and increase transposon expression, suggesting that THO silences transposons by promoting piRNA biogenesis. Here, we show that the thoc7-null mutant combination increases transposon transcription but does not reduce anti-sense piRNAs targeting half of the transcriptionally activated transposon families. These mutations also fail to reduce piRNA-guided H3K9me3 chromatin modification or block Panoramix-dependent silencing of a reporter transgene, and unspliced transposon transcripts co-precipitate with THO through a Piwi- and Panoramix-independent mechanism. Mutations in piwi also dominantly enhance germline defects associated with thoc7-null alleles. THO thus functions in a piRNA-independent transposon-silencing pathway, which acts cooperatively with Piwi to support germline development.

| S-EPMC8567991 | biostudies-literature

Acetyltransferase Enok regulates transposon silencing and piRNA cluster transcription.

Project description:The piRNA pathway is a highly conserved mechanism to repress transposon activation in the germline in Drosophila and mammals. This pathway starts from transcribing piRNA clusters to generate long piRNA precursors. The majority of piRNA clusters lack conventional promoters, and utilize heterochromatin- and HP1D/Rhino-dependent noncanonical mechanisms for transcription. However, information regarding the transcriptional regulation of piRNA clusters is limited. Here, we report that the Drosophila acetyltransferase Enok, which can activate transcription by acetylating H3K23, is critical for piRNA production from 54% of piRNA clusters including 42AB, the major piRNA source. Surprisingly, we found that Enok not only promotes rhino expression by acetylating H3K23, but also directly enhances transcription of piRNA clusters by facilitating Rhino recruitment. Taken together, our study provides novel insights into the regulation of noncanonical transcription at piRNA clusters and transposon silencing.

| S-EPMC7877743 | biostudies-literature

The Drosophila HP1 homolog Rhino is required for transposon silencing and piRNA production by dual-strand clusters.

Project description:Piwi-interacting RNAs (piRNAs) silence transposons and maintain genome integrity during germline development. In Drosophila, transposon-rich heterochromatic clusters encode piRNAs either on both genomic strands (dual-strand clusters) or predominantly one genomic strand (uni-strand clusters). Primary piRNAs derived from these clusters are proposed to drive a ping-pong amplification cycle catalyzed by proteins that localize to the perinuclear nuage. We show that the HP1 homolog Rhino is required for nuage organization, transposon silencing, and ping-pong amplification of piRNAs. rhi mutations virtually eliminate piRNAs from the dual-strand clusters and block production of putative precursor RNAs from both strands of the major 42AB dual-strand cluster, but not of transcripts or piRNAs from the uni-strand clusters. Furthermore, Rhino protein associates with the 42AB dual-strand cluster,but does not bind to uni-strand cluster 2 or flamenco. Rhino thus appears to promote transcription of dual-strand clusters, leading to production of piRNAs that drive the ping-pong amplification cycle.

| S-EPMC2770713 | biostudies-literature

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