Maize (Zea mays L.) is an important food and energy crop, and low phosphate (Pi) availability is one of the major constraints in maize production worldwide. Plants adapt suitably to acclimate to low Pi stress. However, the underlying molecular mechanism of Pi deficiency response is still unclear. In this study, comparative transcriptomic analyses were conducted to investigate the differences of transcriptional responses in two maize genotypes with different tolerances to low phosphorus (LP) stress. LP-tolerant genotype QXN233 maintained higher P and Pi levels in shoots than LP-sensitive genotype QXH0121 suffering from Pi deficiency at seedling stage. Moreover, the transcriptomic analysis identified a total of 1391 Pi-responsive genes differentially expressed between QXN233 and QXH0121 under LP stress. Among these genes, 468 (321 up- and 147 down-regulated) were identified in leaves, and 923 (626 up- and 297 down-regulated) were identified in roots. These Pi-responsive genes were involved in various metabolic pathways, the biosynthesis of secondary metabolites, ion transport, phytohormone regulation, and other adverse stress responses. Consistent with the differential tolerance to LP stress, five maize inorganic Pi transporter genes were more highly up-regulated in QXN233 than in QXH0121. Results provide important information to further study the changes in global gene expression between LP-tolerant and LP-sensitive maize genotypes and to understand the molecular mechanisms underlying maize's long-term response to Pi deficiency.

The mechanism of phosphate (Pi)-mediated salt tolerance in maize is poorly understood. In this study, the effects of Pi (H₂PO₄⁻) on the salt tolerance of two contrasting genotypes was investigated in a pot experiment. We discovered that the application of 3 mM Pi could alleviate salt injury caused by 200 mM NaCl. High amounts of compatible solutes and low amounts of reactive oxygen species (ROS) were also observed under Pi application. Consistent with the increased tolerance, the total number of roots and the growth of shoots increased to relieve salt stress. This phenomenon could be associated with the observed increased expression of nitrate transporters. Furthermore, the seedlings presented a negative relationship between sodium (Na⁺) and Pi (low Na⁺ content and high Pi content), which is related to the genes ZmNHX1, ZmPHT1;8, and ZmPHT1;9, indicating that the exclusion of Na⁺ was promoted by high Pi uptake. However, high Na⁺ and low potassium (K⁺) efflux were detected in the roots, and these were positively correlated with two K⁺ transporters. These observations indicate that Na⁺ exclusion was directly induced by high K⁺ retention rather than Pi absorption. We conclude that maize salt tolerance increased in response to Pi application by promoting Na⁺ exclusion.

Maize is the most important cereal crop globally. However, in recent years, maize production faced numerous challenges from environmental factors due to the changing climate. Salt stress is among the major environmental factors that negatively impact crop productivity worldwide. To cope with salt stress, plants developed various strategies, such as producing osmolytes, increasing antioxidant enzyme activity, maintaining reactive oxygen species homeostasis, and regulating ion transport. This review provides an overview of the intricate relationships between salt stress and several plant defense mechanisms, including osmolytes, antioxidant enzymes, reactive oxygen species, plant hormones, and ions (Na⁺, K⁺, Cl⁻), which are critical for salt tolerance in maize. It addresses the regulatory strategies and key factors involved in salt tolerance, aiming to foster a comprehensive understanding of the salt tolerance regulatory networks in maize. These new insights will also pave the way for further investigations into the significance of these regulations in elucidating how maize coordinates its defense system to resist salt stress.

Maize seedlings are constantly exposed to inorganic phosphate (Pi)-limited environments. To understand how maize cope with low Pi (LP) and high Pi (HP) conditions, physiological and global proteomic analysis of QXN233 genotype were performed under the long-term Pi starvation and supplementation. We investigated the physiological response of QXN233 genotype to LP and HP conditions and detected the changes in ion fluxes by non-invasive micro-test technology and gene expression by quantitative real-time polymerase chain reaction. QXN233 was further assessed using vermiculite assay, and then proteins were isolated and identified by nano-liquid chromatography-mass spectrometry. A negative relationship was observed between Na+ and Pi, and Na+ efflux was enhanced under HP condition. Furthermore, a total of 681 and 1374 were identified in the leaves and roots, respectively, which were mostly involved in metabolism, ion transport, and stress response. Importantly, several key Pi transporters were identified for breeding potential. Several ion transporters demonstrated an elaborate interplay between Pi and other ions, together contributing to the growth of QXN233 seedlings. The results from this study provide insights into the response of maize seedlings to long-term Pi exposure.

