Supplementary Fig. 5: Redundant functions of Urp1 and Urp2 during body-axis straightening.

a, Quantification of the number of beating motile cilia per a.u. in the spinal canal of control embryos and urp1 and uts2ra morphants. NS, not significant; P = 0.42 for urp1 and P = 0.84 for uts2ra. b, Diagram showing the structure of the urp1 gene and sequences of urp1 alleles in wild-type and mutant embryos. The underlining shows the conserved amino acids of the cyclic region of wild-type Urp1; one of the cysteines is mutated in the mutants. c, Percentage of embryos with body curvature defects in wild-type or mutant urp1 mRNA overexpressing embryos, which were collected from cross between two zmynd10 heterozygotes d, Top, reverse transcription (RT)–PCR amplification of the urp2 transcript in wild-type and urp2 SP (Splicing-blocking Morpholino) morphants at 24 h.p.f. Note the decreased level of mature urp2 transcript in the morphants. Bottom, genomic structure of the urp2 gene. The position of the SP morpholino oligonucleotide and primers used for RT–PCR are shown. e, Percentage of embryos with a curly body axis in control, urp1 and urp2 morphants at different combinations as indicated. f, Percentage of embryos with body-curvature defects in wild-type or urp1 mutants injected with urp2 SP morpholino oligonucleotide. In panels c, e and f, the numbers of embryos analyzed are shown on top of each bar.