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Background Grain quality in sweet corn ( Zea mays L .) is primarily determined by pericarp thickness and soluble sugar composition, which influence consumer preference and processing suitability. Despite their importance, the genetic basis of these traits remains insufficiently understood. Elucidating the underlying genetic architecture is essential for developing sweet corn varieties with improved kernel texture and sweetness. Results A panel of 240 sweet corn inbred lines was evaluated across two seasons in Guangzhou, China, using an alpha-lattice design with two replications to enhance phenotypic precision. Phenotypic data for pericarp thickness and sugar-related traits were adjusted using best linear unbiased predictions (BLUPs), and genotyping was performed with a 60 K SNP array. Genome-wide association study (GWAS) identified 174 loci significantly associated with the target traits, of which 84 were consistently detected across both seasons. Candidate genes within these loci were enriched in biological pathways related to cell wall biosynthesis and sugar metabolism. Notable gene families included cellulose synthase, pectin methylesterase, peroxidase, sucrose synthase, sucrose phosphate synthase, and SWEET transporters, all of which are known to contribute to pericarp development or sugar accumulation. Expression profiling of 12 representative candidate genes in contrasting inbred lines revealed consistent differential expression patterns aligned with phenotypic variation, further supporting their role in regulating pericarp thickness and sweetness. Conclusions This study provides a comprehensive analysis of the genetic determinants of grain quality traits in sweet corn. The discovery of stable loci and functionally relevant candidate genes offers new insights into the molecular mechanisms governing kernel texture and sugar accumulation. These findings supply valuable markers and genomic resources for marker-assisted selection and genomic prediction, facilitating the development of improved sweet corn varieties with enhanced quality attributes.

The thickness of the pericarp is a complex characteristic that determines sweet corn's palatability. However, the molecular mechanisms in forming pericarp thickness differences have not been clarified. In this study, we conducted transcriptomics, miRNA analysis, and metabolomics to explore the underlying molecular mechanisms. Scanning electron microscopy (SEM) revealed that the disparity in pericarp thickness is primarily due to variations in the number of cell layers. Our combined multi-omics analysis discovered 6,054 differentially expressed genes (DEGs), 73 differentially expressed miRNAs, 113 differentially accumulated metabolites (DAMs), and several key miRNAs, such as , , , and were identified, which modulate the expression of different transcription factors and regulate the signal transduction of various plant hormones, thereby influencing pericarp thickness. Additionally, our integrated transcriptomic and metabolomic analysis revealed that genes and metabolites involved in plant hormone signal transduction and phenylpropanoids biosynthesis pathway play a significant role in regulating pericarp growth and development. Furthermore, we observed that in the thick pericarp line (M08), the content of cytokinins was significantly reduced, while phenylpropanoid compounds such as 5-O-feruloylquinic acid glucoside, berberine, scopoletin, sinapic alcohol, sinapic acid and 3-O-feruloylquinic acid glucoside accumulated considerably. These findings provide valuable theoretical support and genetic resources.

Camellia fruit is a woody edible oil source with a recalcitrant pericarp, which increases processing costs. However, the relevance of pericarp thickness variations in Camellia species remains unclear. Therefore, this study aimed to identify pericarp differences at the metabolic and transcription levels between thick-pericarp Camellia drupifera BG and thin-pericarp Camellia oleifera SG. Forty differentially accumulated metabolites were screened through non-targeted UHPLC-Q-TOF MS-based metabolite profiling. S-lignin was prominently upregulated in BG compared with SG, contributing to the thick pericarp of BG. KEGG enrichment and coexpression network analysis showed 29 differentially expressed genes associated with the lignin biosynthetic pathway, including 21 genes encoding catalysts and 8 encoding transcription factors. Nine upregulated genes encoding catalysts potentially led to S-lignin accumulation in BG pericarp, and transcription factors NAC and MYB were possibly involved in major transcriptional regulatory mechanisms. Conventional growth-related factors WRKYs and AP2/ERFs were positively associated while pathogenesis-related proteins MLP328 and NCS2 were negatively associated with S-lignin content. Thus, Camellia balances growth and defense possibly by altering lignin biosynthesis. The results of this study may guide the genetic modifications of C. drupifera to optimize its growth–defense balance and improve seed accessibility.

