Redox and hormonal imbalances underpin apical spikelet degeneration in wheat mutant asd1

The number of spikelets is a key factor affecting wheat grain yield. We obtained a winter wheat mutant apical spikelet degeneration 1 (asd1). The apical spikelets of asd1 exhibited delayed development starting from the anther septum formation stage, showing a distinct degenerative phenotype during the tetrad stage. Reactive oxygen species (ROS) detection revealed that superoxide dismutase (SOD) enzyme activity was significantly elevated in the degenerated apical spikelets of asd1, accompanied by hydrogen peroxide (H2O2) accumulation and membrane lipid peroxidation, which resulted in redox imbalance within the cells. The catalase isozyme gene CAT2 and peroxidase genes POD1, POD5, POD8, POD12, and POD21 showed significant expression differences in the degenerated spikelets, leading to a burst of ROS that disrupted the redox homeostasis in the asd1 apical spikelets. At the tetrad stage, the asd1 apical spikelets exhibit PCD-like characteristics, accompanied by disruption of hormonal pathways. The expression patterns of key factors in the biosynthesis and signaling pathways of jasmonic acid (JA), abscisic acid (ABA), and auxin (IAA) were significantly altered, thereby perturbing the hormonal network within the apical spikelet. The expression patterns of known genes on spike development did not align with the apical spikelet degeneration in asd1, indicating that the degeneration was controlled by a novel gene. Our findings not only enhance the understanding of bidirectional interaction between ROS and hormones, but also provide valuable data for subsequent research on the genetic basis and regulatory mechanisms of apical spikelet development in wheat.