Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of C. elegans IG274 wt frIs7 and IG339 nipi-1(fr1) frIs7 after infection with Dreshmeria coniosporia

ABSTRACT: 1.Sample Growth Conditions protocols
Eggs from IG274 wt; frIs7 and IG339 nipi-1(fr1); frIs7 worms cultivated at 25ÃÂ°C were allowed to hatch in the absence of food at 25ÃÂ°C for 16 hours. Synchronised larvae were transferred to NGM agar plates lawned with OP50 and cultivated at 25°C for 48 hours.
2.Sample Treatment protocols
Synchronised IG274 wt; frIs7 and IG339 nipi-1(fr1); frIs7 worms at the young L4 stage were infected with freshly harvested spores of Dreshmeria coniosporia. After 24 hours at 25°C, the worms were collected into trizol for further RNA extraction. Controls worms were non infected.

INSTRUMENT(S): ScanArray 4000XL [PerkinElmer]

ORGANISM(S): Caenorhabditis elegans

DISEASE(S): not infected

SUBMITTER: Jonathan Ewbank

PROVIDER: E-MEXP-1364 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Antifungal innate immunity in C. elegans: PKCdelta links G protein signaling and a conserved p38 MAPK cascade.

Ziegler Katja K Kurz C Léopold CL Cypowyj Sophie S Couillault Carole C Pophillat Matthieu M Pujol Nathalie N Ewbank Jonathan J JJ

Cell host & microbe 20090401 4

Like other multicellular organisms, the model nematode C. elegans responds to infection by inducing the expression of defense genes. Among the genes upregulated in response to a natural fungal pathogen is nlp-29, encoding an antimicrobial peptide. In a screen for mutants that fail to express nlp-29 following fungal infection, we isolated alleles of tpa-1, homologous to the mammalian protein kinase C (PKC) delta. Through epistasis analyses, we demonstrate that C. elegans PKC acts through the p38 ...[more]

PMID: 19380113

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Project description:Filarial nematodes are arthropod-borne nematodes that cause a variety of economically important diseases such as onchocerciasis (river blindness), lymphatic filariasis, and heartworm disease. The most widespread filarial disease of humans is lymphatic filariasis, caused by worms in the genera Wuchereria and Brugia. Lymphatic filariasis is an economic and social burden in endemic countries and affects approximately 119 million people worldwide (Michael, 1997). In humans, the worms live in and block the lymph vessels, causing improper flow of lymph, and inflammation of the lymphatic system. The symptoms are fever, swollen limbs and genitals, generalized malaise, and can progress to a debilitating condition known as elephantiasis This research focuses on the transmission of these worms to the disseminating mosquito host, and it is based on the interesting observation that mf must be at least 7 days old to successfully infect the mosquito (de Hollanda, 1982). Newborn mf that have not â??maturedâ?? cannot successfully penetrate the midgut of the mosquito, and subsequently cannot develop to the L3 stage (Fuhrman, 1987). Previous work done by another group 20 years ago suggests that the molecular makeup of the worm surface changes during this maturation process (Furman, 1983 a and b). We used microarray analysis to characterize changes in gene expression that take place during the mf maturation process. Understanding the gene expression changes that occur as the mf mature will allow us to understand the nature of the philological transition that allows mf to move from the human to the mosquito host. With this information in hand, we can eventually identify parasite molecules that could be targeted to either stop parasite reproduction or prevent transmission of the mf to the mosquito. This would stop parasite transmission in endemic areas. Brugia pahangi mature mf (30 days and older) RNA was compared to immature mf (3 days and younger). Three biological replicates were performed each with two technical replicates

Dataset Information

Transcription profiling of C. elegans IG274 wt frIs7 and IG339 nipi-1(fr1) frIs7 after infection with Dreshmeria coniosporia

Publications

Antifungal innate immunity in C. elegans: PKCdelta links G protein signaling and a conserved p38 MAPK cascade.

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