Proper pericarp thickness protects the maize kernel against pests and diseases, moreover, thinner pericarp improves the eating quality in fresh corn. In this study, we aimed to investigate the dynamic changes in maize pericarp during kernel development and identified the major quantitative trait loci (QTLs) for maize pericarp thickness. It was observed that maize pericarp thickness first increased and then decreased. During the growth and formation stages, the pericarp thickness gradually increased and reached the maximum, after which it gradually decreased and reached the minimum during maturity. To identify the QTLs for pericarp thickness, a BC 4 F 4 population was constructed using maize inbred lines B73 (recurrent parent with thick pericarp) and Baimaya (donor parent with thin pericarp). In addition, a high-density genetic map was constructed using maize 10 K SNP microarray. A total of 17 QTLs related to pericarp thickness were identified in combination with the phenotypic data. The results revealed that the heritability of the thickness of upper germinal side of pericarp (UG) was 0.63. The major QTL controlling UG was qPT1-1 , which was located on chromosome 1 (212,215,145–212,948,882). The heritability of the thickness of upper abgerminal side of pericarp (UA) was 0.70. The major QTL controlling UA was qPT2-1 , which was located on chromosome 2 (2,550,197–14,732,993). In addition, a combination of functional annotation, DNA sequencing analysis and quantitative real-time PCR (qPCR) screened two candidate genes, Zm00001d001964 and Zm00001d002283 , that could potentially control maize pericarp thickness. This study provides valuable insights into the improvement of maize pericarp thickness during breeding.

Pericarp thickness affects the edible quality of sweet corn ( Zea mays L. saccharata Sturt.). Therefore, breeding varieties with a thin pericarp is important for the quality breeding of sweet corn. However, the molecular mechanisms underlying the pericarp development remain largely unclear. We performed an integrative analysis of mRNA and miRNA sequencing to elucidate the genetic mechanism regulating pericarp thickness during kernel development (at 15 days, 19 days, and 23 days after pollination) of two sweet corn inbred lines with different pericarp thicknesses (M03, with a thinner pericarp and M08, with a thicker pericarp). A total of 2,443 and 1,409 differentially expressed genes (DEGs) were identified in M03 and M08, respectively. Our results indicate that phytohormone-mediated programmed cell death (PCD) may play a critical role in determining pericarp thickness in sweet corn. Auxin (AUX), gibberellin (GA), and brassinosteroid (BR) signal transduction may indirectly mediate PCD to regulate pericarp thickness in M03 (the thin pericarp variety). In contrast, abscisic acid (ABA), cytokinin (CK), and ethylene (ETH) signaling may be the key regulators of pericarp PCD in M08 (the thick pericarp variety). Furthermore, 110 differentially expressed microRNAs (DEMIs) and 478 differentially expressed target genes were identified. miRNA164-, miRNA167-, and miRNA156-mediated miRNA–mRNA pairs may participate in regulating pericarp thickness. The expression results of DEGs were validated by quantitative real-time PCR. These findings provide insights into the molecular mechanisms regulating pericarp thickness and propose the objective of breeding sweet corn varieties with a thin pericarp.

Background In recent years, the planting area of sweet corn in China has expanded rapidly. Some new varieties with high yields and good adaptabilities have emerged. However, the improvement of edible quality traits, especially through the development of varieties with thin pericarp thickness, has not been achieved to date. Pericarp thickness is a complex trait that is the key factor determining the edible quality of sweet corn. Genetic mapping combined with transcriptome analysis was used to identify candidate genes controlling pericarp thickness. Results To identify novel quantitative trait loci (QTLs) for pericarp thickness, a sweet corn BC 4 F 3 population of 148 lines was developed using the two sweet corn lines M03 (recurrent parent) and M08 (donor parent). Additionally, a high-density genetic linkage map containing 3876 specific length amplified fragment (SLAF) tags was constructed and used for mapping QTLs for pericarp thickness. Interestingly, 14 QTLs for pericarp thickness were detected, and one stable QTL ( qPT10–5) was detected across multiple years, which explained 7.78–35.38% of the phenotypic variation located on chromosome 10 (144,631,242-145,532,401). Forty-two candidate genes were found within the target region of qPT10–5 . Moreover, of these 42 genes, five genes ( GRMZM2G143402 , GRMZM2G143389 , GRMZM2G143352 , GRMZM6G287947 , and AC234202.1_FG004 ) were differentially expressed between the two parents, as revealed by transcriptome analysis. According to the gene annotation information, three genes might be considered candidates for pericarp thickness. GRMZM2G143352 and GRMZM2G143402 have been annotated as AUX/IAA transcription factor and ZIM transcription factor, respectively, while GRMZM2G143389 has been annotated as FATTY ACID EXPORT 2, chloroplastic. Conclusions This study identified a major QTL and candidate genes that could accelerate breeding for the thin pericarp thickness variety of sweet corn, and these results established the basis for map-based cloning and further functional research.

Mapping QTL for disease resistance and associated traits is important to develop maize (Zea mays L.) hybrids less susceptible to ear rots. A biparental mapping population of 298 F5 recombinant inbreds (RIs), obtained from the cross between LP4637 (moderately resistant) and L4674 (susceptible), was genotyped with 250 single nucleotide polymorphism (SNP) markers. A set of 120 of those RIs, selected by uniRec procedure, and parental inbreds were phenotyped in two environments for pericarp thickness, pericarp content of trans-ferulic acid (tFA) and resistance to Fusarium ear rot. The set of parental inbreds exhibited an average density of one marker every 5 cM, 6% of a residual heterozygosity, and 5% of lost data. Moderate negative genotypic correlations were observed between disease severity and pericarp thickness (rG = − 0.31) and between disease severity and pericarp content of tFA (rG = − 0.32). Quantitative trait loci were mapped for disease severity in bins 1.06, 2.03, 3.06, 5.04, 5.07 and 6.05, for pericarp thickness in bins 1.06, 2.03, 4.02 and 4.05, and for pericarp content of tFA in bins 2.03, 3.06, 4.05 and 6.05. The joint models, including some additive-by-additive epistasis gene effects, explained 56.0–58.2%, 46.6–45.5%, 41.4–47.1% of the phenotypic variability for disease severity, pericarp thickness and pericarp content of tFA, respectively, depending on the environment. The most important QTL for the three traits overlapped in bin 2.03 indicating that genes from this genomic region might contribute to the expression of disease resistance by increasing thickness and tFA content of the pericarp.