Uneven germination is still a common problem in sweet maize planting. The mesocotyl is a key driver for ground-breaking sweet maize, and deep-sowing has a longer mesocotyl. However, the physiological and molecular mechanisms of sweet maize mesocotyl elongation in response to deep-sowing remain unknown. Here we found that sweet maize inbred line Ltx05 could obtain longer mesocotyls in deep soil of 10 cm depth, and that 20 mg/L GA₃ was the optimal concentration to promote mesocotyl elongation and seedling emergence. Microstructure observation showed that the longitudinal cell length of mesocotyl at 10 cm sowing depth was significantly longer than that of 1 cm. Transcriptome analysis showed that microtubule process related differentially expressed genes may contribute to the longitudinal cell elongation. The content of GAs in the mesocotyl at 10 cm sowing depth was markedly higher than that of 1 cm. Combining transcriptome data and qRT-PCR at different developmental stages, ZmGA20ox1, ZmGA20ox4 and ZmGA20ox5 were identified as three positive regulation candidate genes during mesocotyl elongation under deep-sowing conditions, and this was further confirmed by the significant elongation of the hypocotyl in heterologous transformation of Arabidopsis thaliana. These results lay a foundation for improving the ability of sweet maize to tolerate deep-sowing stress and improving the breeding of excellent deep-sowing-tolerant germplasms.

Background: The structural basis of chloroplast and the regulation of chloroplast biogenesis remain largely unknown in maize. Gene mutations in these pathways have been linked to the abnormal leaf color phenotype observed in some mutants. Large scale structure variants (SVs) are crucial for genome evolution, but few validated SVs have been reported in maize and little is known about their functions though they are abundant in maize genomes. Results: In this research, a spontaneous maize mutant, pale green leaf-shandong (pgl-sd), was studied. Genetic analysis showed that the phenotype of pale green leaf was controlled by a recessive Mendel factor mapped to a 156.8-kb interval on the chromosome 1 delineated by molecular markers gy546 and gy548. There were 7 annotated genes in this interval. Reverse transcription quantitative PCR analysis, SV prediction, and de novo assembly of pgl-sd genome revealed that a 137.8-kb deletion, which was verified by Sanger sequencing, might cause the pgl-sd phenotype. This deletion contained 5 annotated genes, three of which, including Zm00001eb031870, Zm00001eb031890 and Zm00001eb031900, were possibly related to the chloroplast development. Zm00001eb031870, encoding a Degradation of Periplasmic Proteins (Deg) homolog, and Zm00001eb031900, putatively encoding a plastid pyruvate dehydrogenase complex E1 component subunit beta (ptPDC-E1-β), might be the major causative genes for the pgl-sd mutant phenotype. Plastid Degs play roles in protecting the vital photosynthetic machinery and ptPDCs provide acetyl-CoA and NADH for fatty acid biosynthesis in plastids, which were different from functions of other isolated maize leaf color associated genes. The other two genes in the deletion were possibly associated with DNA repair and disease resistance, respectively. The pgl-sd mutation decreased contents of chlorophyll a, chlorophyll b, carotenoids by 37.2%, 22.1%, and 59.8%, respectively, and led to abnormal chloroplast. RNA-seq revealed that the transcription of several other genes involved in the structure and function of chloroplast was affected in the mutant. Conclusions: It was identified that a 137.8-kb deletion causes the pgl-sd phenotype. Three genes in this deletion were possibly related to the chloroplast development, which may play roles different from that of other isolated maize leaf color associated genes.