[
WormBook,
2005]
A wide variety of bacterial pathogens, as well as several fungi, kill C. elegans or produce non-lethal disease symptoms. This allows the nematode to be used as a simple, tractable model host for infectious disease. Human pathogens that affect C. elegans include Gram-negative bacteria of genera Burkholderia, Pseudomonas, Salmonella, Serratia and Yersinia; Gram-positive bacteria Enterococcus, Staphylococcus and Streptococcus; and the fungus Cryptococcus neoformans. Microbes that are not pathogenic to mammals, such as the insect pathogen Bacillus thuringiensis and the nematode-specific Microbacterium nematophilum, are also studied with C. elegans. Many of the pathogens investigated colonize the C. elegans intestine, and pathology is usually quantified as decreased lifespan of the nematode. A few microbes adhere to the nematode cuticle, while others produce toxins that kill C. elegans without a requirement for whole, live pathogen cells to contact the worm. The rapid growth and short generation time of C. elegans permit extensive screens for mutant pathogens with diminished killing, and some of the factors identified in these screens have been shown to play roles in mammalian infections. Genetic screens for toxin-resistant C. elegans mutants have identified host pathways exploited by bacterial toxins.
[
WormBook,
2006]
Throughout the C. elegans sequencing project Genefinder was the primary protein-coding gene prediction program. These initial predictions were manually reviewed by curators as part of a "first-pass annotation" and are actively curated by WormBase staff using a variety of data and information. In the WormBase data release WS133 there are 22,227 protein-coding gene, including 2,575 alternatively-spliced forms. Twenty-eight percent of these have every base of every exon confirmed by transcription evidence while an additional 51% have some bases confirmed. Most of the genes are relatively small covering a genomic region of about 3 kb. The average gene contains 6.4 coding exons accounting for about 26% of the genome. Most exons are small and separated by small introns. The median size of exons is 123 bases, while the most common size for introns is 47 bases. Protein-coding genes are denser on the autosomes than on chromosome X, and denser in the central region of the autosomes than on the arms. There are only 561 annotated pseudogenes but estimates but several estimates put this much higher.
[
WormBook,
2008]
Germline apoptosis shares with somatic apoptosis a reliance on key components of the core apoptotic machinery, including CED-3 and CED-4. However, germline apoptosis differs from somatic apoptosis in its regulation. Whereas somatic apoptosis is developmentally programmed by cell lineage, germline apoptosis occurs as part of an oogenesis program. One category of germline apoptosis, dubbed "physiological" germline apoptosis, reduces the number of cells that complete oogenesis, and is independent of the BH3-only apoptosis effecter EGL-1. A second category, termed "stress-induced" germline apoptosis, is triggered by a genomic integrity checkpoint. Some mechanisms that are monitored by this DNA-damage checkpoint are also involved in germ cell "immortality," or preservation of a continuous germ cell lineage over successive generations. In addition, exposure to certain environmental insults or pathogens induces germ cell apoptosis. Here we will review the mechanisms that control each of the pathways leading to germ cell apoptosis and discuss their functional significance. Germline apoptosis is an integral part of oogenesis in many animals, including humans. Because many of the regulators of C. elegans germline apoptosis are conserved, we suggest that this nematode provides a valuable model for understanding controls of germline apoptosis more broadly.