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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. Thesilkless1mutant 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 androeciousdwarf1;silkless1double 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. Thesilkless1mutant can suppress both silks in the ear and the silks in the tassel of JA‐deficient and AP2 transcription factortasselseedmutants. 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 thesilkless1mutant and JA pathway. Thesilkless1mutant did not prevent the formation of pistils in the tassel bynana plant2in double mutants. In addition, we demonstrate that there is more to thesilkless1mutant than just a suppression of pistil growth. We document novel phenotypes ofsilkless1mutants 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. 

SUMMARY Zea mays(maize) makes phytoalexins such as sesquiterpenoid zealexins, to combat invading pathogens. Zealexins are produced from farnesyl diphosphate in microgram per gram fresh weight quantities. As farnesyl diphosphate is also a precursor for many compounds essential for plant growth, the question arises as to howZ. maysproduces high levels of zealexins without negatively affecting vital plant systems. To examine if specific pools of farnesyl diphosphate are made for zealexin synthesis we made CRISPR/Cas9 knockouts of each of the three farnesyl diphosphate synthases (FPS) inZ. maysand examined the resultant impacts on different farnesyl diphosphate‐derived metabolites. We found that FPS3 (GRMZM2G098569) produced most of the farnesyl diphosphate for zealexins, while FPS1 (GRMZM2G168681) made most of the farnesyl diphosphate for the vital respiratory co‐factor ubiquinone. Indeed,fps1mutants had strong developmental phenotypes such as reduced stature and development of chlorosis. The replication and evolution of thefpsgene family inZ. maysenabled it to produce dedicated FPSs for developmentally related ubiquinone production (FPS1) or defense‐related zealexin production (FPS3). This partitioning of farnesyl diphosphate production between growth and defense could contribute to the ability ofZ. maysto produce high levels of phytoalexins without negatively impacting its growth.