Laterality of the ASE neurons. (A) Model of gene regulatory network responsible for the generation of ASE asymmetry (Hobert 2006). (B) mir-273 locus and deletion allele tested in this analysis. The deletion allele is from Miska et al. (2007). (C) mir-273 null mutant animals do not have an ASE asymmetry phenotype. lsy-6 loss-of-function and control data taken from Johnston and Hobert (2003). (D) Alignment of the C. elegans die-1 3′UTR with three other related nematode species. Multiple sequence alignments were generated with T-coffee (Notredame et al. 2000). Only the first 400 bp of the die-1 3′UTR is shown because it contains all regulatory information (see Fig. 3). Gray boxes indicate the most conserved, extended sequenced patches, both of which show matches to the mir-273 family of miRNAs (for miRNA/target pairing, see Supplemental Fig. 1). Sequence elements identified by mutational analysis motifs to be involved in 3′UTR regulation are colored. Red lines indicate the extent of the 25-bp scanning mutagenesis windows (Supplemental Figs. 2, 3).
