Microbial Interactions with Caenorhabditis elegans: Lessons from a Model Organism

Abstract

In recent years, the study of invertebrate innate immune defense responses has been greatly expanded by the use of the powerful tractable model Caenorhabditis elegans. Because of the accessible mechanisms underpinning its innate immune system, the worm has become into a valuable model for identifying core strategies of microbial pathogenicity and host defense. C. elegans-microbial interaction studies have revealed a conservation of both pathogen virulence factors and metazoan immune repertoires. In C. elegans the signaling pathways involved in orchestrating immune responses are: three mitogen-activated protein kinases (p38, JNK and ERK), the unfolded protein response (serine threonine/kinase IRE-1 and PQN/ABU proteins), the transforming growth factor-b (TGF-b), the insulin-like receptor (DAF-2), the Wnt/Wingless b-catenin (BAR-1), and the component of programmed cell death BCL-2 homolog (CED-9). These pathways also serve major developmental, behavioral and metabolic functions. Abbreviations ABUactivated in blocked unfolded protein response AGE-1 aging alteration Apaf-1 apoptosis protease activating factor-1 ASK1 apoptosis signaling-regulating kinase-1 BAR-1 beta-catenin/armadillo related CED cell death abnormality DAF dauer formation abnormal DBL-1 decapentaplegic/BMP-like EGL egg-laying defective

A Model for Evolutionary Ecology of Disease: The Case for Caenorhabditis Nematodes and Their Natural Parasites

“…Before the discovery of these viruses, researchers hypothesized that viruses could not replicate in C. elegans cells, perhaps because of its strong RNAi response (rev. in Gravato-Nobre and Hodgkin, 2005Hodgkin, , 2011 The following studies illustrate the potential for experimental coevolution to answer fundamental questions in evolutionary biology and inform host-parasite interactions in the wild.…”

“…2002). Many reviews cover this diversity in more detail (Aballay and Ausubel, 2002;Couillault and Ewbank, 2002;Ewbank, 2002;Sifri et al, 2005;Gravato-Nobre and Hodgkin, 2011).…”

“…Before the discovery of these viruses, researchers hypothesized that viruses could not replicate in C. elegans cells, perhaps because of its strong RNAi response (rev. in Gravato-Nobre and Hodgkin, 2005Hodgkin, , 2011. In the laboratory, replication of unnatural viruses was obtained only under highly artificial conditions (Flock house virus- Lu et al, 2005) (vesicular stomatitis virus- Schott et al, 2005;Wilkins et al, 2005).…”

A transcriptomic snapshot of early molecular communication between Pasteuria penetrans and Meloidogyne incognita

“…Mutations in genes involved in the building of complex cuticular surface components in C. elegans are known to affect bacterial adhesion [37]. Several differentially expressed transcripts identified in this study are predicted to interfere with attachment of endospores on the nematodes by altering the cuticle surface structure.…”

Knockdown of a mucin‐like gene in Meloidogyne incognita (Nematoda) decreases attachment of endospores of Pasteuria penetrans to the infective juveniles and reduces nematode fecundity

“…Although the roles of the majority of mucins in C. elegans are unknown, it is clear that bah , bus and srf mutants, which show altered bacterial adhesion, are glycosyltransferase mutants; glycosyltransferases are involved in the building of complex glycans on the surface coat of the cuticle (Gravato‐Nobre and Hodgkin, ). One of these mutations in C. elegans , bus‐4 , which confers resistance to Microbacterium nematophilum, Yersinia pestis and Y. pseudotuberculosis , also shows altered mucin expression (Parsons et al ., ).…”