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Mechanistic impacts of bacterial diet on dopaminergic neurodegeneration in a Caenorhabditis elegans α-synuclein model of Parkinson's disease

ABSTRACT: Using distinct mutant strains deficient in key aspects of gene silencing machinery, we provide evidence that neuroprotection appears to stem from dsRNAs that originate from the bacteria themselves, and Systemic RNA Interference Defective (SID) mutants deficient in dsRNA-mediated gene silencing do not allow for neuroprotection from the bacteria. Transcriptomic analysis between worms reared on OP50 and HB101 E. coli for multiple generations in an a-syn background revealed that the primary cellular processes involved in neuroprotection of this nature included but were not limited to endopeptidase activity, transcriptional regulation, calcium ion binding activity, and water channel activity.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE210005 | GEO | 2023/05/19

REPOSITORIES: GEO

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RNA-seq Analysis of wildtype (N2) C. elegans at the L4 stage on diets from the laboratory environment and natural environment

Project description:We analyzed RNA-seq data from C. elegans on six bacterial diets, 3 E. coli diets (OP50, HT115, HB101) found in the laboratory setting and 3 found in C. elegans natural environment (Methylobacterium, Xanthomonas, Sphingomonas). We compared gene expression between L4 worms on the OP50 diet to the other 5 bacterial diets. We found that diet influences many gene expression changes, leading to genes being both up regulated and down regulated in a diet-dependent manner.

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Expression data from the commensal bacteria Escherchia coli strain HB101 interacting with Caenorhabditis elegans and/or Giardia duodenalis

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2015-04-02 | E-GEOD-61092 | biostudies-arrayexpress

Germline- and soma-specific heritable epigenetic silencing at an endogenous locus (small RNA-Seq)

Project description:The emergence and transmission of epigenetic signals across generations can quickly and efficiently alter gene expression in a population. We describe an epigenetic silencing signal whose initiation, transmission properties, genetic requirements and site of action are distinct from previously described epigenetic inheritance in C. elegans. A multi-copy transgene containing the region upstream of sid-1 silences sid-1 and upstream genes. Once established, silencing is stable in the absence of the array and can be maintained without selection for 13 generations. We show that the silenced state can be transmitted to progeny in the absence of the silenced locus, but that inherited silencing is dependent on the nuclear RNAi Argonaute HRDE-1, which stabilizes silencing siRNAs that target sid-1 exons. Notably, at each generation, the RNAi-dependent germline silenced sid-1 locus transitions to a chromatin-dependent silenced state in somatic cells, indicating that the mechanisms of transgenerational silencing in the soma and germline are distinct.

2017-02-16 | GSE81706 | GEO

Germline- and soma-specific heritable epigenetic silencing at an endogenous locus (RNA-Seq)

2017-02-16 | GSE81707 | GEO

Targeted interference of sin3a-tgif1 function by SID decoy treatment inhibits WNT signaling and invasion in triple negative breast cancer cells

Project description:Targeted interference of sin3a-tgif1 function by SID decoy treatment inhibits WNT signaling and invasion in triple negative breast cancer cells. MDA-MB-231 cells were treated with scrambled SID control, 2.5ÂµM SID peptide or untreated for 24h. Sub-confluent cultures of MDA-MB-231 cells were treated with scrambled SID control, 2.5ÂµM SID peptide or untreated for 24h. Experiments were performed as three independent replicates.

2016-07-21 | E-GEOD-84648 | biostudies-arrayexpress

Endocytosed dsRNAs induce lysosomal membrane permeabilization that allows cytosolic dsRNA translocation for Drosophila RNAi response

Project description:RNA interference (RNAi) is a gene-silencing mechanism triggered by the cytosolic entry of double-stranded RNAs (dsRNAs). Many animal cells internalize extracellular dsRNAs via endocytosis for RNAi induction. However, it is not clear how the endocytosed dsRNAs are translocated into the cytosol across the endo/lysosomal membrane. Herein, we show that in Drosophila S2 cells, endocytosed dsRNAs induce lysosomal membrane permeabilization (LMP) that allows cytosolic dsRNA translocation. LMP mediated by dsRNAs requires the lysosomal Cl−/H+ antiporter ClC-b/DmOstm1. In clc-b or dmostm1 knockout S2 cells, extracellular dsRNAs are endocytosed and reach the lysosomes normally but fail to enter the cytosol. Pharmacological induction of LMP restores extracellular dsRNA-directed RNAi in clc-b or dmostm1-knockout cells. Furthermore, clc-b or dmostm1 mutant flies are defective in extracellular dsRNA-directed RNAi and its associated antiviral immunity. Therefore, endocytosed dsRNAs have an intrinsic ability to induce ClC-b/DmOstm1-dependent LMP that allows cytosolic dsRNA translocation for RNAi responses in Drosophila cells.

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2007-02-08 | GSE5793 | GEO

Targeted interference of sin3a-tgif1 function by SID decoy treatment inhibits WNT signaling and invasion in triple negative breast cancer cells

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PTGS induced by different dsRNAs

Project description:Unexpected variations in posttranscriptional silencing induced by differentially produced dsRNAs

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Targeting the SIN3A-PF1 Interaction inhibits Epithelial to Mesenchymal Transition and Maintenance of a Stem Cell Phenotype in Triple Negative Breast Cancer (Expression)

Project description:Triple negative breast cancer (TNBC) is characterized by a poorly differentiated phenotype and limited treatment options. Aberrant epigenetics in this subtype represent a potential therapeutic opportunity, but a better understanding of the mechanisms contributing to the TNBC pathogenesis is required. The SIN3 molecular scaffold performs a critical role in multiple cellular processes, including epigenetic regulation, and has been identified as a potential therapeutic target. Using a competitive peptide corresponding to the SIN3 interaction domain of MAD (Tat-SID), we investigated the functional consequences of selectively blocking the paired amphipathic helix (PAH2) domain of SIN3. Here, we report the identification of the SID-containing adaptor PF1 as a factor required for maintenance of the TNBC stem cell phenotype and epithelial to mesenchymal transition (EMT). Tat-SID peptide blocked the interaction between SIN3A and PF1, leading to epigenetic modulation and transcriptional downregulation of TNBC stem cell and EMT markers. Importantly, Tat-SID treatment led to a reduction in primary tumor growth and disseminated metastatic disease in vivo. In support of these findings, knockdown of PF1 expression phenocopied treatment with Tat-SID both in vitro and in vivo. These results demonstrate a critical role for a complex containing SIN3A and PF1 in TNBC and provide a rational for its therapeutic targeting. Sub-confluent cultures of MDA-MB-231 cells were treated with 1ÂµM Tat-SID peptide or 1ÂµM Tat-Scr scrambled control peptide for 24hr.

2015-11-02 | E-GEOD-73278 | biostudies-arrayexpress

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