Blumenthal et al., 2002: Genomic analysis of operons by microarrays. Authors probed for SL2 sequence, which is recognized by a snRNP responsible for trans-splicing of the polycistronic mRNA. They used SL2/polyA ratio to determine percentage of genes downstream in operons. Their positive control set: confirmed SL2 genes, negative control set: genes first in operon. They assessed distribution of operons in the genome, the number of genes per operon, and distribution of intercistronic distances within operons.

Why have operons? Is it more efficient? (Some operons in yeast, I believe, but not sure whether at a similar frequency as in C. elegans.) Does it relate to synteny at all? Operons ususally consist of genes with similar function or similar regulation, so there must be an evolutionary benefit. Then why not have operons? Authors suggest that it may have to do with the compactness of the C. elegans genome. (How compact is compact? More compact than, say, Drosophila, which doesn’t have operons?) May be present in genomes of other nematode species, which is interesting. Must come hand-in-hand with trans-splicing machinery in eukaryotes.

Kamath et al., 2003: Construction of RNAi library for C. elegans, covering 86% of predicted genes in genome. Authors kept track of knockdown phenotypes, organized into phenotypic classes, which show enrichment for certain gene functions. How stringent is the knockdown? How consistent is the effect on phenotype? Interesting to see the chromosomal distribution of the phenotypic classes, especially in light of the operons mentioned above.