Harnessing landrace diversity empowers wheat breeding.

Harnessing genetic diversity in major staple crops through the development of new breeding capabilities is essential to ensure food security1. Here we examined the genetic and phenotypic diversity of the A.E. Watkins landrace collection2 of bread wheat (Triticum aestivum), a major global cereal, through whole-genome re-sequencing (827 Watkins landraces and 208 modern cultivars) and in-depth field evaluation spanning a decade. We discovered that modern cultivars are derived from just two of the seven ancestral groups of wheat and maintain very long-range haplotype integrity. The remaining five groups represent untapped genetic sources, providing access to landrace-specific alleles and haplotypes for breeding. Linkage disequilibrium (LD) based haplotypes and association genetics analyses link Watkins genomes to the thousands of high-resolution quantitative trait loci (QTL), and significant marker-trait associations identified. Using these structured germplasm, genotyping and informatics resources, we revealed many Watkins-unique beneficial haplotypes that can confer superior traits in modern wheat. Furthermore, we assessed the phenotypic effects of 44,338 Watkins-unique haplotypes, introgressed from 143 prioritised QTL in the context of modern cultivars, bridging the gap between landrace diversity and current breeding. This study establishes a framework for systematically utilising genetic diversity in crop improvement to achieve sustainable food security.

Identification of QTL related to anther color and hull color by RAD sequencing in a RIL population of Setaria italica.

BACKGROUND: Foxtail millet (Setaria italica) is one of the oldest domesticated crops and has been considered as an ideal model plant for C4 grasses. It has abundant type of anther and hull colors which is not only a most intuitive morphological marker for color selection in seed production, but also has very important biological significance for the study of molecular mechanism of regulating the synthesis and metabolism of flavonoids and lignin. However, only a few genetic studies have been reported for anther color and hull color in foxtail millet. RESULTS: Quantitative trait loci (QTL) analysis for anther color and hull color was conducted using 400 F6 and F7 recombinant inbreed lines (RILs) derived from a cross between parents Yugu18 and Jigu19. Using restriction-site associated DNA sequencing, 43,001 single-nucleotide polymorphisms (SNPs) and 3,022 indels were identified between both the parents and the RILs. A total of 1,304 bin markers developed from the SNPs and indels were used to construct a genetic map that spanned 2196 cM of the foxtail millet genome with an average of 1.68 cM/bin. Combined with this genetic map and the phenotypic data observed in two locations for two years, two QTL located on chromosome 6 (Chr6) in a 1.215-Mb interval (33,627,819-34,877,940 bp) for anther color (yellow - white) and three QTL located on Chr1 in a 6.23-Mb interval (1-6,229,734 bp) for hull color (gold-reddish brown) were detected. To narrow the QTL regions identified from the genetic map and QTL analysis, we developed a new method named "inconsistent rate analysis" and efficiently narrowed the QTL regions of anther color into a 60-kb interval (34.13-34.19 Mb) in Chr6, and narrowed the QTL regions of hull color into 70-kb (5.43-5.50 Mb) and 30-kb (5.69-5.72 Mb) intervals in Chr1. Two genes (Seita.6G228600.v2.2 and Seita.6G228700.v2.2) and a cinnamyl alcohol dehydrogenase (CAD) gene (Seita.1G057300.v2.2) with amino acid changes between the parents detected by whole-genome resequencing were identified as candidate genes for anther and hull color, respectively. CONCLUSIONS: This work presents the related QTL and candidate genes of anther and hull color in foxtail millet and developed a new method named inconsistent rate analysis to detect the chromosome fragments linked with the quality trait in RILs. This is the first study of the QTL related to hull color in foxtail millet and clarifying that the CAD gene (Seita.1G057300.v2.2) is the key gene responsible for this trait. It lays the foundation for further cloning of the functional genes and provides a powerful tool to detect the chromosome fragments linked with quality traits in RILs.

Microstructure and properties of SiC ceramic brazed with Zr-Cu composite filler metal.

The microstructure and properties of SiC ceramic brazed with Zr-Cu composite filler metal were investigated. Combined with the brazing experiment, the microstructure of the interface reaction layer and the brazed SiC ceramic joint was analyzed, and the shear strength was used to evaluate the mechanical properties of the joint. The results show that both Zr-Cu + SiCp and Zr-Cu + Mo composite filler metals can braze SiC ceramic, and the products of the interface reaction layer are mainly ZrC and Zr2Si. The addition of SiCp and Mo to Zr-Cu-based composite filler metal improves the nuclear properties of the composite filler metal and its joint, reduces the coefficient of thermal expansion of the composite filler metal and SiC ceramic joint, and improves the mechanical properties of the joint. The shear properties of the joint increase with the increase of the content of SiCp and Mo in the Zr-Cu composite filler metals. The shear strength of the joint reaches the maximum (82 MPa) when the content of SiC particles is 10 vol% of the Zr-Cu + SiCp composite filler metal, and the average value of the shear strength reaches the maximum of 74 MPa when the content of Mo is 6 vol% of the Zr-Cu + Mo composite filler metal.

