Correction: A team of heterochromatin factors collaborates with small RNA pathways to combat repetitive elements and germline stress

McMurchy, Alicia N.; Stempor, Przemyslaw; Gaarenstroom, Tessa; Wysolmerski, Brian; Dong, Yi; Aussianikava, Darya; Appert, Alex; Huang, Ni; Kolasinska-Zwierz, Paulina; Sapetschnig, Alexandra; Miska, Eric A.; Ahringer, Julie

doi:10.7554/elife.32516

Cited by 16 publications

(5 citation statements)

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“…Interestingly, while HP1 homologs directly bind H3K9me2/3 histone modifications via a chromodomain ( 32 , 33 ), H3K9me2/3 is not endogenously required in C. elegans for HPL-2 association ( 30 ). While several C. elegans genes have been suggested to be involved in HPL-2 recruitment, including lin-13 , lin-35 , and let-418 ( 34 – 36 ), the mechanism of HPL-2 association with active genes is unclear. In humans, HP1 coprecipitates with elongating forms of RNA polymerase II (Pol II) ( 26 ) but only localizes to certain genes to affect RNA processing, implying that additional factors must provide the specificity of HP1 association.…”

Section: Introductionmentioning

confidence: 99%

The Caenorhabditis elegans Ortholog of TDP-43 Regulates the Chromatin Localization of the Heterochromatin Protein 1 Homolog HPL-2

Saldi

Gonzales

Garrido-Lecca

et al. 2018

Molecular and Cellular Biology

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Section: Introductionmentioning

confidence: 99%

The Caenorhabditis elegans Ortholog of TDP-43 Regulates the Chromatin Localization of the Heterochromatin Protein 1 Homolog HPL-2

Saldi

Gonzales

Garrido-Lecca

et al. 2018

Molecular and Cellular Biology

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“…Telomeric repeats in C. elegans and humans are enriched in H3K9me2 29 , while human subtelomeres are enriched in H3K9me3 63 , 64 . We found that telomeric foci were perturbed by mutations in either met-2 or set-25 , two histone methyltransferases that create H3K9me2 and H3K9me3, respectively 47 , 65 .…”

Section: Discussionmentioning

confidence: 99%

“…Aside from shelterin, mammalian telomeric DNA interacts with histones that are enriched for H3K9 di- and trimethylation that promote genome silencing 28 . C. elegans telomeres also possess the H3K9 dimethyl histone silencing mark 29 , suggesting that heterochromatin may be a common theme of metazoan telomeres. Loss of heterochromatin in mouse primary cells deficient for the histone methyltransferases Suv39h1 and Suv39h2 is associated with telomere elongation 28 .…”

Section: Introductionmentioning

confidence: 99%

Gametes deficient for Pot1 telomere binding proteins alter levels of telomeric foci for multiple generations

et al. 2021

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Deficiency for telomerase results in transgenerational shortening of telomeres. However, telomeres have no known role in transgenerational epigenetic inheritance. C. elegans Protection Of Telomeres 1 (Pot1) proteins form foci at the telomeres of germ cells that disappear at fertilization and gradually accumulate during development. We find that gametes from mutants deficient for Pot1 proteins alter levels of telomeric foci for multiple generations. Gametes from pot-2 mutants give rise to progeny with abundant POT-1::mCherry and mNeonGreen::POT-2 foci throughout development, which persists for six generations. In contrast, gametes from pot-1 mutants or pot-1; pot-2 double mutants induce diminished Pot1 foci for several generations. Deficiency for MET-2, SET-25, or SET-32 methyltransferases, which promote heterochromatin formation, results in gametes that induce diminished Pot1 foci for several generations. We propose that C. elegans POT-1 may interact with H3K9 methyltransferases during pot-2 mutant gametogenesis to induce a persistent form of transgenerational epigenetic inheritance that causes constitutively high levels of heterochromatic Pot1 foci.

