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Abstract Background Inositol‐requiring enzyme 1 (IRE1) is an endoplasmic reticulum (ER)‐resident transmembrane protein that senses ER stress and mediates an essential arm of the unfolded protein response (UPR). IRE1 reduces ER stress by upregulating the expression of multiple ER chaperones through activation of X‐box‐binding protein 1 (XBP1). Emerging lines of evidence have revealed that IRE1‐XBP1 axis serves as a multipurpose signal transducer during oncogenic transformation and cancer development. In this study, we explore how IRE1‐XBP1 signaling promotes chemoresistance in lung cancer. Methods The expression patterns of UPR components and MRP1 were examined by Western blot. qRT‐PCR was employed to determine RNA expression. The promoter activity was determined by luciferase reporter assay. Chemoresistant cancer cells were analyzed by viability, apoptosis. CUT & Tag (Cleavage under targets and tagmentation)‐qPCR analysis was used for analysis of DNA‐protein interaction. Results Here we show that activation of IRE1α‐XBP1 pathway leads to an increase in MDR‐related protein 1 (MRP1) expression, which facilitates drug extrusion and confers resistance to cytotoxic chemotherapy. At the molecular level, XBP1‐induced c‐Myc is necessary for SREBP1 expression, and SREBP1 binds to the MRP1 promoter to directly regulate its transcription. Conclusions We conclude that IRE1α‐XBP1 had important role in chemoresistance and appears to be a novel prognostic marker for lung cancer.

Screening genotypes with optimal root traits presents a promising breeding strategy for enhancing adaptability to abiotic stresses and improving resource use efficiency. This study evaluated root traits of 100 winter wheat genotypes under four treatments: control (C), low phosphorus (LP), PEG-induced drought (D), and a combination of LP and drought (DLP), using a semi-hydroponic phenotyping platform. Significant variations in root traits were observed 65 days after transplanting, with over 80% of traits being significantly affected by drought, phosphorus, or their interactions. Biomass and phosphorus content decreased under LP and drought, while root length and diameter in deeper layers increased, especially under drought stress. Combined stress led to the most severe reductions in biomass, P-content, and leaf number. Phosphorus acquisition efficiency was positively correlated with root length but inversely related to stress tolerance. High heritability traits, such as root number, root length, maximum root depth, leaf number, and biomass, hold potential for breeding programs focused on environmental adaptation, resource efficiency, and yield improvement. The substantial genotypic variation in root morphology under stress conditions highlights the potential for breeding stress-resilient wheat genotypes. This finding lays a foundation for wheat-breeding initiatives aimed at developing genotypes better suited to prevailing environmental conditions.

BackgroundTo investigate the correlation between albumin-corrected anion gap(ACAG) within the first 24 hours of admission and in-hospital mortality in trauma patients in intensive care unit(ICU).Materials and methodsWe utilized the MIMIC-Ⅲ and MIMIC-Ⅳ databases to examine trauma patients admitted to the ICU. The relationship between ACAG and in-hospital mortality in trauma patients was analyzed using Receiver Operating Characteristic(ROC) curve, Kaplan-Meier (K-M) survival curve, and Cox regression model. Propensity score matching (PSM) and subgroup analysis were conducted to enhance stability and reliability of the findings. Mortality at 30-day and 90-day served as secondary outcomes.ResultsThe study enrolled a total of 1038 patients. The AUC for ACAG (0.701, 95%CI: 0.652-0.749) was notably higher than that for anion gap and albumin. The Log-rank test revealed that the optimal cut-off point of ACAG for predicting in-hospital mortality was determined to be 20.375mmol/L. The multivariate Cox regression analysis demonstrated an independent association between high ACAG level and a higher risk of in-hospital mortality (HR = 3.128, 95% CI: 1.615-6.059). After PSM analysis, a matched cohort consisting of 291 subjects was obtained. We found no signifcant interaction in most stratas. Finally, The in-hospital, 30-day, and 90-day survival rates in the high ACAG group exhibited a statistically decrease compared to those in the low ACAG group both pre- and post-matching.ConclusionThe elevated level of ACAG was found to be independently associated with increased in-hospital mortality among trauma patients in the ICU.

