Caenorhabditis elegans
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ABSTRACT:
PROVIDER: PRJNA184925 | ENA |
REPOSITORIES: ENA
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Project description:Birt-Hogg-Dubé syndrome is an autosomal dominantly inherited disorder that is characterized by the clinical triad of benign skin tumors - so-called fibrofolliculomas, recurrent pneumothoraces due to pulmonary cysts and the formation of kidney tumors. The molecular function of Folliculin (FLCN), the protein product of the BHD gene mutated in this syndrome, has remained elusive to a large extent. Animal models such as mouse, rat and canine models have been used to elucidate parts of the pathway in which FLCN plays a role showing it to interfere with AMP-kinase and mTOR signaling. Caenorhabditis elegans provides - due to its simple genetic amenability and large brood size - the perfect tool to study signal transduction pathways in detail. Thus, we decided to examine F22D3.2 (flcn-1) - a putative orthologue of FLCN in the nematode. We established the first gene expression profiles of a strain harboring a mutation in flcn-1 compared to WTN2 allowing for a first insight into the function of this gene in C. elegans. This study examines the transcriptome of the flcn-1 mutant strain RB1035 in comparison to WTN2 in order to identify differentially regulated genes. RNA was prepared from pre-reproductive adults in both WTN2 and RB1035 (harboring a flcn-1 mutant allele, mutant worms had been backcrossed wo WTN2 8 times) using biological triplicates. RNA was labeled and hybridized to Agilent C. elegans whole genome microarrays and scanned using a Agilent Technologies Scanner G2505C US22502540.
2012-12-31 | E-GEOD-43207 | biostudies-arrayexpress
Project description:Birt-Hogg-Dubé syndrome is an autosomal dominantly inherited disorder that is characterized by the clinical triad of benign skin tumors - so-called fibrofolliculomas, recurrent pneumothoraces due to pulmonary cysts and the formation of kidney tumors. The molecular function of Folliculin (FLCN), the protein product of the BHD gene mutated in this syndrome, has remained elusive to a large extent. Animal models such as mouse, rat and canine models have been used to elucidate parts of the pathway in which FLCN plays a role showing it to interfere with AMP-kinase and mTOR signaling. Caenorhabditis elegans provides - due to its simple genetic amenability and large brood size - the perfect tool to study signal transduction pathways in detail. Thus, we decided to examine F22D3.2 (flcn-1) - a putative orthologue of FLCN in the nematode. We established the first gene expression profiles of a strain harboring a mutation in flcn-1 compared to WTN2 allowing for a first insight into the function of this gene in C. elegans. This study examines the transcriptome of the flcn-1 mutant strain RB1035 in comparison to WTN2 in order to identify differentially regulated genes.
2012-12-31 | GSE43207 | GEO
Project description:Identification of genes expressed in C. elegans touch receptor neurons
| PRJNA92957 | ENA
Project description:Genomic identification and functional characterization of essential genes in Caenorhabditis elegans
| PRJNA416306 | ENA
Project description:Expression analysis of C. elegans genes kin-1 and crh-1 mutant
| PRJNA175021 | ENA
Project description:Expression analysis of C. elegans genes daf-9 and daf-12 mutant
| PRJNA177847 | ENA
Project description:Purpose: The goal of this study is to identify differentially expressed genes in pry-1/Axin mutant compare to N2 wild-type (WT). Our study represents the first analysis of Axin transcriptome in C. elegans and facilitates investigations of axin mediated processes.
2018-03-01 | GSE94412 | GEO
Project description:Purpose: The goal of this study is to identify differentially expressed microRNAs in pry-1/Axin mutant compare to N2 wild-type (WT). Our study represents the first microRNA analysis of Axin transcriptome in C. elegans and facilitates investigations of axin mediated processes.
2019-04-19 | GSE130039 | GEO
Project description:Background: The ability of an organism to repair DNA damage is implicated in carcinogenesis and aging. Interestingly expression profiling of Nucleotide Excision Repair (NER) deficient segmental progeroid mice revealed gene expression changes resembling these observed in aged wild type animals. Our previous transcriptional profiling of NER-deficient C. elegans xpa-1 mutant showed overrepresentation of genes involved in lifespan determination and upregulation of several oxidative stress response genes (Fensgard et al. Aging 2010). However, since an independent study performed by Boyd and coworkers (Boyd et al. Mut Res 2010) showed limited number of changes in xpa-1 mutant. Therefore to independently validate that transcriptome modulation does take place in xpa-1 mutants, we performed another global gene expression profiling based on 5 independent biological replicates allowing more stringent statistical analysis. Results: In agreement with what was observed by Boyd and coworkers (Boyd et al. Mut Res 2010) current transcriptomic analysis detected fewer changes in xpa-1 C. elegans mutant with only a few genes regulated more than 4-fold. Nevertheless, Gene Ontology (GO) enrichment analysis performed on statistically significantly regulated unique protein coding genes revealed overrepresentation of aging gene cluster. Moreover, as before, overexpression of several genes involved in oxidative stress responses was detected. Conclusion: More stringent statistical analysis predictably resulted in a smaller number of regulated genes and thus overrepresented GOs comparing to the earlier paper. However, major conclusions of the previous study can be still regarded as valid, as the most important aging GO is still overrepresented. Activation of oxidative stress-responses and downregulation of insulin-like signaling (ILS) is seen in Nucleotide Excision Repair (NER) deficient segmental progeroid mice. Evidence suggests that this is a survival response to persistent transcription-blocking DNA damage, although the relevant lesions have not been identified. Here we provide evidence for transcriptional reprogramming in NER-deficient C. elegans xpa-1 by transcriptomic and proteomic approaches. This reprograming is accompanied by increased intracellular ROS and ATP levels and lifespan shortening in xpa-1 mutant. Moreover we show that Base Excision Repair DNA glycosylase NTH-1 is upstream form the signaling events leading to transcriptomic changes, as its downregulation reverses overexpression of sod-3, gst-4 and aqp-1 genes, reduces intracellular ROS and ATP levels and reverses lifespan shortening observed in xpa-1 mutant. Surprisingly, however, these responses appear to not depend on cyclopurine levels, since these lesions are lower in xpa-1 C. elegans mutant than in the wild type. Finally, we also explore here which other upstream factors are necessary for transcriptional reprograming in xpa-1 mutant.
2013-05-03 | GSE39252 | GEO