Transcriptome Analysis of Caenorhabditis elegans Lacking Heme Peroxidase SKPO-1 Reveals an Altered Response to Enterococcus faecalis
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ABSTRACT:
PROVIDER: PRJNA641409 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12076114_1.fastq.gz | Fastqsanger.gz | |||
| SRR12076114_2.fastq.gz | Fastqsanger.gz | |||
| SRR12076115_1.fastq.gz | Fastqsanger.gz | |||
| SRR12076115_2.fastq.gz | Fastqsanger.gz | |||
| SRR12076116_1.fastq.gz | Fastqsanger.gz |
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Project description:The nematode Caenorhabditis elegans is commonly used as a model organism in studies of development and the host immune response. The worm encodes twelve peroxidase-cyclooxygenase superfamily members. SKPO-1 was localized to the hypodermis of the animals where it also affected cuticle development. In this work, a better understanding of how loss of skpo-1 impacts both sensitivity to pathogen as well as cuticle development was sought by subjecting a deletion mutant of skpo-1 to transcriptome analysis using RNA sequencing following exposure to control (Escherichia coli) and pathogenic (E. faecalis) feeding conditions.
2020-06-24 | GSE153088 | GEO
Project description:The nematode Caenorhabditis elegans is commonly used as a model organism in studies of the host immune response. The worm encodes twelve peroxidase-cyclooxygenase superfamily members, making it an attractive model in which to study the functions of heme peroxidases. In previous work, loss of one of these peroxidases, SKPO-1 (ShkT-containing peroxidase), rendered C. elegans more sensitive to the human, Gram-positive pathogen Enterococcus faecalis. SKPO-1 was localized to the hypodermis of the animals where it also affected cuticle development as indicated by a morphological phenotype called "dumpy." In this work, a better understanding of how loss of skpo-1 impacts both sensitivity to pathogen as well as cuticle development was sought by subjecting a deletion mutant of skpo-1 to transcriptome analysis using RNA sequencing following exposure to control (Escherichia coli) and pathogenic (E. faecalis) feeding conditions. Loss of skpo-1 caused a general upregulation of genes encoding collagens and other proteins related to cuticle development. On E. faecalis, these animals also failed to upregulate guanylyl cyclases that are often involved in environmental sensing. Hoechst straining revealed increased permeability of the cuticle and atomic force microscopy exposed the misalignment of the cuticular annuli and furrows. These findings provide a basis for better understanding of the morphological as well as the pathogen sensitivity phenotypes associated with loss of SKPO-1 function.
| S-EPMC8022988 | biostudies-literature
Project description:In mice lacking the heme exporter, FLVCR, differentiation fails at the CFU-E/proerythroblast stage from excessive heme and reactive oxygen species. We show that Flvcr1-deleted CFU-E/proerythroblasts have low GATA1 mRNA and GATA1-target gene mRNAs along with increased ribosomal protein mRNAs as a direct result of increased heme. Thus heme increases ribosomal protein transcription when globin production needs to be increased, and when heme is excessive, GATA1 is reduced allowing for normal termination of erythroid differentiation. This demonstrates that heme and GATA1 are co-master regulators of erythroid differentiation.
2019-02-07 | GSE94905 | GEO
Project description:The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue. Two experimental groups: Group 1: three 4um Controls vs. three 4uM hrg-2 Mutants; Group 2: three 20um Controls vs. three 20uM hrg-2 Mutants
2013-01-01 | E-GEOD-34471 | biostudies-arrayexpress
Project description:The roundworm Caenorhabditis elegans is a heme auxotroph that requires the coordinated actions of HRG-1 heme permeases to transport environmental heme into the intestine and HRG-3, a secreted protein, to deliver intestinal heme to other tissues including the embryo. Here we show that heme homeostasis in the extraintestinal hypodermal tissue is facilitated by the transmembrane protein HRG-2. Systemic heme deficiency upregulates hrg-2 mRNA expression over 200-fold in the main body hypodermal syncytium hyp 7. HRG-2 is a type I membrane protein which binds heme and localizes to the endoplasmic reticulum and apical plasma membrane. Cytochrome heme profiles are aberrant in HRG-2 deficient worms, a phenotype that is partially suppressed by heme supplementation. Heme-deficient yeast strain, ectopically expressing worm HRG-2, reveal significantly improved growth at submicromolar concentrations of exogenous heme. Taken together, our results implicate HRG-2 as a facilitator of heme utilization in the C. elegans hypodermis and provide a mechanism for regulation of heme homeostasis in an extraintestinal tissue.
