Frame-shift Mutation Causes the Function Loss of TaMYB-A1 Regulating Anthocyanin Biosynthesis in Triticum aestivum

Abstract

Red coleoptile is an easily observed trait in Triticum aestivum and can provide some protection against stress. Here, TaMYB-A1 or TuMYB-A1, homologous to TaMYB-D1, which controls red coleoptile formation in the common wheat cultivar ‘Gy115’, was isolated from eight T. aestivum and 34 T. urartu cultivars. The genome sequence of TaMYB-A1 was 867 bp with an intron of 93 bp, which was similar to the MYBs regulating anthocyanin biosynthesis in T. aestivum but different from other MYB transcription factors regulating anthocyanin biosynthesis. TaMYB-A1 had an integrated DNA-binding domain of 102 amino acids and a transcriptional domain of 42 amino acids, which was responsible for regulating anthocyanin biosynthesis. TaMYB-A1 was assigned to the same branch as the MYBs regulating anthocyanin biosynthesis in a phylogenetic tree. A transient expression analysis showed that TaMYB-A1 induced ‘Opata’ coleoptile cells to synthesize anthocyanin with the help of ZmR. A non-functional allele of TaMYB-a1 existed in common wheat cultivars containing rc-a1. One single nucleotide was deleted 715 bp after the start codon in TaMYB-a1 compared with TaMYB-A1. The deletion caused a frame shift mutation, destroyed the DNA transcription activator domain, and resulted in TaMYB-a1 losing its ability to regulate anthocyanin biosynthesis in ‘Opata’ coleoptile cells. Those cultivars with functional TaMYB-A1 or TuMYB-A1 have red coleoptiles. The isolation of TaMYB-A1 should aid in understanding the molecular mechanisms of coleoptile traits in T. aestivum.