- Cell death
The death of a cell is a highly regulated process that occurs frequently throughout development. Current research shows that there are four different ways a cell can die, programmed cell death, necrosis, autophagy, and cytotoxic cell death. Research in C. elegans pioneered the discovery of the molecular pathway responsible for programmed cell death. More recent work using this model organism has made headways into elucidating the genes involved in regulating and impacting these other methods of cell death. There is controversy as to whether or not cell death by autophagy has been observed in C. elegans animals; however, an aspect of autophagy, macroautophagy, has been reported.
- Aging
Aging in C. elegans involves measurable declines in morphology, reproduction, and behavior. Understanding the cellular and molecular processes leading to senescence in this nematode began in the early 1980s with the targeted identification of mutants with extended life spans (an AGE phenotype). These studies identified at least two key regulators of life span, DAF-2, an insulin/IGF receptor ortholog, and DAF-16, a Forkhead-related transcription factor. Since then many more genes and pathways involved in senescence have been identified. Almost all of these genes play important roles in cellular and organismal-level processes other than aging, such as dauer formation, stress response, feeding, and chemosensation. A common marker for aging in C. elegans is the accumulation of lysosomal deposits of lipofuscin, resulting in an increase in intestinal autofluorescence over time.
- Mechanosensation
Mechanosensation converts mechanical energy into electrical signals allowing an organism to use physical cues from the environment or from internal sensors to affect its behavior. Mechanical stimuli are received through mechanosensory receptor neurons (MRNs). In C. elegans, there are 30 putative MRNs in hermaphrodites while an additional 52 MRNs are found in males. More than 40 of these male-specific MRNs are found in the male tail, hook, post-cloacal sensilla and spicule and are required for male mating. MRNs transmit electrical signals to other neurons through electrical or chemical synapses. MRNs may or may not have ciliated dendrite endings, which is some cases are exposed to the outside. Mechanical stimuli initiate as well as modulate many behaviors of the worm. MRNs allow the worm to respond to light touch, such as stroking with an eyelash as well as harsh touch, such as prodding with a pick.
- 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.
- Trans-splicing
Trans-splicing is an RNA processing event that fuses together sections of two different pre-mRNA sequences. In C. elegans, ~70% of mRNAs are trans-spliced to one of two 22 nucleotide spliced leaders, SL1 or SL2, with more than half of all transcripts undergoing SL1 splicing. During SL1 splicing, the 5' ends of pre-mRNAs are removed and replaced with SL1 sequence in a process very closely related to cis-splicing (intron/exon processing). SL1 sequence is ~100nt and is donated by small nuclear ribonucleoprotein particles (snRNPs). The remaining genes are trans-spliced by SL2. These genes are all downstream genes in closely spaced gene clusters similar to bacterial operons. They are transcribed from a promoter at the 5' end of the cluster of between 2 and 8 genes. This transcription makes a polycistronic pre-mRNA that is co-transcriptionally processed by cleavage and polyadenylation at the 3' end of each gene, and this event is closely coupled to the SL2 trans-splicing event that occurs only ~100 nt further downstream. Recent studies on the mechanism of SL2 trans-splicing have revealed that one of the 3' end formation proteins, CstF, interacts with the only protein known to be specific to the SL2 snRNP.