Genetic variations in ZmSAUR15 contribute to the formation of immature embryo-derived embryonic calluses in maize

The ability of immature maize (Zea mays) embryos to form embryonic calluses (ECs) is highly genotype dependent, which limits transgenic breeding development in maize. Here, we report the association map-based cloning of ZmSAUR15 using an association panel (AP) consisting of 309 inbred lines with diverse formation abilities for ECs. We demonstrated that ZmSAUR15, which encodes a small auxin-upregulated RNA, acts as a negative effector in maize EC induction. Polymorphisms in the ZmSAUR15 promoter that influence the expression of ZmSAUR15 transcripts modulate the EC induction capacity in maize. ZmSAUR15 is involved in indole-3-acetic acid biosynthesis and cell division in immature embryo-derived callus. The ability of immature embryos to induce EC formation can be improved by the knockout of ZmSAUR15, which consequently increases the callus regeneration efficiency. Our study provides new insights into overcoming the genotypic limitations associated with EC formation and improving genetic transformation in maize.

Automated summary

The ability of immature maize embryos to form embryonic calluses is genotype dependent, with ZmSAUR15 playing a negative role in EC induction. Modulating the expression of ZmSAUR15 transcripts through polymorphisms in its promoter can influence EC induction capacity in maize. Knocking out ZmSAUR15 improves EC formation and callus regeneration efficiency, providing insights into overcoming genotypic limitations for genetic transformation in maize.