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Figure Caption
Fig. S2 Loss of msgn1 does not enhance the tail deficiency of ntl–/– mutants. The progeny of a double heterozygous msgn1+/– ;ntl+/– cross were sorted into three distinguishable phenotypic classes and subsequent genotyping showed that embryos with a normal tail phenotype were wt (A), embryos with an enlarged tailbud were msgn1–/– (B) and embryos with similar severe tail truncations were either ntl–/– or msgn1–/–;ntl–/– double mutants (C). Genotypes were present at the expected ratios.
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