Wnt signaling pathway
Wnt glycoproteins are signaling molecules that control a wide range of developmental processes and is a conserved feature of metazoan development. In C. elegans Wnt signaling has been shown to play a role in cell fate specification and determination of cell polarity, cell migration, and axis determination during axon outgrowth. A 'canonical' Wnt signaling pathway has been elucidated in vertebrate and invertebrate model systems where Wnt binding leads to the stabilization of the transcription factor beta-catenin, which then enters the nucleus to regulate Wnt pathway target genes. Like other species, the C. elegans genome encodes multiple genes for Wnt ligands, EGL-20, LIN-44, MOM-2, CWN-1, CWN-2) and Wnt receptors (LIN-17, MOM-5, MIG-1, CFZ-2, LIN-18). Canonical Wnt signaling in C. elegans, utilizes the beta-catenin BAR-1 to convert POP-1 into an activator and controls the expression of several homeobox genes. However, unlike vertebrates or Drosophila, the C. elegans genome encodes multiple beta-catenin genes (HMP-2, BAR-1, SYS-1, WRM-1), which give rise to noncanonical Wnt signalling pathways: for example, the endoderm induction pathway requires the beta-catenin WRM-1 and parallel input from a mitogen-activated kinase (MAPK) pathway to downregulate POP-1.
Mitochondrial DNA maintenance and expression
The mitochondrial genome is a vital component of animal metabolism, physiology, and development. C. elegans mitochondrial DNA (mtDNA) is typical of animal mitochondrial genomes in its size, 13,794 nucleotides in length, and gene content of 32 genes: 2 ribosomal RNAs, 22 transfer RNAs, and 12 protein subunits of the mitochondrial respiratory chain (MRC). Unlike nuclear DNA, mtDNA is maternally inherited and can be present at tens to tens of thousands of copies per cell. Its copy number is developmentally regulated, with mtDNA increasing about 30-fold between the L1 and the adult stages. Blocking mtDNA increase leads to larval arrest. Underlying its essential role in the biology of C. elegans, over 200 nuclear genes are needed to replicate, transcribe, and maintain the mitochondrial genome and to assemble the translation machinery required for expressing mitochondrial proteins. Disruptions in these processes have shown that the mitochondrion plays a critical role in aging, life span determination, reactive oxygen species response, the unfolded protein response, and apoptosis. Oddly, despite the essential role of mtDNA encoded genes in the cellular and organismal biology of C. elegans, mutations in mtDNA have not been reported. By contrast, over 300 lesions in human mtDNA have been described, many associated with neurological, endocrinological or muscle diseases.