Functional Analysis of ZmABA8ox1b in Regulating Maize Seed Germination via ABA Catabolism and Multi-Hormone Signaling Crosstalk

Seed germination is a critical determinant of seedling establishment, stress resistance, and final yield. ABA catabolism plays a central role in releasing seed dormancy and promoting germination, and ABA8ox is the key rate-limiting enzyme in this process. In this study, we used wild-type maize B73, and ZmABA8ox1b CRISPR-Cas9 knockout mutant as materials to investigate the biological function of ZmABA8ox1b. Compared with the wild type, the zmaba8ox1b mutant significantly delayed seed germination and enhanced the sensitivity to exogenous ABA. Endogenous ABA content in mutant embryos was drastically increased, indicating that ZmABA8ox1b is essential for ABA degradation during germination. The loss of ZmABA8ox1b function led to the activation of the ABA signaling pathway and severely impaired the responsiveness to exogenous ABA. Moreover, the mutation disturbed the expression and ABA responsiveness of auxin, gibberellin, ethylene, jasmonic acid, and brassinosteroid pathways, leading to a hormonal network imbalance. In conclusion, ZmABA8ox1b positively regulates maize seed germination by coordinating ABA catabolism and multi-hormone signal crosstalk. This study preliminarily clarifies the molecular mechanism of ZmABA8ox1b in germination control and provides important gene resources and theoretical support for breeding maize varieties.