2013-01-01 | GSE34471 | GEO
Project description:In mice lacking the heme exporter, FLVCR, differentiation fails at the CFU-E/proerythroblast stage from excessive heme and reactive oxygen species. We show that Flvcr1-deleted CFU-E/proerythroblasts have low GATA1 mRNA and GATA1-target gene mRNAs along with increased ribosomal protein mRNAs as a direct result of increased heme. Thus heme increases ribosomal protein transcription when globin production needs to be increased, and when heme is excessive, GATA1 is reduced allowing for normal termination of erythroid differentiation. This demonstrates that heme and GATA1 are co-master regulators of erythroid differentiation.
2019-02-07 | GSE94898 | GEO
Project description:The goal was to identify genes regulated by YvcL (EF0768) by assessing changes in the yvcL deletion mutant relative to the isogenic wild-type. Wild-type E. faecalis OG1 and the mutant lacking yvcL were cultured in Mueller-Hinton broth to exponential phase. Total RNA was purified, depleted for rRNA, and subjected to preparation of mRNA libraries.
2024-03-08 | GSE234500 | GEO
Project description:The goal was to identify genes that are regulated by cell wall stress (bacitracin treatment) in wild-type cells but not in mutant cells lacking CroR, thereby revealing genes of the CroR regulon. Cells of a mutant lacking CroR or its otherwise isogenic wild-type E. faecalis OG1 were cultured in Mueller-Hinton broth and treated (or not) with bacitracin for 15 min. Total RNA was purified, depleted for rRNA, and subjected to preparation of TruSeq stranded mRNA libraries before sequencing on a NextSeq 550 (76-bp single read run).
2022-07-25 | GSE193042 | GEO
Project description:Hemes are essential but potentially cytotoxic cofactors that participate in critical and diverse biological processes. Although the pathway and intermediates for heme biosynthesis have been well defined, the intracellular networks which mediate heme trafficking remain unknown. Caenorhabditis elegans and related helminths are natural heme auxotrophs requiring environmental heme for growth and development. We exploited this auxotrophy to identify HRG-1 and HRG-4 in C. elegans and show that they are essential for heme homeostasis and normal vertebrate development. We demonstrate that heme deficiency upregulates expression of hrg-4 and its evolutionarily conserved paralog hrg-1. Depletion of either HRG-1 or HRG-4 in worms results in disruption of organismal heme sensing and abnormal response to heme analogs. HRG-1 and HRG-4 are novel transmembrane proteins that bind heme and have evolutionarily conserved functions. Transient knockdown of hrg-1 in zebrafish leads to hydrocephalus, yolk tube malformations, and, most strikingly, profound defects in erythropoiesis - phenotypes that are fully rescued by worm HRG-1. These findings reveal unanticipated and conserved pathways for cellular heme trafficking in animals that defines the paradigm for eukaryotic heme transport. Uncovering the mechanisms of heme transport in C. elegans will provide novel insights into human disorders of heme metabolism and generate unique anthelmintics to combat worm infestations. Keywords: dose-response
2008-06-13 | GSE8696 | GEO
Project description:The biofilm proteome profile of endodontic and systemic pathogen E. faecalis has been analysed in this study to identify markers associated with its biofilm formation. Strong and weak biofilm forming E. faecalis clinical isolates were compared with two standard ATCC strains of E. faecalis in order to elucidate the biological pathways associated with the biofilm formation capability of E. faecalis.
2018-01-29 | PXD006542 | Pride