The Hessian fly (HF, Mayetiola destructor) is one of the destructive pests of wheat (Triticum aestivum L.) worldwide. Resistant cultivars can effectively minimize wheat damage due to this insect pest. To identify new quantitative trait loci (QTL) for HF resistance, a population of recombinant inbred lines (RILs) was developed from a cross between the HF-resistant wheat cultivar ‘Chokwang’ and susceptible wheat ‘Ning 7840’, and phenotyped for responses to HF attack. A linkage map was constructed using 1147 single nucleotide polymorphism (SNP) markers generated from genotyping-by-sequencing (GBS). One major QTL, QHf.hwwg-6BS, for HF-resistance was identified on chromosome arm 6BS, which explained up to 84.0% of the phenotypic variation and was contributed by Chokwang. Two RILs showed recombination in the candidate interval of QHf.hwwg-6BS, which delimited QHf.hwwg-6BS to a 4.75 Mb physical interval between 6,028,601 bp and 10,779,424 bp on chromosome arm 6BS of IWGSC Chinese Spring reference genome RefSeq v2.0. Seven GBS-SNPs in the candidate interval were converted into Kompetitive allele specific polymerase chain reaction (KASP) markers. Two of them, KASP-6B112698 and KASP-6B7901215, were validated in a U.S. winter wheat panel. KASP-6B112698 was nearly diagnostic, thus can be used to screen QHf.hwwg-6BS and pyramid it with other resistance genes in breeding programs.

Wheat resistance to Fusarium head blight (FHB) has often been associated with some undesirable agronomic traits. To study the relationship between wheat FHB resistance and agronomic traits, we constructed a linkage map of single nucleotide polymorphisms (SNPs) using an F6:8 population from G97252W × G97380A. The two hard winter wheat parents showed contrasts in FHB resistance, plant height (HT), heading date (HD), spike length (SL), spike compactness (SC), kernel number per spike (KNS), spikelet number per spike (SNS), thousand-grain weight (TGW) and grain size (length and width). Quantitative trait locus (QTL) mapping identified one major QTL (QFhb.hwwg-2DS) on chromosome arm 2DS for the percentage of symptomatic spikelets (PSS) in the spike, deoxynivalenol (DON) content and Fusarium damaged kernel (FDK). This QTL explained up to 71.8% of the phenotypic variation for the three FHB-related traits and overlapped with the major QTL for HT, HD, SL, KNS, SNS, TGW, and grain size. QTL on chromosome arms 2AL, 2DS, 3AL and 4BS were significant for the spike and grain traits measured. G97252W contributed FHB resistance and high SNS alleles at QFhb.hwwg-2DS, high KNS alleles at the QTL on 2AL and 2DS, and high TGW and grain size alleles at QTL on 3AL; whereas G97380A contributed high TGW and grain size alleles at the QTL on 2AL and 2DS, respectively, and the high KNS allele at the 4BS QTL. Combining QFhb.hwwg-2DS with positive alleles for spike and grain traits from other chromosomes may simultaneously improve FHB resistance and grain yield in new cultivars. [ABSTRACT FROM AUTHOR]

To solve the problem of low removal rate and poor N2 selectivity in direct electrochemical ammonia oxidation (EAO), commercial Ni foam and Cu foam were used as anode and cathode of the EAO system, respectively. The coupling effect between the cathode and anode promoted nitrogen cycling during the reaction process, which improved N2 selectivity of the reaction system and promoted it to achieve a high ammonia removal rate. This study showed that the thin Ni(OH)2 with oxygen vacancy formed on the surface of Ni foam anode played an effective role in the dimerization of intermediate products in ammonia oxidation to form N2. This electrochemical system was used to treat real goose wastewater containing 422.5 mg/L NH4+-N and 94.5 mg/L total organic carbon (TOC). After treatment, this electrochemical system achieved good performance with an ammonia removal rate of 87%, N2 selectivity of 77%, and TOC removal rate of 72%. Therefore, this simple and efficient system with Ni foam anode and Cu foam cathode is a promising method for treating ammonia nitrogen wastewater. HIGHLIGHTS The use of commercial electrodes has increased the practicality of this system.; The anode was responsible for the ammonia oxidation.; The cathode was responsible for the reduction of nitrate.; The nitrogen cycle between the electrodes enabled this system to achieve high performance.; The electrochemical system had achieved significant results in practical goose wastewater treatment.;

