The process by which an embryo forms and develops, marking a time of rapid cell proliferation, specification, and differentiation. Embryogenesis in C. elegans takes about fourteen hours at 22 degrees C, starting with fertilization of the oocyte with self-sperm from the hermaphrodite or sperm from a male. During the first two hours, the zygote forms and early cleavages establish the embryonic axes. Somatic and germ-line founder cell fates are also determined. During the next five hours, most cell proliferation completes, the embryo undergoes gastrulation, and cell differentiation and organogenesis begins. Cell differentiation, organogenesis and morphogenesis are completed during the final stage of embryogenesis. The nervous system becomes active and muscles are stimulated during this last stage, resulting in the embryo twitching within its egg shell and eventually hatching as an L1 larva.
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.
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.