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Soybean is an important economic crop in the world, which provides plant protein, oil and a variety of active substances beneficial to human health. In order to comprehensively identify the quality characters of soybean resources abundant in China, 16 kinds of seed quality traits of 520 soybean germplasms in Huang-Huai-Hai ecoregion were evaluated in 6 environments across 2 years with reference to the national standard method. The results showed that the genetic variations of the tested seed quality traits were abundant in the soybean germplasms, and the variation coefficients of isoflavone and tocopherol contents were relative high, while the variation coefficients of protein, oil and fatty acid components were relatively low. Meanwhile, there were significant correlations among the 16 seed quality traits. Principal component analysis showed that the 16 quality traits could be attributed to 5 principal components. Based on the results of principal component analysis, 520 germplasms could be divided into 3 categories by cluster analysis with significant differences. Based on the above results and high stability coefficient analysis, 35 germplasms with multiple or single elite seed quality traits were screened out, which provided important resources for genetic improvement of seed quality traits in soybean. [ABSTRACT FROM AUTHOR]

Chlorophyll is an essential pigment for plant photosynthesis. Drought tolerance affects chlorophyll synthesis, reduces photosynthetic efficiency, and decreases soybean yield. In order to explore the genetic loci of chlorophyll content in soybean under drought stress, drought resistance index (DRI) were calculated by chlorophyll contents under drought and well-watered conditions. Moreover, based on the DRI and re-sequenced genotypes of the soybean natural population (199 accessions) at 20x sequencing depth, the genome-wide association study (GWAS) was performed. The results showed that 237 single nucleotide polymorphisms (SNPs) in 18 loci on the chromosomes 1, 2, 3, 7, 10, 16, 17 and 18 were identified to associate with DRI. Moreover, 181 SNPs (76.37% of the total) were located on chromosome 16, of which 9 SNPs were located in the gene introns, 17 in exons, 21 in upstream or downstream, and 1 in 3' UTR. Based on these, 57 candidate genes flanking the associated SNPs were found, and according to the gene annotation, SNP mutation, and RNA expression, 3 candidate genes, Glyma.16G063600 (F-box protein), Glyma. 10G007000 (AP2-EREBP), and Glyma. 17G143900 (AP2/ERF) were screened out which might be responsible for the drought tolerance in soybean. Above results provided important theoretical foundation for drought tolerance genetic improvement in soybean. [ABSTRACT FROM AUTHOR]

Sugars are always transported to the other organs via sugar transporters to play their important functions in plants. SWEET (sugars will eventually be exported transporters) is a kind of sugar transporters which plays important function in plant growth and development as well as in resistance or tolerance to diverse biotic and abiotic stresses. To analyze the expressions of SWEET genes during pod and seed developments and under different stress conditions in soybean, the SWEET genes were firstly analyzed based on the newly published cultivated and wild soybean genomes in the present study. Subsequently, the gene expressions were evaluated during pod and seed developments, as well as in resistance to soybean mosaic virus (SMV) and tolerance to low phosphorus. The results showed that 48 SWEET genes were identified in the cultivated soybean genome (Wm82a4v1), which encoded protein with length 174~354 amino acids and located on 15 chromosomes. Meanwhile, 51 SWEET genes were identified in the wild soybean genome (W05), which encoded length of 84~392 amino acids and located on 16 chromosomes. The phylogenetic tree of SWEET genes in cultivated and wild soybeans showed that they were clustered into 3 sub-groups. Moreover, 16 SWEET genes were expressed in soybean pods with the expressions of Glyma. 06G122200, Glyma. 14G159900 and Glyma. 14G160100 etc. increased during the pod development process. 12 SWEET genes were expressed in soybean seeds, and the expressions of Glyma.08G025100, Glyma.13G041300 and Glyma.14G120300 were increased during the seed development, suggesting their important roles for soybean seed development. The SWEET genes showed different expressions after the inoculation of SMV, and the expressions of Glyma.08G009900 and Glyma.13G264400 were induced in leaves of resistant variety, while had no change in the sensitive variety, implying that they might involve in SMV resistance. The expressions of Glyma.04G198400, Glyma.14G160100 and Glyma.15G211800 were induced in soybean roots after low phosphorus treatment, indicating their important functions in the tolerance to low phosphorus stress. In addition, the single nucleotide polymorphism(SNP)analysis of SWEET genes showed that 43 genes contained 220 nonsynonymous SNPs with 103 located in the conserved domains of encoding proteins. Thus, above results provided candidate genes for molecular breeding of soybean pod and seed yield and diverse stress resistances. [ABSTRACT FROM AUTHOR]