Inflammatory macrophages play a crucial role in atherosclerosis development. The long non-coding RNA growth arrest-specific 5 (GAS5) regulates THP-1 macrophage inflammation by sponging microRNAs. The purpose of this study was to investigate the regulatory mechanism of GAS5 in atherosclerosis development. GSE40231, GSE21545, and GSE28829 datasets from the Gene Expression Omnibus database were integrated after adjusting for batch effect. Differential analysis was performed on the integrated dataset and validated using the Genotype-Tissue Expression and GSE57691 datasets. Potential biological functions of GAS5 and annexin A2 (ANXA2) were identified using gene set enrichment analysis (GSEA). ssGSEA, CIBERSORTx, and ImmuCellAI algorithms were used to identify immune infiltration in plaque samples. GAS5 and ANXA2 expression levels in RAW264.7 cells treated with oxidized low-density lipoprotein (ox-LDL) were measured by qRT-PCR and Western blot. Small interfering and short hairpin RNA were used to silence GAS5 expression. Plasmids of ANXA2 were used to establish ANXA2 overexpression. Apoptosis and inflammatory markers in macrophages were detected by Western blot. Aortic samples from APOE−/− mice were collected to validate the expression of GAS5 and ANXA2. GAS5 expression was significantly increased during atherosclerosis. GAS5 expression was positively correlated with macrophage activation and ANXA2 expression in plaques. Furthermore, ANXA2 upregulation was also related to the activation of macrophage. GSEA indicated similar biological functions for GAS5 and ANXA2 in plaques. Moreover, in vitro experiments showed that both GAS5 and ANXA2 contributed to macrophage apoptosis and inflammation. Rescue assays revealed that the inflammatory effects of GAS5 on macrophages were ANXA2-dependent. In vivo experiments confirmed the highly expression of Gas5 and Anxa2 in the plaque group. We identified the atherogenic roles of GAS5 and ANXA2 in the inflammatory response of macrophages. The inflammatory response in ox-LDL-treated macrophages was found to be mediated by GAS5-ANXA2 regulation, opening new avenues for atherosclerosis therapy.

An increasing body of studies has demonstrated the significance of long non-coding RNA (lncRNA) growth arrest specific 5 (GAS5) in inflammation and myocardial injury in septic shock. This research aims to determine whether GAS5 contributes to the pathological development of sepsis-induced cardiac damage and NLRP3 inflammasome-mediated myocardial cell pyroptosis. Cecal ligation and puncture (CLP) surgery was used to cause septic shock in C57BL/6 wild-type mice. After CLP, inflammatory, pyroptosis parameters of myocardial tissue, survival rate, and Murine Sepsis Score (MSS) were assessed to evaluate the involvement of GAS5 in the mouse myocardial depression. To investigate GAS5's function in lipopolysaccharide (LPS) induced myocardial cell pyroptosis, gain- and loss-of-function experiments were conducted in vitro on HL-1 cells. Our findings indicated that CLP dramatically reduced survival rates, MSS, SIRT3 and p-AMPK expression, and activated the Nuclear factor-κB (NF-κB) pathway and NLRP3 inflammasome-mediated pyroptosis. The NF-κB and pyroptosis pathways were greatly elevated while SIRT3/p-AMPKα was dramatically decreased as a result of GAS5 being downregulated. Meanwhile, the regulatory effect could be suppressed by SIRT3 and AMPKα activator. Our observations supported the idea that GAS5 has a crucial protective impact against myocardial inflammation and pyroptosis in sepsis.

Characterisation of macrophages from human carotid artery plaques and in vitro assays reveal that macrophages regulate vascular smooth muscle cell function during atherosclerosis progression through the IL-1β/STAT3 axis.

