Genetic evidence that brassinosteroids suppress pistils in the maize tassel independent of the jasmonic acid pathway.

Abstract

The developmental genetics of reproductive structure control in maize must consider both the staminate florets of the tassel and the pistillate florets of the ear synflorescences. Pistil abortion takes place in the tassel florets, and stamen arrest is affected in ear florets to give rise to the monoecious nature of maize. Gibberellin (GA) deficiency results in increased tillering, a dwarfed plant syndrome, and the retention of anthers in the ear florets of maize. The silkless1 mutant results in suppression of silks in the ear. We demonstrate in this study that jasmonic acid (JA) and GA act independently and show additive phenotypes resulting in androecious dwarf1;silkless1 double mutant plants. The persistence of pistils in the tassel can be induced by multiple mechanisms, including JA deficiency, GA excess, genetic control of floral determinacy, and organ identity. The silkless1 mutant can suppress both silks in the ear and the silks in the tassel of JA-deficient and AP2 transcription factor tasselseed mutants. We previously demonstrated that GA production was required for brassinosteroid (BR) deficiency to affect persistence of pistils in the tassel. We find that BR deficiency affects pistil persistence by an independent mechanism from the silkless1 mutant and JA pathway. The silkless1 mutant did not prevent the formation of pistils in the tassel by nana plant2 in double mutants. In addition, we demonstrate that there is more to the silkless1 mutant than just a suppression of pistil growth. We document novel phenotypes of silkless1 mutants including weakly penetrant ear fasciation and anther persistence in the ear florets. Thus, the JA/AP2 mechanism of pistil retention in the tassel and silk growth in the ear are similarly sensitive to loss of the SILKLESS1 protein, while the BR/GA mechanism is not.