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. 2017 Oct 11;8:869. doi: 10.1038/s41467-017-00945-2

Fig. 3.

Fig. 3

Identity of male sterility inducing lesions within TaMs1 and in vivo complementation of ms1d/ms1d by TaMs1. a Schematic representation of the TaMs1 (the three exons are shown as black boxes) gene depicting the relative positions (indicated by solid lines with arrowheads) of EMS-derived lesions (chromatogram insets) for ms1d, ms1e, ms1f and ms1h. Polymorphisms cause either a frame shift (ms1d, ms1e) or an amino acid transition in a conserved residue of TaMs1 (ms1f, ms1h). b Sequence chromatogram comparison between both mutant (ms1d) and wild-type genomic cDNAs. Polymorphism G329A of ms1d induces the use of a cryptic splice site (highlighted by a 7 bp insertion) within TaMs1. c Stable complementation of the ms1d mutant by TaMs1. Mature inflorescences of male-sterile ms1d/ms1d, and three independent transformants (Events 1–3), each homozygous for ms1d, and showing a self-seed set (arrow). Scale bars: 1 cm