Unknown,Transcriptomics,Genomics,Proteomics

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Transcripts regulated by elevated DKF-2 (WT background)


ABSTRACT: Transcriptional profiling was used to determine why DKF-2 (protein kinase D) deficiency and surfeit caused hypersensitivity and resistance, respectively, to a bacterial pathogen (P. aeruginosa 14). The studies show that DKF-2 contributes to C. elegans innate immunity by inducing expression of >75 genes that protect against pathogenic bacteria. Keywords: Induced imune response Three independent biological replicates were isolated for each strain. The strains for each replicate were grown and harvested in parallel.

ORGANISM(S): Caenorhabditis elegans

SUBMITTER: Charles Rubin 

PROVIDER: E-GEOD-12456 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Protein kinase D is an essential regulator of C. elegans innate immunity.

Ren Min M   Feng Hui H   Fu Ya Y   Land Marianne M   Rubin Charles S CS  

Immunity 20090401 4


Protein kinase D (PKD) mediates signal transduction downstream from phospholipase C and diacylglycerol (DAG). PKDs are activated by hormones and stress in cell lines, but little is known about PKD functions and regulation in vivo. Here, we show that DKF-2, a C. elegans PKD, regulates innate immunity. Animals lacking DKF-2 were hypersensitive to killing by bacteria that are pathogens of C. elegans and humans. DKF-2 induced 85 mRNAs, which encode antimicrobial peptides and proteins that sustain in  ...[more]

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