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Title:
Germ granule dysfunction is a hallmark and mirror of Piwi mutant sterility | Nature Communications
Description:
In several species, Piwi/piRNA genome silencing defects cause immediate sterility that correlates with transposon expression and transposon-induced genomic instability. In C. elegans, mutations in the Piwi-related gene (prg-1) and other piRNA deficient mutants cause a transgenerational decline in fertility over a period of several generations. Here we show that the sterility of late generation piRNA mutants correlates poorly with increases in DNA damage signaling. Instead, sterile individuals consistently exhibit altered perinuclear germ granules. We show that disruption of germ granules does not activate transposon expression but induces multiple phenotypes found in sterile prg-1 pathway mutants. Furthermore, loss of the germ granule component pgl-1 enhances prg-1 mutant infertility. Environmental restoration of germ granule function for sterile pgl-1 mutants restores their fertility. We propose that Piwi mutant sterility is a reproductive arrest phenotype that is characterized by perturbed germ granule structure and is phenocopied by germ granule dysfunction, independent of genomic instability. Piwi deficiency results in sterility and is associated with transposon expression and genomic instability. Here the authors show that sterility of C. elegans Piwi prg-1 mutant is not associated with transposon-induced DNA damage but is associated with and is phenocopied by dysfunction of germ granules.
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Keywords {🔍}
mutants, sterile, germ, pubmed, granule, piwi, pgl, article, sterility, germline, mutant, nrde, elegans, google, scholar, prg, cas, fig, pathway, cell, adults, germlines, animals, granules, central, genome, lategeneration, fertile, rnai, cells, silencing, rna, small, wild, type, dysfunction, expression, day, genes, nature, reproductive, transposon, found, arrest, caenorhabditis, hrde, worms, fertility, dna, wildtype,
Topics {✒️}
nature portfolio open scientific question privacy policy precision genome editing poly-l-lysine-coated slide research infrastructure programs advertising small-rna-mediated transgenerational silencing piwi-interacting small rnas gene editing medical research research design libraries language reprints donkey anti-rabbit cy5 late-generation prg-1/piwi mutants rna-dependent rna polymerase nature 403 nature 557 nature 489 nature 465 nature piwi/pirna genome silencing small anti-sense rnas cy-5 donkey anti-rabbit germ-line-specific cytoplasmic granules piwi-interacting rnas suggesting post-transcriptional regulation goat anti-rat cy2 predicted rna-binding component cy3 donkey anti-mouse donkey anti-mouse fitc rna-seq data reported male germ-cell differentiation promote genome silencing open biol multigenerational epigenetic memory granule-depleted animals matured nrde rna-seq data nrde-2 rna-seq data constitutive germ-granule components granule rnai exhibit late-generation prg-1 mutant18 fertile late-generation siblings late-generation fertile siblings vectashield mounting media phospho-specific antibody targeting sterile late-generation animals reprogramming epigenetic memory
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headline:Germ granule dysfunction is a hallmark and mirror of Piwi mutant sterility
description:In several species, Piwi/piRNA genome silencing defects cause immediate sterility that correlates with transposon expression and transposon-induced genomic instability. In C. elegans, mutations in the Piwi-related gene (prg-1) and other piRNA deficient mutants cause a transgenerational decline in fertility over a period of several generations. Here we show that the sterility of late generation piRNA mutants correlates poorly with increases in DNA damage signaling. Instead, sterile individuals consistently exhibit altered perinuclear germ granules. We show that disruption of germ granules does not activate transposon expression but induces multiple phenotypes found in sterile prg-1 pathway mutants. Furthermore, loss of the germ granule component pgl-1 enhances prg-1 mutant infertility. Environmental restoration of germ granule function for sterile pgl-1 mutants restores their fertility. We propose that Piwi mutant sterility is a reproductive arrest phenotype that is characterized by perturbed germ granule structure and is phenocopied by germ granule dysfunction, independent of genomic instability. Piwi deficiency results in sterility and is associated with transposon expression and genomic instability. Here the authors show that sterility of C. elegans Piwi prg-1 mutant is not associated with transposon-induced DNA damage but is associated with and is phenocopied by dysfunction of germ granules.
datePublished:2021-03-03T00:00:00Z
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headline:Germ granule dysfunction is a hallmark and mirror of Piwi mutant sterility
description:In several species, Piwi/piRNA genome silencing defects cause immediate sterility that correlates with transposon expression and transposon-induced genomic instability. In C. elegans, mutations in the Piwi-related gene (prg-1) and other piRNA deficient mutants cause a transgenerational decline in fertility over a period of several generations. Here we show that the sterility of late generation piRNA mutants correlates poorly with increases in DNA damage signaling. Instead, sterile individuals consistently exhibit altered perinuclear germ granules. We show that disruption of germ granules does not activate transposon expression but induces multiple phenotypes found in sterile prg-1 pathway mutants. Furthermore, loss of the germ granule component pgl-1 enhances prg-1 mutant infertility. Environmental restoration of germ granule function for sterile pgl-1 mutants restores their fertility. We propose that Piwi mutant sterility is a reproductive arrest phenotype that is characterized by perturbed germ granule structure and is phenocopied by germ granule dysfunction, independent of genomic instability. Piwi deficiency results in sterility and is associated with transposon expression and genomic instability. Here the authors show that sterility of C. elegans Piwi prg-1 mutant is not associated with transposon-induced DNA damage but is associated with and is phenocopied by dysfunction of germ granules.
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