BackgroundDespite a growing body of evidence that acne impacts mental disorders, the actual causality has not been established for the possible presence of recall bias and confounders in observational studies.MethodsWe performed a two-sample Mendelian randomization (MR) analysis to evaluate the effect of acne on the risk of six common mental disorders, i.e., depression, anxiety, schizophrenia, obsessive–compulsive disorder (OCD), bipolar disorder, and post-traumatic stress disorder (PTSD). We acquired genetic instruments for assessing acne from the largest genome-wide association study (GWAS) of acne (N = 615,396) and collected summary statistics from the largest available GWAS for depression (N = 500,199), anxiety (N = 17,310), schizophrenia (N = 130,644), OCD (N = 9,725), bipolar disorder (N = 413,466), and PTSD (N = 174,659). Next, we performed the two-sample MR analysis using four methods: inverse-variance weighted method, MR-Egger, weighted median, and MR pleiotropy residual sum and outliers. Sensitivity analysis was also performed for heterogeneity and pleiotropy tests.ResultsThere was no evidence of a causal impact of acne on the risk of depression [odds ratio (OR): 1.002, p = 0.874], anxiety (OR: 0.961, p = 0.49), OCD (OR: 0.979, p = 0.741), bipolar disorder (OR: 0.972, p = 0.261), and PTSD (OR: 1.054, p = 0.069). Moreover, a mild protective effect of acne against schizophrenia was observed (OR: 0.944; p = 0.033).ConclusionThe increased prevalence of mental disorders observed in patients with acne in clinical practice was caused by modifiable factors, and was not a direct outcome of acne. Therefore, strategies targeting the elimination of potential factors and minimization of the occurrence of adverse mental events in acne should be implemented.

Summary: To determine the effect of aerobic exercise in different intensities on renal injury and epithelial-mesenchymal transformation (EMT) in the kidney of spontaneously hypertensive rats (SHR) and explore possible mechanisms, we subjected SHR to different levels of 14-week aerobic treadmill training. We tested the effects of aerobic exercise on irisin level, renal function, and EMT modulators in the kidney. We also treated angiotensin II-induced HK-2 cells with irisin and tested the changes in EMT levels. The data showed low and moderate aerobic exercise improved renal function and inhibited EMT through promoting irisin expression in SHR. However, high-intensity exercise training had no effect on renal injury and EMT in SHR but did significantly activate STAT3 phosphorylation in the kidney. These results clarify the mechanisms of exercise in improving hypertension-related renal injury and suggest that irisin might be a therapeutic target for patients with kidney injury.

Abstract Enhancer RNAs (eRNAs) are a subclass of non-coding RNAs that are generated during the transcription of enhancer regions and play an important role in tumourigenesis. In this study, we focused on the crucial eRNAs that participate in immune responses in invasive breast cancer (IBC). We first used The Cancer Genome Atlas and Human enhancer RNA Atlas to screen for tissue-specific eRNAs and their target genes. Through Pearson correlation analysis with immune genes, the eRNA WAKMAR2 was identified as a key candidate involved in IBC. Our further research suggested that WAKMAR2 is crucial in regulating the tumour microenvironment and may function by regulating immune-related genes, including IL27RA, RAC2, FABP7, IGLV1-51, IGHA1, and IGHD. Quantitative reverse transcription-polymerase chain reaction was used to detect the expression of WAKMAR2 in IBC and normal tissues, and the effect of WAKMAR2 on the regulation of downstream genes in MB-231 and MCF7 cells was studied in vitro. WAKMAR2 was found to be highly involved in tumour immunity and was downregulated in IBC tissues. Furthermore, the expression of WAKMAR2 and its target genes was observed at the pan-cancer level. This study provides evidence to suggest new potential targets for the treatment of breast cancer.

Abstract Background Numerous studies have revealed the relationship between lipid expression and increased cardiovascular risk in ST-segment elevation myocardial infarction (STEMI) patients. Nevertheless, few investigations have focused on the risk stratification of STEMI patients using machine learning algorithms. Methods A total of 1355 STEMI patients who underwent percutaneous coronary intervention were enrolled in this study during 2015–2018. Unsupervised machine learning (consensus clustering) was applied to the present cohort to classify patients into different lipid expression phenogroups, without the guidance of clinical outcomes. Kaplan-Meier curves were implemented to show prognosis during a 904-day median follow-up (interquartile range: 587–1316). In the adjusted Cox model, the association of cluster membership with all adverse events including all-cause mortality, all-cause rehospitalization, and cardiac rehospitalization was evaluated. Results All patients were classified into three phenogroups, 1, 2, and 3. Patients in phenogroup 1 with the highest Lp(a) and the lowest HDL-C and apoA1 were recognized as the statin-modified cardiovascular risk group. Patients in phenogroup 2 had the highest HDL-C and apoA1 and the lowest TG, TC, LDL-C and apoB. Conversely, patients in phenogroup 3 had the highest TG, TC, LDL-C and apoB and the lowest Lp(a). Additionally, phenogroup 1 had the worst prognosis. Furthermore, a multivariate Cox analysis revealed that patients in phenogroup 1 were at significantly higher risk for all adverse outcomes. Conclusion Machine learning-based cluster analysis indicated that STEMI patients with increased concentrations of Lp(a) and decreased concentrations of HDL-C and apoA1 are likely to have adverse clinical outcomes due to statin-modified cardiovascular risks. Trial registration ChiCTR1900028516 ( http://www.chictr.org.cn/index.aspx ).

