Cuticle biogenesis
The C. elegans cuticle is a protective exoskeleton of specialized extracellular matrix (ECM) consisting primarily of collagen, lipids, and glycoproteins and is required for viability. (Chisholm and Hardin 2005; Page and Johnstone 2007). The cuticle determines the shape of the body and, through connection from the epidermis to muscle, provides anchoring points for muscle contraction. The cuticle also serves as a model for ECM formation and function with molecules and pathways involved in cuticle biogenesis conserved in vertebrates (Page and Johnstone 2007). The outer epithelial layer, the epidermis, of the embryo undergoes a series of cell fusions to make large multinucleate, or syncytial, epidermal cells, which secrete the materials needed to make up the cuticle. This protective layer is produced five times during C. elegans development, with each molt ending with an entirely new cuticle.
Response to pathogens
C. elegans is susceptible to disease or death brought on by a number of different microbial or fungal pathogens. While some of these pathogens, e.g., Drechmeria conispora and Microbacterium nematophilum are more specific to nematodes, other pathogens, e.g., Pseudomonas aeruginosa, Salmonella enterica, etc., are also pathogenic to humans. Genetic studies of C. elegans response to these pathogens have shown the nematode to employ three main mechanisms to defend against pathogen attack. First, as a behavioral response, C. elegans has been shown to use olfactory cues to distinguish different bacteria and respond with avoidance to those that are deemed harmful. Second, C. elegans has evolved physical barriers to infection that include a cuticle of collagen and chitin that protects the worm from its environment. This cuticle is also replaced at each larval molt, decreasing the worm's exposure to harmful bacteria that may be hitching a ride. In addition, C. elegans has evolved a pharyngeal grinder capable of pulverizing bacteria, keeping live bacteria from entering the gut. Third, C. elegans nematodes have inducible innate immune responses that are analogous to stress response pathways present in other organisms, for example, the PMK-1/P38 MAPK signaling pathway induced in response to Salmonella enterica.