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Bread wheat expanded its habitat from a core area of the Fertile Crescent to global environments within ~10,000 years. The genetic mechanisms of this remarkable evolutionary success are not well understood. By whole-genome sequencing of populations from 25 subspecies within the genera Triticum and Aegilops, we identified composite introgression from wild populations contributing to a substantial portion (4-32%) of the bread wheat genome, which increased the genetic diversity of bread wheat and allowed its divergent adaptation. Meanwhile, convergent adaptation to human selection showed 2- to 16-fold enrichment relative to random expectation-a certain set of genes were repeatedly selected in Triticum species despite their drastic differences in ploidy levels and growing zones, indicating the important role of evolutionary constraints in shaping the adaptive landscape of bread wheat. These results showed the genetic necessities of wheat as a global crop and provided new perspectives on transferring adaptive success across species for crop improvement.

Background: Hepatocellular carcinoma (HCC) is one of the most common malignancies with high invasion and metastasis capacities. Circular RNAs (circRNAs) were evidenced to take part in the progression of multifarious cancers, including HCC. However, the role of circ_0091579 in HCC progression has not been fully described. This study aimed to explore the function of circ_0091579 and its potential regulatory mechanism in the progression of HCC. Materials and Methods: The expression of circ_0091579, microRNA-490-5p (miR-490-5p), and cancer susceptibility candidate 3 (CASC3) in HCC tissues and cells was detected by quantitative real-time polymerase chain reaction. The circular characteristic and stability of circ_0091579 were verified by RNase R digestion and actinomycin D reaction assays. Cell proliferation, migration, and invasion were determined by methyl thiazolyl tetrazolium assay and Transwell assay, respectively. The level of glycolysis was evaluated by glucose consumption and lactate production. The levels of proteins were examined by Western blot. The interaction between miR-490-5p and circ_0091579 or CASC3 was certified by Dual-luciferase reporter assay. Results: circ_0091579 and CASC3 were upregulated, while miR-490-5p was downregulated in HCC tissues and cells. Silencing of either circ_0091579 or CASC3 suppressed cell proliferation, migration, invasion, and glycolysis in HCC cells. Moreover, miR-490-5p was verified to directly bind to circ_0091579 and CASC3. Circ_0091579 upregulated CASC3 by sponging miR-490-5p in HCC cells to promote cell proliferation, invasion, and migration. Conclusion: circ_0091579 promoted cell proliferation, migration, invasion, and glycolysis partially through miR-490-5p/CASC3 axis in HCC cells.

The size of the top three leaves of rice plants is strongly associated with yield; thus, it is important to consider quantitative traits representing leaf size (e.g., length and width) when breeding novel rice varieties. It is challenging to measure such traits on a large scale in the field, and little is known about the genetic factors that determine the size of the top three leaves. In the present study, a population of recombinant inbred lines (RILs) and reciprocal single chromosomal segment substitution lines (SSSLs) derived from the progeny of a japonica Asominori × indica IR24 cross were grown under four diverse environmental conditions. Six morphological traits associated with leaf size were measured, namely length and flag leaf, length and flag, second and third leaves. In the RIL population, 49 QTLs were identified that clustered in 30 genomic region. Twenty-three of these QTLs were confirmed in the SSSL population. A comparison with previously reported genes/QTLs revealed eight novel genomic regions that contained uncharacterized ORFs associated with leaf size. The QTLs identified in this study can be used for marker-assisted breeding and for fine mapping of novel genetic elements controlling leaf size in rice.

Objectives: Intracranial atherosclerotic stenosis (ICAS) is one of the most common causes of stroke worldwide and, in particular, has been implicated as a leading cause of recurrent ischemic stroke. We adapted a rat model of atherosclerosis to study brain intracranial atherosclerosis, and further investigated the effect of omega-3 fatty acids (O3FA) in attenuating development of ICAS. Materials and methods: Adult male Sprague–Dawley rats were divided into control normal-cholesterol or high-cholesterol diet groups with or without O3FA for up to 6 weeks. During the first 2 weeks, NG-nitro- l -arginine methyl ester ( l -NAME, 3 mg/mL) was added to the drinking water of the high-cholesterol groups. The rats received supplementation with O3FA (5 mg/kg/day) by gavages. Blood lipids including low density lipoprotein (LDL), cholesterol (CHO), triglycerides (TG) and high density lipoprotein (HDL) were measured at 3 and 6 weeks. The lumen of middle cerebral artery (MCA) and the thickness of the vessel wall were assessed. Inflammatory molecular markers were assessed by Western blot. Results: A high-cholesterol diet exhibited a significant increase in the classic blood markers (LDL, CHO, and TG) for atherosclerosis, as well as a decrease in HDL. These markers were found to be progressively more severe with time. Lumen stenosis and intimal thickening were increased in MCA. O3FA showed attenuation of blood lipids with an absence of morphological changes. O3FA significantly reduced the inflammatory marker CD68 in MCA and prevented monocyte chemotactic protein (MCP-1) and interferon-γ (IFN-γ) expression in the brain. O3FA similarly decreased inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-α), and interleukin 6 (IL-6), markers affiliated with monocyte activity in atherosclerosis. Furthermore, O3FA significantly inhibited the expression of vascular cell adhesion molecule-1 (VCAM-1), a marker for endothelial activation. Lastly, O3FA increased ATP-binding cassette transporter A1 (ABCA1) protein expression via silent information regulator 1 (SIRT1) activation, thus increasing cholesterol efflux from macrophages to HDL. Conclusions: Long-term O3FA dietary supplementation prevents the development of intracranial atherosclerosis. This O3FA effect appears to be mediated by its prevention of macrophage infiltration into the vessel wall, therefore reducing inflammation and intimal thickening. While similar effects in humans need to be determined, O3FA dietary supplement shows promising results in the prevention of ICAS.

Intracranial atherosclerotic stenosis (ICAS) is one of the most common causes of stroke worldwide and, in particular, has been implicated as a leading cause of recurrent ischemic stroke. We developed a new rat model to study intracranial atherosclerosis.Twelve-week-old male Sprague-Dawley rats were divided into a control (on a maintain diet) and a high-cholesterol group (on a daily 1% cholesterol diet) for up to 6 weeks. During the first two weeks, NG-nitro-L-arginine methylester (L-NAME, 3 mg/mL) was added to the drinking water in the high-cholesterol group to induce intimal changes making the rats susceptible to atherosclerosis. Blood lipids, including low-density lipoprotein (LDL), cholesterol (CHO), triglycerides (TG), and high-density lipoprotein (HDL), were measured after 3 and 6 weeks. Histological sections of the brains, including internal carotid artery (ICA), middle cerebral artery (MCA), and basilar artery (BA), were prepared to study intracranial artery morphometry and intimal thickening. The levels of CD68, an inflammatory marker, within the vessel walls as determined by immunohistochemistry were also measured.The high-cholesterol diet increased the levels of classic blood markers of atherosclerosis, LDL, CHO, and TG as well as decreased HDL, which became progressively more intensive with time. Rats showed increased intimal thickening in the ICA, MCA, and BA. This protocol also increased the levels of CD68 immunoreactivity within the vessel walls.A rat model of intracranial atherosclerosis was effectively developed by high-cholesterol diet and L-NAME administration. This clinically relevant model would be beneficial for studying ICAS.