GT1 and ZmHB13/VRL1 regulate flower sexual differentiation by modulating jasmonate biosynthesis and signaling in maize.

Abstract

As a typical monoecious plant, maize (Zea mays L.) produces unisexual male and female flowers comprising tassels and ears, respectively. However, the molecular mechanisms underlying unisexual flower development remain largely unclear. Here, we identify a pair of homeodomain-leucine zipper (HD-ZIP) transcription factors, Grassy tiller1 (GT1) and ZmHB13 (also termed VRS1-like1, VRL1), which act synergistically to control carpel development in maize. Mutations in GT1, but not ZmHB13/VRL1, cause defects in carpel abortion in the tassels, resulting in feminized tassels. The gt1 Zmhb13 double mutants show a notably more severe phenotype and a defect in the abortion of the lower floret in the ear spikelet, resulting in extra fertile flowers and seed setting. We demonstrate that GT1 and ZmHB13/VRL1 bind directly to the promoters of 2 jasmonate (JA) biosynthesis genes, ZmLOX3 and ZmOPR7, and upregulate their expression in the developing flowers. The application of methyl jasmonate (MeJA) rescues the feminized tassel phenotype of the gt1 Zmhb13 double mutants. Additionally, GT1 and ZmHB13/VRL1 interact with the key JA-pathway repressors ZmJAZ4 and ZmJAZ26, thus releasing the key JA-pathway activators ZmMYC2a and ZmMYC2b to activate the downstream JA signaling processes. Our findings indicate that GT1 and ZmHB13/VRL1 function synergistically to regulate maize carpel development through modulating JA biosynthesis and signaling.