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Argonaute CSR-1A promotes H3K9me3 maintenance to protect somatic development in offspring

ABSTRACT: Paternal stress can be encoded into altered epigenetic information to influence their offspring. How environment-induced perturbation in sperm epigenome is reprogrammed to protect offspring is less well understood. In the nematode Caenorhabditis elegans, parental Argonaute and small RNA pathway defend offspring against viruses, starvation, and pathogenic bacteria. Here we report that, when challenged by universal heat-shock stress, paternal Argonaute CSR-1A potentiates recovery of spermic H3K9me3 to secure the late somatic developmental competence of offspring. CSR-1A employs its repetitive RG motif to engage with SET-25/32, putative histone 3 lysine 9 (H3K9) methyltransferases, and helps germ cell to rescue suppressive chromatin marks H3K9me3 following stress, protecting the late development of somatic cells in the progeny. Finally, among the genes regulated by CSR-1A, we identified dim-1, at which decreased H3K9me3 persists in the progeny, and RNAi of dim-1 mitigates the somatic defects associated with csr-1a loss under stress. Thus, CSR-1A coordinates the epigenetic machinery to shield the latter stages of a progeny's development from the influences of the paternal environment. We speculate that, driven by both natural environmental stressors and the unique characteristics of spermatogenic chromatin, the emergence of multiple RG motif-featured and spermatogenesis-specific CSR-1A and small RNA serves as an adaptive strategy to safeguard against variability in the orchestration of inherited developmental programs from the paternal lineage.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE262244 | GEO | 2025/02/07

REPOSITORIES: GEO

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Argonaute CSR-1A promotes H3K9me3 maintenance to protect somatic development in offspring

Project description:Paternal stress can be encoded into altered epigenetic information to influence their offspring. How environment-induced perturbation in sperm epigenome is reprogrammed to protect offspring is less well understood. In the nematode Caenorhabditis elegans, parental Argonaute and small RNA pathway defend offspring against viruses, starvation, and pathogenic bacteria. Here we report that, when challenged by universal heat-shock stress, paternal Argonaute CSR-1A potentiates recovery of spermic H3K9me3 to secure the late somatic developmental competence of offspring. CSR-1A employs its repetitive RG motif to engage with SET-25/32, putative histone 3 lysine 9 (H3K9) methyltransferases, and helps germ cell to rescue suppressive chromatin marks H3K9me3 following stress, protecting the late development of somatic cells in the progeny. Finally, among the genes regulated by CSR-1A, we identified dim-1, at which decreased H3K9me3 persists in the progeny, and RNAi of dim-1 mitigates the somatic defects associated with csr-1a loss under stress. Thus, CSR-1A coordinates the epigenetic machinery to shield the latter stages of a progeny's development from the influences of the paternal environment. We speculate that, driven by both natural environmental stressors and the unique characteristics of spermatogenic chromatin, the emergence of multiple RG motif-featured and spermatogenesis-specific CSR-1A and small RNA serves as an adaptive strategy to safeguard against variability in the orchestration of inherited developmental programs from the paternal lineage.

2025-02-07 | GSE262243 | GEO

Argonaute CSR-1A promotes H3K9me3 maintenance to protect somatic development in offspring

Project description:Argonaute CSR-1A promotes H3K9me3 maintenance to protect somatic development in offspring

| PRJNA1090892 | ENA

Argonaute CSR-1A promotes H3K9me3 maintenance to protect somatic development in offspring

Project description:Argonaute CSR-1A promotes H3K9me3 maintenance to protect somatic development in offspring

| PRJNA1090893 | ENA

CSR-1A post-translational modification

Project description:CSR-1 is an essential Argonaute protein that binds to a subclass of 22G-RNAs targeting most germline-expressed genes. Here we show that the two isoforms of CSR-1 have distinct expression patterns; CSR-1B is ubiquitously expressed throughout the germline and during all stages of development while CSR-1A expression is restricted to germ cells undergoing spermatogenesis. Furthermore, CSR-1A associates preferentially with 22G-RNAs mapping to spermatogenesis-specific genes whereas CSR-1B-bound small RNAs map predominantly to oogenesis-specific genes. Interestingly, the exon unique to CSR-1A contains multiple dimethylarginine modifications, which are necessary for the preferential binding of CSR-1A to spermatogenesis-specific 22G-RNAs. Thus, we have discovered a regulatory mechanism for C. elegans Argonaute proteins that allows for specificity of small RNA binding between similar Argonaute proteins with overlapping temporal and spatial localization.

2021-06-17 | PXD021227 | Pride

Arginine methylation promotes siRNA-binding specificity for a spermatogenesis-specific isoform of the Argonaute protein CSR-1

2021-06-04 | GSE151828 | GEO

Two isoforms of the essential C. elegans Argonaute CSR-1 differentially regulate sperm and oocyte fertility through distinct small RNA classes

