Copper deficiency alters shoot architecture and reduces fertility of both gynoecium and androecium in .

Copper deficiency reduces plant growth, male fertility, and seed set. The contribution of copper to female fertility and the underlying molecular aspects of copper deficiency-caused phenotypes are not well known. We show that among copper deficiency-caused defects in were also the increased shoot branching, delayed flowering and senescence, and entirely abolished gynoecium fertility. The increased shoot branching of copper-deficient plants was rescued by the exogenous application of auxin or copper. The delayed flowering was associated with the decreased expression of the floral activator, . Copper deficiency also decreased the expression of senescence-associated genes, and , but increased the expression of . The reduced fertility of copper-deficient plants stemmed from multiple factors including the abnormal stigma papillae development, the abolished gynoecium fertility, and the failure of anthers to dehisce. The latter defect was associated with reduced lignification, the upregulation of copper microRNAs and the downregulation of their targets, laccases, implicated in lignin synthesis. Copper-deficient plants accumulated ROS in pollen and had reduced cytochrome oxidase activity in both leaves and floral buds. This study opens new avenues for the investigation into the relationship between copper homeostasis, hormone-mediated shoot architecture, gynoecium fertility, and copper deficiency-derived nutritional signals leading to the delay in flowering and senescence.