Oxidative stress can adversely affect the health status of the body, more specifically by causing intestinal damage by disrupting the permeability of the intestinal barrier. This is closely related to intestinal epithelial cell apoptosis caused by the mass production of reactive oxygen species (ROS). Baicalin (Bai) is a major active ingredient in Chinese traditional herbal medicine that has antioxidant, anti-inflammatory, and anti-cancer properties. The purpose of this study was to explore the underlying mechanisms by which Bai protects against hydrogen peroxide (H2O2)-induced intestinal injury in vitro. Our results indicated that H2O2 treatment caused injury to IPEC-J2 cells, resulting in their apoptosis. However, Bai treatment attenuated H2O2-induced IPEC-J2 cell damage by up-regulating the mRNA and protein expression of ZO-1, Occludin, and Claudin1. Besides, Bai treatment prevented H2O2-induced ROS and MDA production and increased the activities of antioxidant enzymes (SOD, CAT, and GSH-PX). Moreover, Bai treatment also attenuated H2O2-induced apoptosis in IPEC-J2 cells by down-regulating the mRNA expression of Caspase-3 and Caspase-9 and up-regulating the mRNA expression of FAS and Bax, which are involved in the inhibition of mitochondrial pathways. The expression of Nrf2 increased after treatment with H2O2, and Bai can alleviate this phenomenon. Meanwhile, Bai down-regulated the ratio of phosphorylated AMPK to unphosphorylated AMPK, which is indicative of the mRNA abundance of antioxidant-related genes. In addition, knockdown of AMPK by short-hairpin RNA (shRNA) significantly reduced the protein levels of AMPK and Nrf2, increased the percentage of apoptotic cells, and abrogated Bai-mediated protection against oxidative stress. Collectively, our results indicated that Bai attenuated H2O2-induced cell injury and apoptosis in IPEC-J2 cells through improving the antioxidant capacity through the inhibition of the oxidative stress-mediated AMPK/Nrf2 signaling pathway. [ABSTRACT FROM AUTHOR]

Excessive amounts of molybdenum (Mo) and cadmium (Cd) are toxicant, but their combined immunotoxicity are not clearly understood. To estimate united impacts of Mo and Cd on pyroptosis and autophagy by PI3K/AKT axis in duck spleens, Mo or/and Cd subchronic toxicity models of ducks were established by feeding diets with different dosages of Mo or/and Cd. Data show that Mo or/and Cd cause oxidative stress by increasing MDA concentration, and decreasing T‐AOC, CAT, GSH‐Px and T‐SOD activities, restrain PI3K/AKT axis by decreasing PI3K, AKT, p‐AKT expression levels, which evokes pyroptosis and autophagy by elevating IL‐1β, IL‐18 concentrations and NLRP3, Caspase‐1, ASC, GSDME, GSDMA, NEK7, IL‐1β, IL‐18 expression levels, promoting autophagosomes, LC3 puncta, Atg5, LC3A, LC3B, LC3II/LC3I and Beclin‐1 expression levels, and reducing expression levels of P62 and Dynein. Furthermore, the variations of abovementioned indexes are most pronounced in co‐treated group. Overall, results reveal that Mo or/and Cd may evoke pyroptosis and autophagy by PI3K/AKT axis in duck spleens. The association of Mo and Cd exacerbates the changes. [ABSTRACT FROM AUTHOR]