Project description:The C. elegans genome encodes nineteen functional Argonaute proteins that utilize 22G-RNAs, 26G-RNAs, miRNAs, or piRNAs to regulate their target transcripts. Only one of these proteins is essential under normal laboratory conditions: CSR-1. While CSR-1 has been studied in various developmental and functional contexts, nearly all studies investigating CSR-1 have overlooked the fact that the csr-1 locus encodes two isoforms. These isoforms differ by an additional 163 amino acids present in the N-terminus of CSR-1a. Using CRISPR-Cas9 genome editing to introduce GFP::3xFLAG epitopes into the long (CSR-1a) and short (CSR-1b) isoforms of CSR-1, we identified differential expression patterns for the two isoforms. CSR-1a is expressed specifically during spermatogenesis and in select somatic tissues, including the intestine. In contrast, CSR-1b, is expressed constitutively in the germline. Essential functions of csr-1 described in the literature coincide with CSR-1b. In contrast,CSR-1a plays tissue specific functions during spermatogenesis, where it integrates into a spermatogenesis sRNA regulatory network including ALG-3, ALG-4, and WAGO-10 that is necessary for male fertility. CSR-1a is also required in the intestine for the silencing of repetitive transgenes. Sequencing of small RNAs associated with each CSR-1 isoform reveals that CSR-1a engages with 22G- and 26G-RNAs, while CSR-1b interacts with only 22G-RNAs to regulate distinct groups of germline genes and regulate both sperm and oocyte-mediated fertility.

2020-07-19 | GSE154678 | GEO

Exercise during pregnancy prevents parental obesity-induced decline of metabolic function in adult offspring [Bisulfite-Seq]

Project description:It is known that both maternal and paternal health/disease can influence the early development and later metabolic homeostasis of the offspring. We investigated whether maternal exercise during gestation alone could protect the offspring from the adverse effects of either maternal or paternal obesity induced by high-fat diet (HFD). To understand the underlying mechanisms we performed transcriptomics, whole-genome DNA methylation and targeted DNA methylation analysis at the metabolic master regulator, peroxisome proliferator-activated receptor g coactivator-1a (Pgc-1a) promoter in the adult offspring skeletal muscle. Both maternal and paternal HFD resulted in impaired glucose tolerance in the offspring at 9 months of age. Maternal exercise during gestation completely mitigated this metabolic impairment induced by either maternal or paternal HFD. Adult offspring exposed to either maternal or paternal HFD without exercise during gestation had skeletal muscle transcriptional profiles enriched in genes regulating inflammation and immune responses, whereas maternal exercise resulted in a transcriptional profile that was more similar to control offspring from normal chow fed parents. Changes in promoter and CpG DNA methylation were detected between the groups but did not explain the transcriptional changes. Maternal HFD increased methylation of the Pgc-1α promoter at CpG -260, which was prevented by maternal exercise. Paternal HFD did not affect the methylation of the Pgc-1α promoter. These findings demonstrate the negative consequences of maternal and paternal obesity for the offspring’s metabolic outcomes later in life and the clear benefits of maternal exercise during gestation. The mechanisms involve transcriptional regulation of skeletal muscle likely through multiple types of epigenetic modifications.

2021-07-30 | GSE144111 | GEO

Exercise during pregnancy prevents parental obesity-induced decline of metabolic function in adult offspring [RNA-Seq]

2021-07-30 | GSE144109 | GEO

Translation and codon usage regulate Argonaute slicer activity to trigger small RNA biogenesis

Project description:In the Caenorhabditis elegans germline, thousands of mRNAs are concomitantly expressed with antisense 22G-RNAs, which are loaded into the Argonaute CSR-1. Despite their essential functions for animal fertility and embryonic development, how CSR-1 22G-RNAs are produced remains unknown. Here, we show that CSR-1 slicer activity is primarily involved in triggering the synthesis of small RNAs on the coding sequences of germline mRNAs and post-transcriptionally regulates a fraction of targets. CSR-1-cleaved mRNAs prime the RNA-dependent RNA polymerase, EGO-1, to synthesize 22G-RNAs in phase with ribosome translation in the cytoplasm, in contrast to other 22G-RNAs mostly synthesized in germ granules. Moreover, codon optimality and efficient translation antagonize CSR-1 slicing and 22G-RNAs biogenesis. We propose that codon usage differences encoded into mRNA sequences might be a conserved strategy in eukaryotes to regulate small RNA biogenesis and Argonaute targeting

2021-04-23 | PXD020293 | Pride

Paternal microbiome perturbations impact offspring fitness

Project description:<p>The gut microbiota operates at the interface of host-environment interactions to influence human homeostasis and metabolic networks. Environmental factors that unbalance gut microbial ecosystems can therefore elicit physiological and disease-associated responses across somatic tissues. However, the systemic impact of the gut microbiome on the germline - and consequently on the F1 offspring it gives rise to - is unexplored. Here we show that the gut microbiota act as a key interface between paternal preconception environment and intergenerational health in mice. Perturbations to the gut microbiota of prospective fathers increase the probability of their offspring presenting with low birth weight, severe growth restriction and premature mortality. Transmission of disease risk occurs via the germline and is provoked by pervasive gut microbiome perturbations, including non-absorbable antibiotics or osmotic laxatives, but is rescued by restoring the paternal microbiota before conception. This effect is linked with a dynamic response to induced dysbiosis in the male reproductive system, including impaired leptin signalling, altered testicular metabolite profiles and remapped small RNA payloads in sperm. As a result, dysbiotic fathers trigger an elevated risk of in utero placental insufficiency, revealing a placental origin of mammalian intergenerational effects. Our study defines a regulatory ‘gut-germline axis’ in males, which is sensitive to environmental exposures and programs offspring fitness through impacting placental function.</p>

2024-02-12 | MTBLS1629 | MetaboLights

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