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“…Several causes of sterility for late-generation prg-1 mutants have been proposed, including misrouting of pro-and anti-silencing small RNAs (de Albuquerque et al 2015), expression of high levels of transposon or repetitive RNAs (Simon et al 2014), transposition of the Mirage transposon (McMurchy et al 2017), disruption of gene expression (Reed et al 2020), excessive silencing of histone genes (Barucci et al 2020) and disruption of germ granules (Spichal et al 2021). A recent intriguing study suggested that the fertility of late-generation prg-1 mutants may be compromised by accumulation of high levels of small RNAs that are homologous to rRNA as well as the presence of extrachromosomal rDNA circles (Wahba et al 2021), although rRNA levels appear unaffected in prg-1 mutants (Reed et al 2020).…”

Section: Discussionmentioning

confidence: 99%

“…Freshly outcrossed prg-1/Piwi mutants display normal fertility for a number of generations, but their fertility then progressively declines and ultimately culminates in complete sterility (Simon et al 2014;Barucci et al 2020;Reed et al 2020). The PRG-1/Piwi pathway promotes silencing of foreign genetic elements like transposons whose expression might promote prg-1 mutant sterility (Simon et al 2014;McMurchy et al 2017). However, PRG-1/piRNAs also repress the inappropriate silencing of some germline genes, possibly in response to an imbalance of silencing factors and 22G RNAs that arises in the absence of Piwi/piRNAs (Montgomery et al 2021;de Albuquerque et al 2015;Barucci et al 2020;Reed et al 2020).…”

Section: Introductionmentioning

confidence: 99%

Piwi mutant germ cells transmit a form of heritable stress that promotes longevity

Heestand

Simon

Frenk

et al. 2018

Preprint

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The C. elegans Piwi Argonaute protein PRG-1 and associated piRNAs protect the genomes of germ cells by suppressing the expression of transposons and potentially deleterious foreign nucleic acids. Deficiency for prg-1 compromises germ cell immortality, resulting in normal fertility for many generations followed by progressively reduced fertility and ultimately sterility. The sterility phenotype of prg-1 mutants was recently shown to be a form of reproductive arrest, which implies that prg-1 mutants may become sterile in response to a form of heritable stress. The DAF-16 stress resistance and longevity factor can promote germ cell immortality of prg-1 mutants by activating a systemic RNAi pathway. We found that this RNAi pathway was not required for the somatic longevity function of DAF-16. Given that prg-1 mutant germ cells may transmit a form of heritable stress, we studied the somatic longevity of prg-1 mutant adults. We found that early generation prg-1 mutants had normal lifespans, but that lategeneration adults that displayed reduced fertility or sterility were long lived. Germ cells of long-lived late-generation prg-1 mutants gave rise to F1 cross progeny that were heterozygous for prg-1, fertile and also long lived. However, in the absence of DAF-16, the heritable stress transmitted by prg-1 mutant germ cells was deleterious and caused lifespan to shorten. We conclude that deficiency for the genomic surveillance factor PRG-1/Piwi results in germ cells that transmit a heritable stress that promotes somatic longevity via DAF-16/Foxo, which could be relevant transgenerational regulation of aging.All rights reserved. No reuse allowed without permission.(which was not peer-reviewed) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.

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Correction: A team of heterochromatin factors collaborates with small RNA pathways to combat repetitive elements and germline stress

Cited by 16 publications

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The Caenorhabditis elegans Ortholog of TDP-43 Regulates the Chromatin Localization of the Heterochromatin Protein 1 Homolog HPL-2

The Caenorhabditis elegans Ortholog of TDP-43 Regulates the Chromatin Localization of the Heterochromatin Protein 1 Homolog HPL-2

Gametes deficient for Pot1 telomere binding proteins alter levels of telomeric foci for multiple generations

Piwi mutant germ cells transmit a form of heritable stress that promotes longevity

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