(1) Background: As a high-biomass cereal crop, maize provides substantial raw materials for food, animal feed, and processing industries. Plant root systems, vital for nutritional support, are directly vulnerable to diverse stressors that result in developmental abnormalities. Anthocyanins function as essential antioxidants, serving not only as natural pigments, but also playing crucial roles in plant stress resistance. As an essential plant hormone, jasmonic acid (JA) mediates plant stress adaptation and developmental processes, and is frequently employed to stimulate anthocyanin production. (2) Methods: Due to scarce reports on JA functions in maize, we specifically examined JA-triggered developmental regulation and anthocyanin biosynthesis using transcriptomic and metabolomic analysis. (3) Results: Phenotypic analyses revealed that exogenous JA application promoted culm development and intensified pigmentation, while enlarging the areas of stems and primary roots. Combined with phenotypic variations, our integrated transcriptomic and metabolomic analyses of root tissues also indicated that significantly altered metabolites specifically clustered within the flavonoid biosynthesis pathway. Moreover, GO and KEGG enrichment analyses of the associated differentially expressed genes confirmed their participation in this synthetic pathway with high confidence. These findings strongly suggest that methyl jasmonate (MeJA) exposure primarily modulates flavonoid biosynthesis, particularly through regulation of F3H and DFR gene expression, thereby enhancing flavonoid/anthocyanin accumulation in roots. Additionally, our correlation analysis of transcription factors revealed that Zm00001d018097 (MYB), Zm00001d029963 (MYB), and Zm00001d000236 (bHLH) likely participate in regulating the expression of structural genes, thereby promoting the upregulation of functional gene expression. (4) Conclusions: These results provide a robust framework for deciphering the MeJA-mediated regulation of anthocyanin biosynthesis in maize radicles, specifically demonstrating that Zm00001d018097 (MYB), Zm00001d029963 (MYB), and Zm00001d000236 (bHLH) coordinately enhance the expression of F3H and DFR.

Cytoplasmic male sterility (CMS) plays an important role in the application of heterosis in wheat (Triticum aestivum L.). However, the molecular mechanism underlying CMS remains unknown. This study provides a comprehensive morphological and proteomic analysis of the anthers of a P-type CMS wheat line (P) and its maintainer line, Yanshi 9 hao (Y). Cytological observations indicated that the P-type CMS line shows binucleate microspore abortion. In this line, the tapetum degraded early, leading to anther cuticle defects, which could not provide the nutrition needed for microspore development in a timely manner, thus preventing the development of the microspore to the normal binucleate stage. Proteomic analysis revealed novel proteins involved in P-type CMS. Up to 2576 differentially expressed proteins (DEPs) were quantified in all anthers, and these proteins were significantly enriched in oxidative phosphorylation, glycolysis/gluconeogenesis, citrate cycle (TCA cycle), starch and sucrose metabolism, phenylpropanoid biosynthesis, and pyruvate metabolism pathways. These proteins may comprise a network that regulates male sterility in wheat. Based on the function analysis of DEPs involved in the complex network, we concluded that the P-type CMS line may be due to cellular dysfunction caused by disturbed carbohydrate metabolism, inadequate energy supply, and disturbed protein synthesis. These results provide insights into the molecular mechanism underlying male sterility and serve as a valuable resource for researchers in plant biology, in general, and plant sexual reproduction, in particular.

Heterosis has been widely accepted as an effective strategy to increase yields in plant breeding. Notably, the chemical hybridization agent SQ-1 induces male sterility in wheat, representing a critical potential tool in hybrid seed production. However, the mechanisms underlying the male sterility induced by SQ-1 still remain poorly understood. In this study, a cyclin-dependent kinase inhibitor gene, TaICK1, which encodes a 229 amino acid protein, was identified as a potential contributor to male sterility in common wheat. The expression of TaICK1 was upregulated during the development of anthers in Xinong1376 wheat treated with SQ-1. Meanwhile, the seed setting rate was found to be significantly decreased in TaICK1 transgenic rice. Furthermore, we identified two cyclin proteins, TaCYCD2;1 and TaCYCD6;1, as interactors through yeast two-hybrid screening using TaICK1 as the bait, which were validated using bimolecular fluorescence complementation. Subcellular localization revealed that the proteins encoded by TaICK1, TaCYCD2;1, and TaCYCD6;1 were localized in the cell nucleus. The expression levels of TaCYCD2;1 and TaCYCD6;1 were lower in Xinong1376 treated with SQ-1. A further analysis demonstrated that the expression levels of OsCYCD2;1 and OsCYCD6;1 were lower in transgenic TaICK1 rice lines as well. Taken together, these results suggest that the upregulation of TaICK1, induced by SQ-1, may subsequently suppress the expression of TaCYCD2;1 and TaCYCD6;1 in anthers, resulting in male sterility. This study provides new insights into the understanding of SQ-1-induced wheat male sterility, as well as the developmental mechanisms of anthers.

Plant height is a key agronomic trait that is closely to the plant morphology and lodging resistance in wheat. However, at present, the few dwarf genes widely used in wheat breeding have narrowed wheat genetic diversity. In this study, we selected a semi-dwarf wheat mutant dwarf33 that exhibits decreased plant height with little serious negative impact on other agronomic traits. Genetic analysis and mutant gene mapping indicated that dwarf33 contains a new recessive semi-dwarf gene Rht-SN33d, which was mapped into ~1.3 Mb interval on the 3DL chromosome. The gibberellin metabolism-related gene TraesCS3D02G542800, which encodes gibberellin 2-beta-dioxygenase, is considered a potential candidate gene of Rht-SN33d. Rht-SN33d reduced plant height by approximately 22.4% in mutant dwarf33. Further study revealed that shorter stem cell length may be the main factor causing plant height decrease. In addition, the coleoptile length of dwarf33 was just 9.3% shorter than that of wild-type Shaannong33. These results will help to expand our understanding of new mechanisms of wheat height regulation, and obtain new germplasm for wheat improvement.