Assembly of the functional complexes of the mitochondrial respiratory chain requires sophisticated and efficient regulatory mechanisms. In plants, the subunit composition and assembly factors involved in the biogenesis of cytochrome c oxidase (complex IV) are substantially less defined than in mammals and yeast. In this study, we cloned maize (Zea mays) Small kernel 11 (Smk11) via map-based cloning. Smk11 encodes a mitochondria-localized tetratricopeptide repeat (TPR) protein. Disruption of Smk11 severely affected the assembly and activity of mitochondrial complex IV, leading to delayed plant growth and seed development. Protein interactions studies revealed that SMK11 might interact with four putative complex IV assembly factors, Inner membrane peptidase 1A (ZmIMP1A), MYB domain protein 3R3 (ZmMYB3R-3), Cytochrome c oxidase 23 (ZmCOX23), and Mitochondrial ferredoxin 1 (ZmMFDX1), among which ZmMFDX1 might interact with subunits ZmCOX6a and ZmCOX-X1; ZmMYB3R-3 might also interact with ZmCOX6a. The mutation of SMK11 perturbed the normal assembly of these subunits, leading to the inactivation of complex IV. The results of this study revealed that SMK11 serves as an accessory assembly factor required for the normal assembly of subunits into complex IV, which will accelerate the elucidation of the assembly of complex IV in plant mitochondria.

Leaf senescence is a key developmental process influencing photosynthesis, carbon allocation, and crop productivity, all tightly regulated by source–sink balance. In maize (Zea mays), abscisic acid signaling and nonstructural carbohydrate partitioning have been proposed as major determinants of senescence timing under sink limitation. Through multiyear, multigenotype analyses, we refine the current understanding by identifying starch-induced chloroplast disruption as the primary trigger of sink-removal-induced senescence, whereas abscisic acid acts mainly as a secondary, modulatory signal. We also reveal a respiration-linked metabolic compensation mechanism that stabilizes leaf function in genotypes with delayed senescence. In early-senescing genotypes, ear removal induced significant chlorophyll loss, anthocyanin accumulation, and severe sugar/starch overaccumulation that disrupted chloroplast ultrastructure, coinciding with reduced leaf protein contents and impaired photosynthesis. By contrast, genotypes with delayed senescence maintained pigment stability, displaying enhanced dark respiration, balanced carbohydrate metabolism, and chloroplast integrity. Shading experiments further confirmed that starch overaccumulation, rather than abscisic acid elevation, is the dominant driver of sink-removal-induced senescence. Metabolomic analyses showed that early-senescing genotypes accumulate soluble sugars and phosphoenolpyruvate-pathway intermediates, whereas genotypes with delayed senescence exhibited reduced tricarboxylic acid cycle activity and elevated aspartate-family amino acids. Transcriptomics revealed downregulation of sucrose transporters (eg ZmSUT7) and starch degradation genes (eg ZmBmy3) alongside upregulation of anthocyanin and carbohydrate metabolism genes in early-senescing genotypes. Coexpression network analysis further identified hub genes associated with carbohydrate and amino acid metabolism, linking transcriptional regulation to genotype-specific metabolic adjustments. Together, these findings refine current source–sink regulatory models and offer potential physiological and metabolic targets for improving source–sink coordination and enhancing yield resilience in maize.

BAHD acyltransferases are a specialized class of plant enzymes involved in the acylation of secondary metabolites, yet their roles in seed development remain poorly understood. In this study, we identified the defective kernel 601 (dek601) mutant in the maize (Zea mays) W22 genetic background, which exhibits defective embryo and endosperm development, leading to smaller and shrunken kernels compared to the wild type. Using positional cloning, we localized the causal gene, Zm00001d039535 (also known as Disorganized wall 1, Dow1), to chromosome 3. A mutation in this gene causes a frameshift and disrupts protein function, which was confirmed through complementation tests. Dek601 encodes a BAHD family acyltransferase, and its expression is regulated by the transcription factors Opaque2 (O2), Ethylene-Responsive Element Binding Protein 58 (EREB58), and Ethylene-Responsive Element Binding Protein 177 (EREB177). These factors bind to the Dek601 promoter and modulate its expression. Furthermore, DEK601 interacts with the acyl-activating enzyme 19 (ZmAAE19), suggesting their potential functional synergy in downstream enzymatic processes. Metabolomic analysis of dek601 kernels revealed significant shifts in metabolic profiles, including a downregulation of carbohydrate compounds and an upregulation of amino acids and metabolites from the phenylpropanoid and flavonoid pathways. This study demonstrates that the Opaque2–OHP2–EREB58–EREB177 regulatory module controls Dek601 expression, and DEK601 and ZmAAE19 likely collaborate to influence metabolite biosynthesis, thereby regulating kernel development in maize.

Agronomic advancements have led to significant increases in maize yield per hectare in Northeast China, primarily through improved density tolerance. However, the genetic mechanism underlying grain yield responses to density stress remains poorly understood. Here, a population of 193 recombinant inbred lines (RILs) derived from the cross between ZM058 and PH1219 was employed to identify quantitative trait loci (QTLs) under two planting densities across three locations over two years. Six yield-related traits were investigated: ear tip-barrenness length (BEL), cob diameter (CD), ear diameter (ED), ear length (EL), kernel number per row (KNR), and kernel row number (KRN). These traits exhibited distinct and divergent responses to density stress, with the values of CD, ED, EL, KNR and KRN decreasing as planting density increased, except for BEL. A total of 81 QTLs were identified for these traits: 39 were unique to low planting density, 22 to high planting density, and 20 were shared across both conditions. Additionally, nine QTL clusters implicated in the development of multiple traits were detected. The results indicate that planting density significantly affects yield traits, primarily through the interaction of numerous minor QTLs with multiple effects. This insight enhances our understanding of the genetic basis of yield-related traits and provides valuable guidance for breeding high-density-tolerant varieties.