BackgroundIn recent years, frontal fibrosing alopecia (FFA), a type of scarring alopecia, has attracted increasing attention. Several studies have reported the frequent occurrence of rosacea in FFA; however, the association between FFA and rosacea and the underlying pathogenesis have not been thoroughly clarified. Thus, this study aimed to quantify these relationships and investigate their shared molecular mechanisms.MethodsWe evaluated the association between FFA and rosacea by analyzing clinical data from nine observational studies. We then analyzed the gene expression profiles of FFA and rosacea. First, differential expression analysis and weighted gene co-expression network analysis were used to identify the common differentially expressed genes (DEGs). Later, we conducted a functional enrichment analysis and protein-protein interaction network and used seven algorithms to identify hub genes. Then, we performed a correlation analysis between the hub genes and the gene set variation analysis scores of common pathways in the gene set enrichment analysis (GSEA). The results were validated using different datasets. Finally, transcription factors were predicted and verified, and CIBERSORT and single-sample GSEA were used to estimate the infiltrating immune cells.ResultsPatients with FFA had significantly higher odds for rosacea (pooled odds ratio [OR], 2.46; 95% confidence interval [CI], 1.78–3.40), and the pooled prevalence of rosacea in patients with FFA was 23% (95% CI, 14–23%). Furthermore, we identified 115 co-DEGs and 13 hub genes (CCR5, CCL19, CD2, CD38, CD83, CXCL8, CXCL9, CXCL10, CXCL11, CXCR4, IRF1, IRF8, and PTPRC). Seven pathways showed a high correlation with these hub genes. In addition, one TF, STAT1, was highly expressed in both diseases, and the results of the immune infiltration analysis indicated the importance of M1 macrophages and effector memory CD8+ T cells.ConclusionThis study contributes to the understanding of the relationship between FFA and rosacea, and based on the hub genes, we reveal the potential pathologies shared by the two diseases. This finding provides new insights of underlying molecular mechanisms and it may inspire future research on this comorbidity.

Background: Imbalance of testosterone/estradiol ratio are frequently reported to be associated with the risk of cardiometabolic diseases; however, studies have yet to report the testosterone/estradiol ratio and its relationship to cardiometabolic diseases in women at menopause transition. This study aimed to explore the association between testosterone/estradiol ratio with cardiometabolic diseases in women during their menopausal transition age. Methods: 551 women aged from 45 to 55 years old were involved in this study. Their baseline information, disease comorbidity, blood biochemical tests, echocardiography and serum sex hormones were collected. Women were categorized by tertile distribution of testosterone/estradiol ratio. We used binary logistic regression model (for odds ratio) and poissoon loglinear model (for prevalence ratio) to evaluate the association between testosterone/estradiol ratio with cardiometabolic diseases. Results: The mean age of the study population was 48.6 ± 3.5 years old. Taking testosterone/estradiol ratio

