Parastagonospora nodorum is an important pathogen of wheat. The contribution of secondary metabolites to this pathosystem is poorly understood. A biosynthetic gene cluster (SNOG_08608-08616) has been shown to be upregulated during the late stage of P. nodorum wheat leaf infection. The gene cluster shares several homologues with the Cercospora nicotianae CTB gene cluster encoding the biosynthesis of cercosporin. Activation of the gene cluster by overexpression (OE) of the transcription factor gene (SNOG_08609) in P. nodorum resulted in the production of elsinochrome C, a perelyenequinone phytotoxin structurally similar to cercosporin. Heterologous expression of the polyketide synthase gene elcA from the gene cluster in Aspergillus nidulans resulted in the production of the polyketide precursor nortoralactone common to the cercosporin pathway. Elsinochrome C could be detected on wheat leaves infected with P. nodorum, but not in the elcA disruption mutant. The compound was shown to exhibit necrotic activity on wheat leaves in a light-dependent manner. Wheat seedling infection assays showed that ΔelcA exhibited reduced virulence compared with wild type, while infection by an OE strain overproducing elsinochrome C resulted in larger lesions on leaves. These data provided evidence that elsinochrome C contributes to the virulence of P. nodorum against wheat.
To distinguish the immune genes with low-level expression in HBV-induced HCC, but high-level expression in HCV-induced HCC, the concept of distinction immune gene is proposed. A filter is then designed to screen these genes. By using gene positive network with strong correlations between genes, the genes are further filtered to form the set of key distinction immune genes. The 23 key distinction immune genes are screened, which are divided into four clusters, T cells, B cells, immune signalling and major histocompatibility complex. It is evident that the screened genes are important immune genes, which are activated in HCV-induced HCC, but inactivated in HBV-induced HCC. In HCV-induced HCC, the structures of HCV adaptively update, so that they are difficult to be identified by antigens. Therefore, the clinic advice is either to increase the update speed of antigens or reduce the update speed of the viruses during the treatment of HCV-induced HCC. Moreover, it is also advised to add T cells or add the expression levels of T cells to strengthen the ability to kill cancer cells. In contrast, HBV updates slowly, but the immunity system in HBV-induced HCC has been damaged seriously. As a result, the clinic advice is to improve the immune ability of patients subjected to HBV-induced HCC, such as increasing immunoglobulin, T cells and B cells and so forth.
A non-linear kinetic model to predict the consumption of different sugars (glucose, fructose and sucrose) as a substrate, during an apple wine yeast fermentation with Saccharomyces cerevisiae strain CCTCC M201022 is proposed. This model was used to predict sugar utilization by this yeast beginning at various initial sugar concentrations. After observation of the experimental data, a model based on the logistic equation of yeast growth, growthassociated production of ethanol with a lag time, and consumption of sugars for biomass formation and maintenance, was developed. After experimental model fitting, kinetic parameters in the model were estimated. The experimental verification of the model was performed using flask-scale fermentations, and the model obtained predicted the fermentation performance effectively, using different sugars as the substrate set at various initial sugar concentrations. Based on estimated kinetic parameters and the characteristics of sugar utilization, the yeast examined appeared to be glucophilic. The effects of different sugars with various initial concentrations on the fermentation performance by this yeast were investigated, and some applications of kinetic parameters are discussed.
The hancockiamides are an unusual new family of N-cinnamoylated piperazines from the Australian soil fungus Aspergillus hancockii, originating from mixed nonribosomal peptide and phenylpropanoid pathways.
Vaccination with attenuated live varicella zoster virus (VZV) can prevent zoster reactivation, but protection is incomplete especially in an older population. To decipher the molecular mechanisms underlying variable vaccine responses, T- and B-cell responses to VZV vaccination were examined in individuals of different ages including identical twin pairs. Contrary to the induction of VZV-specific antibodies, antigen-specific T cell responses were significantly influenced by inherited factors. Diminished generation of long-lived memory T cells in older individuals was mainly caused by increased T cell loss after the peak response while the expansion of antigen-specific T cells was not affected by age. Gene expression in activated CD4 T cells at the time of the peak response identified gene modules related to cell cycle regulation and DNA repair that correlated with the contraction phase of the T cell response and consequently the generation of long-lived memory cells. These data identify cell cycle regulatory mechanisms as targets to reduce T cell attrition in a vaccine response and to improve the generation of antigen-specific T cell memory, in particular in an older population.
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