The rigid hull encasing Tartary buckwheat seeds necessitates a laborious dehulling process before flour milling, resulting in considerable nutrient loss. Investigation of lignin composition is pivotal in understanding the structural properties of tartary buckwheat seeds hulls, as lignin is key determinant of rigidity in plant cell walls, thus directly impacting the dehulling process. Here, the lignin composition of seed hulls from 274 Tartary buckwheat accessions is analyzed, unveiling a unique lignin chemotype primarily consisting of G lignin, a common feature in gymnosperms. Furthermore, the hardness of the seed hull showed a strong negative correlation with the S lignin content. Genome‐wide detection of selective sweeps uncovered that genes governing the biosynthesis of S lignin, specifically two caffeic acid O‐methyltransferases (COMTs) and one ferulate 5‐hydroxylases, are selected during domestication. This likely contributed to the increased S lignin content and decreased hardness of seed hulls from more domesticated varieties. Genome‐wide association studies identified robust associations between FtCOMT1 and the accumulation of S lignin in seed hull. Transgenic Arabidopsis comt1 plants expressing FtCOMT1 successfully reinstated S lignin content, confirming its conserved function across plant species. These findings provide valuable metabolic and genetic insights for the potential redesign of Tartary buckwheat seed hulls.

Summary: The peduncle vascular system of maize is critical for the transport of photosynthetic products, nutrients, and water from the roots and leaves to the ear. Accordingly, it positively affects the grain yield. However, the genetic basis of peduncle vascular bundle (PVB)‐related traits in maize remains unknown. Thus, 15 PVB‐related traits of 386 maize inbred lines were investigated at three locations (Yongcheng, 17YC; Kaifeng, 20KF; and Yuanyang, 20YY). The repeatability for the 15 traits ranged from 35.53% to 92.13%. A genome‐wide association study was performed and 69 non‐redundant quantitative trait loci (QTL) were detected, including 9, 41, and 27 QTL identified at 17YC, 20KF, and 20YY, respectively. These QTL jointly explained 4.72% (SLL) to 37.30% (NSVB) of the phenotypic variation. Eight QTL were associated with the same trait at two locations. Furthermore, four pleiotropic QTL were identified. Moreover, one QTL (qPVB44), associated with NSVB_20KF, was co‐localized with a previously reported locus related to kernel width, implying qPVB44 may affect the kernel width by modulating the number of small vascular bundles. Examinations of the 69 QTL identified 348 candidate genes that were classified in five groups. Additionally, 26 known VB‐related homologous genes (e.g. VLN2, KNOX1, and UGT72B3) were detected in 20 of the 69 QTL. A comparison of the NSVB between a Zmvln2 EMS mutant and its wild type elucidated the function of the candidate gene ZmVLN2. These results are important for clarifying the genetic basis of PVB‐related traits and may be useful for breeding new high‐yielding maize cultivars.

In Arabidopsis (Arabidopsis thaliana), stomatal closure mediated by abscisic acid (ABA) is redundantly controlled by ABA receptor family proteins (PYRABACTIN RESISTANCE 1 (PYR1)/PYR1-LIKE [PYLs]) and subclass III SUCROSE NONFERMENTING 1 (SNF1)-RELATED PROTEIN KINASES 2 (SnRK2s). Among these proteins, the roles of PYR1, PYL2, and SnRK2.6 are more dominant. A recent discovery showed that ABA-induced accumulation of reactive oxygen species (ROS) in mitochondria promotes stomatal closure. By analyzing stomatal movements in an array of single and higher order mutants, we revealed that the mitochondrial protein VOLTAGE-DEPENDENT ANION CHANNEL 3 (VDAC3) jointly regulates ABA-mediated stomatal closure with a specialized set of PYLs and SnRK2s by affecting cellular and mitochondrial ROS accumulation. VDAC3 interacted with nine PYLs and all three subclass III SnRK2s. Single mutation in VDAC3, PYLs (except PYR1 and PYL2), or SnRK2.2/2.3 had little effect on ABA-mediated stomatal closure. However, knocking out PYR1, PYL1/2/4/8, or SnRK2.2/2.3 in vdac3 mutants resulted in significantly delayed or attenuated ABA-mediated stomatal closure, despite the presence of other PYLs or SnRK2s conferring redundant functions. We found that cellular and mitochondrial accumulation of ROS induced by ABA was altered in vdac3pyl1 mutants. Moreover, H₂O₂ treatment restored ABA-induced stomatal closure in mutants with decreased stomatal sensitivity to ABA. Our work reveals that VDAC3 ensures redundant control of ABA-mediated stomatal closure by canonical ABA signaling components.

Maize vivipary, precocious seed germination on the ear, affects yield and seed quality. The application of multi-omics approaches, such as transcriptomics or metabolomics, to classic vivipary mutants can potentially reveal the underlying mechanism. Seven maize vivipary mutants were selected for transcriptomic and metabolomic analyses. A suite of transporters and transcription factors were found to be upregulated in all mutants, indicating that their functions are required during seed germination. Moreover, vivipary mutants exhibited a uniform expression pattern of genes related to abscisic acid (ABA) biosynthesis, gibberellin (GA) biosynthesis, and ABA core signaling. NCED4 (Zm00001d007876), which is involved in ABA biosynthesis, was markedly downregulated and GA3ox (Zm00001d039634) was upregulated in all vivipary mutants, indicating antagonism between these two phytohormones. The ABA core signaling components (PYL-ABI1-SnRK2-ABI3) were affected in most of the mutants, but the expression of these genes was not significantly different between the vp8 mutant and wild-type seeds. Metabolomics analysis integrated with co-expression network analysis identified unique metabolites, their corresponding pathways, and the gene networks affected by each individual mutation. Collectively, our multi-omics analyses characterized the transcriptional and metabolic landscape during vivipary, providing a valuable resource for improving seed quality.