This study aimed to investigate the morphological and biochemical traits associated with resistance to the fruit and shoot borer ( Leucinodes orbonalis Guenée) in eggplant, with the goal of identifying promising genotypes for breeding programs. Fifty-five eggplant genotypes were evaluated under field conditions in Dhaka, Bangladesh, and assessed for their levels of pest infestation in relation to key physical and chemical plant characteristics. Genotypes bearing green, oblong, or round fruits with high seed counts, spines, and light-colored flowers exhibited lower infestation levels. Among morphological traits, fruit diameter (r = 0.66), pericarp thickness (r = 0.63), and number of primary branches (r = 0.33) were positively correlated with fruit infestation, while stem girth (r = 0.80) showed a significant positive correlation with shoot infestation. Conversely, trichome density (r = −0.76), number of fruits per plant (r = −0.52), fruit yield per plant (r = −0.37), and fruit length (r = −0.27) were negatively associated with infestation. Biochemical analysis revealed negative correlations between fruit infestation and total phenols (r = −0.74) and flavonoids (r = −0.71), while total sugars (r = 0.66), chlorophyll (r = 0.74), moisture content (r = 0.77), and total soluble solids (r = 0.61) were positively correlated. Genotypes G7, G11, G31, and G57 demonstrated strong resistance traits and are recommended as parental lines in resistance breeding. These results emphasize that host plant physical and biochemical defenses reduce herbivore damage by lowering tissue palatability and digestibility, thereby decreasing reliance on chemical pesticides and increasing the sustainability of the defense mechanism of host resistance.

Delayed and uneven germination of acorns has a negative effect on seedling quality and yield in seedlings. To address this issue, the effects of different mechanical treatments were studied, including a control (CK), removal of cup scar (RS), removal of pericarp (RP), removal of pericarp and 1/2 of the cotyledon (HC) and removal of pericarp and 2/3 cotyledon (TC), on the germination of Quercus variabilis, Q. wutaishanica and Q. robur acorns and pericarp thickness. The results showed that (1) RP and HC treatments significantly decreased root and shoot mean germination time, increased rooting and shooting germination percentage, and improved the root and shoot synchronization and vigor indexes of the three species’ acorns; (2) the acorns from the TC treatment significantly reduced root and shoot mean germination time and significantly induced the root and shoot synchronization index for all three species; and (3) the RS treatment significantly reduced the root and shoot mean germination time of the three species. Therefore, RP and HC treatments can effectively accelerate germination and regular seedling, which are important in the propagation of Q. variabilis, Q. wutaishanica and Q. robur seedlings. Even and quick germination help reduce acorn predation.

Pericarp thickness and ear traits are important selection criteria for breeding fresh market waxy corn. This research was conducted to better understand genetic control of these traits in popular South Korean germplasm now grown in Illinois. Pericarp thickness on five kernel regions, and ten inflorescence architecture traits were measured on ears from 264 F 2:3 families from a cross between Korean inbreds BH20 and BH30. All five pericarp thickness traits showed high heritabilities and were highly correlated. Multivariate principal components analysis (PCA) revealed that just one principal component (PC) explained most of the total phenotypic variation. A number of univariate quantitative trait loci (QTL) were detected and most were associated with more than one kernel pericarp region. Four out of seven PC-QTL were located in chromosome positions where three or more pericarp thickness univariate QTL were detected. Conversely, three PC-QTL were found in regions with just a single or two univariate QTL, indicating that these QTL regions may be more important for overall pericarp thickness than suggested by univariate analysis. The PCA, QTL, and PC-QTL results indicate that pericarp thickness on different kernel regions may be controlled by common genes with pleiotropic effects. Additive effects of QTL for thinner pericarp thickness came from both BH20 and BH30. For ear architecture traits, heritability varied from 0.38 to 0.72, and several traits were correlated. The PCA reduced these traits into three independent PCs, and all substantial component traits for these PCs were also significantly correlated. A number of univariate QTL were clustered closely, and some PC-QTL were detected in these regions. Some PC-QTL were found in chromosome regions where univariate QTL were not detected, again suggesting that these regions may have larger overall effects on ear architecture than suggested by univariate analyses. Collectively, these QTL may be useful for marker assisted introgression into germplasm more adapted to the U.S.