Background: The coronary atherosclerotic burden in patients with ST-segment elevation myocardial infarction (STEMI) has been identified as the main predictor of prognosis. However, the association of lipoprotein(a) [Lp(a)], a well-established proatherogenic factor, with atherosclerotic burden in patients with STEMI is unclear.Methods: In total, 1,359 patients who underwent percutaneous coronary intervention (PCI) for STEMI were included in analyses. Three prespecified models with adjustment for demographic parameters and risk factors were evaluated. Generalized additive models and restricted cubic spline analyses were used to assess the relationships of Lp(a) with Gensini scores and the no-reflow phenomenon. Kaplan–Meier curves were generated to explore the predictive value of Lp(a) for long-term all-cause mortality. Furthermore, mRNA expression levels of LPA in different groups were compared using the GEO database.Results: Patients in the highest tertile according to Lp(a) levels had an increased incidence of heart failure during hospitalization. Furthermore, patients with high levels of Lp(a) (>19.1 mg/dL) had sharply increased risks for a higher Gensini score (Pfor trend = 0.03) and no-reflow (Pfor trend = 0.002) after adjustment for demographic parameters and risk factors. During a median follow-up of 930 days, 132 deaths (9.95%) were registered. Patients with high levels of Lp(a) (>19.1 mg/dL) had the worst long-term prognosis (Pfor trend < 0.0001). In a subgroup analysis, patients with higher Lp(a) still had the highest all-cause mortality. Additionally, the mRNA expression levels of LPA in patients with STEMI with lower cardiac function were higher than those in other groups (P = 0.003). A higher coronary atherosclerotic burden was correlated with higher LPA expression (P = 0.01).Conclusion: This study provides the first evidence that Lp(a) (at both the protein and mRNA levels) is independently associated with coronary atherosclerotic lesions and prognosis in patients with STEMI treated with PCI.Clinical Trial Registration:http://www.chictr.org.cn/index.aspx, identifier: ChiCTR1900028516.

Increasing evidence has indicated that modulation of epigenetic mechanisms, especially methylation and long-non-coding RNA (lncRNA) regulation, plays a pivotal role in the process of atherosclerosis; however, few studies focused on revealing the epigenetic-related subgroups during atherosclerotic progression using unsupervised clustering analysis. Hence, we aimed to identify the epigenetics-related differentially expressed genes associated with atherosclerosis subtypes and characterize their clinical utility in atherosclerosis. Eighty samples with expression data (GSE40231) and 49 samples with methylation data (GSE46394) from a large artery plaque were downloaded from the GEO database, and aberrantly methylated–differentially expressed (AMDE) genes were identified based on the relationship between methylation and expression. Furthermore, we conducted weighted correlation network analysis (WGCNA) and co-expression analysis to identify the core AMDE genes strongly involved in atherosclerosis. K-means clustering was used to characterize two subtypes of atherosclerosis in GSE40231, and then 29 samples were recognized as validation dataset (GSE28829). In a blood sample cohort (GSE90074), chi-square test and logistic analysis were performed to explore the clinical implication of the K-means clusters. Furthermore, significance analysis of microarrays and prediction analysis of microarrays (PAM) were applied to identify the signature AMDE genes. Moreover, the classification performance of signature AMDE gene-based classifier from PAM was validated in another blood sample cohort (GSE34822). A total of 1,569 AMDE mRNAs and eight AMDE long non-coding RNAs (lncRNAs) were identified by differential analysis. Through the WGCNA and co-expression analysis, 32 AMDE mRNAs and seven AMDE lncRNAs were identified as the core genes involved in atherosclerosis development. Functional analysis revealed that AMDE genes were strongly related to inflammation and axon guidance. In the clinical analysis, the atherosclerotic subtypes were associated with the severity of coronary artery disease and risk of adverse events. Eight genes, including PARP15, SERGEF, PDGFD, MRPL45, UBR1, STAU1, WIZ, and LSM4, were selected as the signature AMDE genes that most significantly differentiated between atherosclerotic subtypes. Ultimately, the area under the curve of signature AMDE gene-based classifier for atherosclerotic subtypes was 0.858 and 0.812 in GSE90074 and GSE34822, respectively. This study identified the AMDE genes (lncRNAs and mRNAs) that could be implemented in clinical clustering to recognize high-risk atherosclerotic patients.

With the increase in consumer demand, wheat grain quality improvement has become a focus in China and worldwide. Transcriptome analysis is a powerful approach to research grain traits and elucidate their genetic regulation. In this study, two cDNA libraries from the developing grain and leaf-stem components of bread wheat cultivar, Nongda211, were sequenced using Roche/454 technology. There were 1061274 and 1516564 clean reads generated from grain and leaf-stem, respectively. A total of 61393 high-quality unigenes were obtained with an average length of 1456 bp after de novo assembly. The analysis of the 61393 unigenes involved in the biological processes of the grain showed that there were 7355 differentially expressed genes upregulated in the grain library. Gene ontology enrichment and the Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed that many transcription products and transcription factors associated with carbohydrate and protein metabolism were abundantly expressed in the grain. These results contribute to excavate genes associated with wheat quality and further study how they interact.