Abstract
Little is known about the relative contributions and importance of antibacterial effectors in the nematode C. elegans, despite extensive work on the innate immune responses in this organism. We report an investigation of the expression, function and regulation of the six ilys (invertebrate-type lysozyme) genes of C. elegans. These genes exhibited a surprising variety of tissue-specific expression patterns and responses to starvation or bacterial infection. The most strongly expressed, ilys-3, was investigated in detail. ILYS-3 protein was expressed constitutively in the pharynx and coelomocytes, and dynamically in the intestine. Analysis of mutants showed that ILYS-3 was required for pharyngeal grinding (disruption of bacterial cells) during normal growth and consequently it contributes to longevity, as well as being protective against bacterial pathogens. Both starvation and challenge with Gram-positive pathogens resulted in ERK-MAPK-dependent up-regulation of ilys-3 in the intestine. The intestinal induction by pathogens, but not starvation, was found to be dependent on MPK-1 activity in the pharynx rather than in the intestine, demonstrating unexpected communication between these two tissues. The coelomocyte expression appeared to contribute little to normal growth or immunity. Recombinant ILYS-3 protein was found to exhibit appropriate lytic activity against Gram-positive cell wall material.
Highlights
Most animal epithelia possess innate defense systems that sense pathogenic and toxic insults and transmit stranger/danger signals to activate appropriate counter measures
We examined the expression and relative importance of a gene family encoding six invertebrate-type lysozymes in the much-studied nematode C. elegans
We focused our attention on the ilys-3 gene because this was one of highly expressed genes induced in C. elegans upon exposure to M. nematophilum and its reporter showed strong induction under various conditions
Summary
Most animal epithelia possess innate defense systems that sense pathogenic and toxic insults and transmit stranger/danger signals to activate appropriate counter measures. The transcriptional programs that control the epithelial production of antimicrobials and mucosal homeostasis both act via coordinated activation of common innate immune receptors: Toll-like receptors (TLR), Nodlike receptors (NLR) and the cytosolic helicases RIG-1 and MDA5. Some of these function as sensors of endogenous or exogenous damage-associated molecular patterns [1]. The invertebrate C. elegans has proved a valuable model to deconstruct biological processes that deal with the way animals detect danger signals and respond to life-threatening events such as toxic chemicals, DNA damage, metabolic stress and pathogens. Damage inflicted on nematode tissues can trigger a variety of functionally conserved molecular events aimed at limiting and repairing damage or sustaining viability while adverse conditions persist (reviewed elsewhere [2,3,4,5,6])
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