Search

Extensive lead (Pb) accumulation in plants exerts toxic effects on plant growth and development and enters the human food chain. Combining linkage mapping, transcriptome analysis, and association studies, we cloned the ZmbZIP54 transcription factor, which confers maize tolerance to Pb. Combined overexpression and knockdown confirmed that ZmbZIP54 mitigates Pb toxicity in maize by alleviating Pb absorption into the roots. Yeast one-hybrid and dual-luciferase assays revealed that ZmbZIP54 binds to the ZmPRP1 promoter and promotes its transcription. Yeast two-hybrid and bimolecular fluorescence complementation assays indicated that ZmFdx5 interacts with ZmbZIP54 in the nucleus. ZmFdx5 acts as a switch that controls the regulation of ZmPRP1 expression by ZmbZIP54 when maize encounters Pb stress. Furthermore, we revealed that variation in the 5'-UTR of ZmbZIP54 affects its expression level under Pb stress and contributes to the difference in Pb tolerance among maize lines. Finally, we proposed a model to summarize the role of ZmbZIP54 in Pb tolerance, which involves the cooperative effect of ZmbZIP54 and ZmFdx5 on the ZmPRP1 transcription in maize response to Pb. This study provides novel insights into the development of Pb-tolerant maize varieties and bioremediation of Pb-contaminated soils.

The ability of immature maize (Zea mays) embryos to form embryonic calluses (ECs) is highly genotype dependent, which limits transgenic breeding development in maize. Here, we report the association map-based cloning of ZmSAUR15 using an association panel (AP) consisting of 309 inbred lines with diverse formation abilities for ECs. We demonstrated that ZmSAUR15, which encodes a small auxin-upregulated RNA, acts as a negative effector in maize EC induction. Polymorphisms in the ZmSAUR15 promoter that influence the expression of ZmSAUR15 transcripts modulate the EC induction capacity in maize. ZmSAUR15 is involved in indole-3-acetic acid biosynthesis and cell division in immature embryo-derived callus. The ability of immature embryos to induce EC formation can be improved by the knockout of ZmSAUR15, which consequently increases the callus regeneration efficiency. Our study provides new insights into overcoming the genotypic limitations associated with EC formation and improving genetic transformation in maize.

The heavy metals lead and cadmium have become important pollutants in the environment, which exert negative effects on plant morphology, growth and photosynthesis. It is particularly significant to uncover the genetic loci and the causal genes for lead and cadmium tolerance in plants. This study used an IBM Syn10 DH population to identify the quantitative trait loci (QTL) controlling maize seedling tolerance to lead and cadmium by linkage mapping. The broad-sense heritability of these seedling traits ranged from 65.8–97.3% and 32.0–98.8% under control (CK) and treatment (T) conditions, respectively. A total of 53 and 64 QTL were detected under CK and T conditions, respectively. Moreover, 42 QTL were identified using lead and cadmium tolerance coefficient (LCTC). Among these QTL, five and two major QTL that explained > 10% of phenotypic variation were identified under T condition and using LCTC, respectively. Furthermore, eight QTL were simultaneously identified by T and LCTC, explaining 5.23% to 9.21% of the phenotypic variations. Within these major and common QTL responsible for the combined heavy metal tolerance, four candidate genes (Zm00001d048759, Zm00001d004689, Zm00001d004843, Zm00001d033527) were previously reported to correlate with heavy metal transport and tolerance. These findings will contribute to functional gene identification and molecular marker-assisted breeding for improving heavy metal tolerance in maize.