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Summary: Carotenoids are indispensable to plants and critical components of the human diet. The carotenoid metabolic pathway is conserved across plant species, but our understanding of the genetic basis of carotenoid variation remains limited for the seeds of most cereal crops. To address this issue, we systematically performed linkage and association mapping for eight carotenoid traits using six recombinant inbred line (RIL) populations. Single linkage mapping (SLM) and joint linkage mapping (JLM) identified 77 unique additive QTLs and 104 pairs of epistatic QTLs. Among these QTLs, we identified 22 overlapping hotspots of additive and epistatic loci, highlighting the important contributions of some QTLs to carotenoid levels through additive or epistatic mechanisms. A genome‐wide association study based on all RILs detected 244 candidate genes significantly associated with carotenoid traits, 23 of which were annotated as carotenoid pathway genes. Effect comparisons suggested that a small number of loci linked to pathway genes have substantial effects on carotenoid variation in our tested populations, but many loci not associated with pathway genes also make important contributions to carotenoid variation. We identified ZmPTOX as the causal gene for a QTL hotspot (Q10/JLM10/GWAS019); this gene encodes a putative plastid terminal oxidase that produces plastoquinone‐9 used by two enzymes in the carotenoid pathway. Natural variants in the promoter and second exon of ZmPTOX were found to alter carotenoid levels. This comprehensive assessment of the genetic mechanisms underlying carotenoid variation establishes a foundation for rewiring carotenoid metabolism and accumulation for efficient carotenoid biofortification. [ABSTRACT FROM AUTHOR]

AIM: To investigate the protective effect of total flavonoids from Patrina villosa Juss (PJF) on the lung in an experimental rat model of acute lung injury (ALI), and to elucidate the potential mechanism. METHODS: The ALI rat model was established by instilling 5 mg/kg of lipopolysaccharide (LPS) into the airway. Sixty male SD rats were randomly divided into 4 groups: control, LPS, LPS+low-dose PJF (receiving 100 mg/kg PJF one hour before ALI modeling) and LPS+high-dose PJF (receiving 300 mg/kg PJF one hour before ALI modeling). Each group consisted of 15 animals. Lung tissues and bronchoalveolar lavage fluid (BALF) were collected from all groups 24 h after modeling. For assessment of lung tissue morphology, HE staining was performed. The wet/dry weight ratio of the lung tissue was determined using the wet/dry weighing method. Evans blue staining was conducted to assess epithelial barrier permeability in lung tissues. ELISA was used to detect the levels of inflammatory factors tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 in the BALF, as well as oxidative stress markers including superoxide dismutase (SOD), myeloperoxi-dase (MPO) and glutathione peroxidase (GSH-Px) activity, and malondialdehyde (MDA) content in the lung tissue. The expression levels of C/EBP homologous protein (CHOP), glucose-regulated protein 78 (GRP78) and X-box binding protein 1 (XBP1) in the lung tissue were analyzed by Western blotting. RESULTS: Compared with control group, the rats in LPS group exhibited a blurred alveolar structure with a significant infiltration of inflammatory cells. The ALI score and the wet/dry weight ratio of the lung tissue were increased (P<0. 05). Concurrently, the levels of IL-6, IL-1β and TNF-α in the BALF, along with MDA content and MPO activity in the lung tissue, were elevated (P<0. 05). Additionally, the protein levels of CHOP, GRP78 and XBP1 were up-regulated in the lung tissue (P<0. 05), while the SOD and GSH-Px activity was significantly decreased (P<0. 05). Compared with LPS group, PJF intervention exerted beneficial effects on the lung tissue morphology with reduced ALI score and lower lung wet/dry weight ratio (P<0. 05). Moreover, the levels of IL-6, IL-1β and TNF-α in BALF, as well as MDA content, MPO activity and the protein levels of CHOP, GRP78 and XBP1 in the lung tissue were all significantly decreased (P<0. 05), while the SOD and GSH-Px activity was significantly increased (P<0. 05). The efficacy in high-dose group exceeded that in low-dose group. CONCLUSION: The PJF have protective effect on the lungs of rats with ALI, and its mechanism may be related to the inhibition of inflammation, oxidative stress and endoplasmic reticulum stress. [ABSTRACT FROM AUTHOR]