The accumulation of copper (Cu) in the organisms could lead to kidney damage by causing mitochondrial dysfunction. Given that mitochondria are one of the targets of Cu poisoning, this study aimed to investigate the role of mitophagy in Cu‐induced mitochondrial dysfunction in renal tubular epithelial cells to understand the mechanism of Cu nephrotoxicity. Hence, the cells were treated with different concentrations of Cu sulfate (CuSO4) (0, 100, and 200 μM), and mitophagy inhibitor (Cyclosporine A, 0.5 μM) and/or 200 μM CuSO4 in the combination for 12 h. Results showed that Cu caused mitochondrial swelling, vacuoles, and cristae fracture; increased the number of mitochondrial and lysosome fluorescent aggregation points; upregulated the mRNA levels of mitophagy‐associated genes (LC3A, LC3B, P62, BNIP3, NIX, OPTN, NDP52, Cyp D LAMP1, and LAMP2) and protein levels of LC3II/LC3I, BNIP3, and NIX, downregulated the mRNA and protein levels of P62; reduced the mitochondrial membrane potential (MMP), ATP content, mitochondrial respiratory control rate (RCR), mitochondrial respiratory control rate (OPR), and the mRNA and protein levels of PGC‐1α, TOMM20, and Mfn2, but increased the mRNA and protein levels of Drp1. Besides, cotreatment with Cu and CsA dramatically decreased the level of mitophagy, but increased mitochondrial division, further reduced MMP, ATP content, RCR, and OPR, mitochondrial fusion and thereby reduced mitochondrial biogenesis. Taken together, these data indicated that Cu exposure induced BNIP3/NIX‐dependent mitophagy in duck renal tubular epithelial cells, and inhibition of mitophagy aggravated Cu‐induced mitochondrial dysfunction. [ABSTRACT FROM AUTHOR]

High molybdenum (Mo) and cadmium (Cd) are harmful to the body, but pulmonary toxicity induced by Mo and Cd co‐exposure is unknown. To assess the combined impacts of Mo and Cd on fibrosis through M1 polarization in the lung of ducks, 80 healthy 8‐day‐old Shaoxing ducks (Anas platyrhyncha) were randomly assigned to 4 groups and fed with containing unequal doses of Mo or/and Cd diet. Lung tissues were collected on the 16th week. Results indicated that Mo or/and Cd significantly increased their contents in the lungs, and led to trace elements disorder and histological abnormality, and oxidative stress accompanied by promoting contents of H2O2 and MDA and decreasing activities of T‐SOD, GSH‐Px, and CAT, then activated the TLR4/NF‐κB/NLRP3 pathway accompanied by upregulating Caspase‐1, ASC, IL‐18, IL‐1β, TLR4, NF‐κB, and NLRP3 expression levels, and disrupted M1/M2 balance to divert toward M1, which evoked the TGF‐β/Smad2/3‐mediated fibrosis by elevating TGF‐β1, Smad2, Smad3, COL1A1, α‐SMA, and MMP2 expression levels, and decreasing Smad7 and TIMP2 expression levels. The changes of the combined group were most obvious. To sum up, the research demonstrated that Mo or/and Cd may cause macrophages to polarize toward M1 by oxidative stress‐mediated the TLR4/NF‐κB/NLRP3 pathway, then result in fibrosis through the TGF‐β1/Smad2/3 pathway in duck lungs. Mo and Cd may worsen lung damage. [ABSTRACT FROM AUTHOR]

Cadmium (Cd) is detrimental to animals, but nephrotoxic effects of Cd on duck have not been fully elucidated. To evaluate the impacts of Cd on Ca homeostasis and autophagy via PLC‐IP3‐IP3R pathway, primary duck renal tubular epithelial cells were exposed to 2.5 μM and 5.0 μM Cd, and combination of 5.0 μM Cd and 10.0 μM 2‐APB or 0.125 μM U‐73122 for 12 h (U‐73122 pretreated for 1 h). These results evidenced that Cd induced [Ca2+]c overload mainly came from intracellular Ca store. Cd caused [Ca2+]mit and [Ca2+]c overload with [Ca2+]ER decrease, elevated Ca homeostasis related factors (GRP78, GRP94, CRT, CaN, CaMKII, and CaMKKβ) expression, PLC and IP3 activities and IP3R expression, but subcellular Ca2+ redistribution was reversed by 2‐APB. PLC inhibitor U‐73122 dramatically relieved the changes of the above indicators induced by Cd. Additionally, U‐73122 obviously reduced the number of autophagosomes and LC3 accumulation spots, Atg5, LC3A, LC3B mRNA levels and LC3II/LC3I, Beclin‐1 protein levels induced by Cd, and markedly elevated p62 mRNA and protein levels. Overall, the results verified that Cd induced [Ca2+]c overload mainly originated from ER Ca2+ release mediated by PLC‐IP3‐IP3R pathway, then triggered autophagy in duck renal tubular epithelial cells. [ABSTRACT FROM AUTHOR]