Inhibition of extracellular signal-regulated kinase 1 by adenovirus mediated small interfering RNA attenuates hepatic fibrosis in rats.

UNLABELLED: Extracellular signal-regulated kinase 1 (ERK1) is a critical part of the mitogen-activated protein kinase signal transduction pathway, which is involved in hepatic fibrosis. However, the effect of down-regulation of ERK1 on hepatic fibrosis has not been reported. Here, we induced hepatic fibrosis in rats with dimethylnitrosamine administration or bile duct ligation. An adenovirus carrying small interfering RNA targeting ERK1 (AdshERK1) was constructed to determine its effect on hepatic fibrosis, as evaluated by histological and immunohistochemical examination. Our results demonstrated that AdshERK1 significantly reduced the expression of ERK1 and suppressed proliferation and levels of fibrosis-related genes in hepatic stellate cells in vitro. More importantly, selective inhibition of ERK1 remarkably attenuated the deposition of the extracellular matrix in fibrotic liver in both fibrosis models. In addition, both hepatocytes and biliary epithelial cells were proven to exert the ability to generate the myofibroblasts depending on the insults of the liver, which were remarkably reduced by AdshERK1. Furthermore, up-regulation of ERK1 paralleled the increased expression of transforming growth factor beta1 (TGF-beta1), vimentin, snail, platelet-derived growth factor-BB (PDGF-BB), bone morphogenetic protein 4 (BMP4), and small mothers against decapentaplegic-1 (p-Smad1), and was in reverse correlation with E-cadherin in the fibrotic liver. Nevertheless, inhibition of ERK1 resulted in the increased level of E-cadherin in parallel with suppression of TGF-beta1, vimentin, snail, PDGF-BB, BMP4, and p-Smad1. Interestingly, AdshERK1 treatment promoted hepatocellular proliferation. CONCLUSION: Our study provides the first evidence for AdshERK1 suppression of hepatic fibrosis through the reversal of epithelial-mesenchymal transition of both hepatocytes and biliary epithelial cells without interference of hepatocellular proliferation. This suggests that ERK1 is implicated in hepatic fibrogenesis and selective inhibition of ERK1 by small interfering RNA may present a novel option for hepatic fibrosis treatment.

[Genetic analysis of HAV strains isolated from patients with acute hepatitis in Hebei Shijiazhuang of China].

OBJECTIVE: To characterize the hepatitis A virus (HAV) wild type strains circulating in Hebei Shijiazhuang of China during 2005-2007, to provide the bases for further investigation of the sources of HAV infection. METHODS: The VP1/P2A junction regions were detected by RT-PCR from HAV IgM positives serum samples during 2005 and 2007, the 34 RT-PCR positive samples were sequenced and subjected to phylogenetic analysis by Neighbor Joining (NJ) method. RESULTS: All the detected HAV strains were identified as sub-genotype I A, the homology of nucleotide sequence in the VP1-2A imation region ranged from 95%-100%, the amino acid sequences of HAV strains almost had no difference. CONCLUSION: There are different HAV strains existing in Hebei Shijiazhuang of China, same HAV strain may exist in different areas; or in one area, identical or different HAV strains may be detected. This work provides the bases for further investigation of the sources of HAV infection and also for effectively control measures to prevent the spread of the disease.

Differentiation therapy of hepatocellular carcinoma in mice with recombinant adenovirus carrying hepatocyte nuclear factor-4alpha gene.

UNLABELLED: Previous studies have shown that hepatocyte nuclear factor-4alpha (HNF4alpha) is a central regulator of differentiated hepatocyte phenotype and forced expression of HNF4alpha could promote reversion of tumors toward a less invasive phenotype. However, the effect of HNF4alpha on cancer stem cells (CSCs) and the treatment of hepatocellular carcinoma (HCC) with HNF4alpha have not been reported. In this study, an adenovirus-mediated gene delivery system, which could efficiently transfer and express HNF4alpha, was generated to determine its effect on hepatoma cells (Hep3B and HepG2) in vitro and investigate the anti-tumor effect of HNF4alpha in mice. Our results demonstrated that forced re-expression of HNF4alpha induced the differentiation of hepatoma cells into hepatocytes, dramatically decreased "stemness" gene expression and the percentage of CD133(+) and CD90(+) cells, which are considered as cancer stem cells in HCC. Meanwhile, HNF4alpha reduced cell viability through inducing apparent apoptosis in Hep3B, while it induced cell cycle arrest and cellular senescence in HepG2. Moreover, infection of hepatoma cells by HNF4alpha abolished their tumorigenesis in mice. Most interestingly, systemic administration of adenovirus carrying the HNF4alpha gene protected mice from liver metastatic tumor formation, and intratumoral injection of HNF4alpha also displayed significant antitumor effects on transplanted tumor models. CONCLUSION: The striking suppression effect of HNF4alpha on tumorigenesis and tumor development is attained by inducing the differentiation of hepatoma cells--especially CSCs--into mature hepatocytes, suggesting that differentiation therapy with HNF4alpha may be an effective treatment for HCC patients. Our study also implies that differentiation therapy may present as one of the best strategies for cancer treatment through the induction of cell differentiation by key transcription factors.