Trichoderma harzianum strain SQR-T37 and its bio-organic fertilizer could control Rhizoctonia solani damping-off disease in cucumber seedlings mainly by the mycoparasitism

Damping-off disease is caused by Rhizoctonia solani and leads to serious loss in many crops. Biological control is an efficient and environmentally friendly way to prevent damping-off disease. Optical micrographs, scanning electron micrographs, and the determination of hydrolytic enzymes were used to investigate the antagonism of Trichoderma harzianum SQR-T37 (SQR-T37) against R. solani. Experiments were performed in pots to assess the in vivo disease-control efficiency of SQR-T37 and bio-organic fertilizer. The results indicate that the mycoparasitism was the main mechanism accounting for the antagonistic activity of SQR-T37. In one experiment, the population of R. solani was decreased from 10⁶ internal transcribed spacer (ITS) copies per gram soil to 10⁴ ITS copies per gram soil by the presence of the antagonist. In this experiment, 45% of the control efficiency was obtained when 8 g of SQR-T37 hyphae per gram soil was applied. In a second experiment, as much as 81.82% of the control efficiency was obtained when bio-organic fertilizer (SQR-T37 fermented organic fertilizer, BIO) was applied compared to only 27.27% of the control efficiency when only 4 g of SQR-T37 hyphae per gram soil was applied. Twenty days after incubation, the population of T. harzianum was 4.12 × 10⁷ ITS copies per gram soil in the BIO treatment, which was much higher than that in the previous treatment (8.77 × 10⁵ ITS copies per gram soil), where only SQR-T37 was applied. The results indicated that SQR-T37 was a potent antagonist against R. solani in a mycoparasitic way that decreased the population of the pathogen. Applying BIO was more efficient than SQR-T37 application alone because it stabilized the population of the antagonist.     

Intentionally introduced species: more easily invited than removed

Alien species are brought into countries world wide on a massive scale for agricultural production, ex situ conservation, landscape aesthetics, gardens, and ecosystem restoration. Unfortunately, some of these species have escaped and adversely impacted on regional as well as global biodiversity conservation and agricultural production. To reduce such risks, it is necessary to implement specific and effective measures. Since various government departments and institutions are involved in the management of alien species, it is difficult to prevent native and agroecosystems from being invaded by invited species. We propose the establishment of a supervision and inspection continuum over intentional species introduction, similar to that which exists in some countries over unintentional species introductions. Namely, a justification of the necessity to import, a risk assessment, assurances as to provision of an adequate containment facility assessment, and a damage-limitation protocol should that need to be invoked. These requirements should be satisfied before an alien species is knowingly imported, and the necessary follow-up supervision is important post- importation.     

A comprehensive gene network for fine tuning floral development in poplar

Herbaceous model species, especially Arabidopsis has provided a wealth of information about the genes involved in floral induction and development of inflorescences and flowers. While the genus Populus is an important model system for the molecular biology of woody plant. These two genuses differ in many ways. This study was designed to improve understanding of flower development in poplar at a system level, as its regulatory pathway to a large extent remains poorly known, owing to the presently limited mutant pool. To address this issue, a poplar GeneChip was employed to detect genes expressed during the whole floral developmental process. Using the expressed floral genes, a systematic gene network was constructed with the aid of functional association with Arabidopsis. The results suggested that autonomous, gibberellin, vernalization, photoperiod, ethylene, brassinosteroid, stress-induced and floral suppression pathways are involved in poplar flowering. Modularity analysis revealed several pathways in common with Arabidopsis, such as autonomous, gibberellin, vernalization and photoperiod pathways. In addition, brassinosteroid, stress-induced and floral suppression pathways were implicated as additional novel pathways. Notably, a difference in vernalization between Arabidopsis and poplar was revealed. Autonomous, gibberellin, vernalization, photoperiod, ethylene, brassinosteroid, stress-induced and floral suppression pathways integrated into a systematic gene network in floral development of poplar. Compared to Arabidopsis, brassinosteroid, stress-induced and floral suppression pathways are additional in poplar, and FLC is absent in vernalization pathway in poplar. Preliminary conclusions drawn here provide a basis for both identification of key genes and elucidation of molecular mechanisms involved in poplar floral development.     

Iron metabolism in diabetes-induced Alzheimer’s disease: a focus on insulin resistance in the brain

Alzheimer’s disease (AD) is characterized by an excessive accumulation of toxic amyloid beta (Aβ) plaques and memory dysfunction. The onset of AD is influenced by age, genetic background, and impaired glucose metabolism in the brain. Several studies have demonstrated that diabetes involving insulin resistance and glucose tolerance could lead to AD, ultimately resulting in cognitive dysfunction. Even though the relationship between diabetes and AD was indicated by significant evidences, the critical mechanisms and metabolic alterations in diabetes induced AD are not clear until now. Recently, iron metabolism has been shown to play multiple roles in the central nervous system (CNS). Iron deficiency and overload are associated with neurodegenerative diseases. Iron binds to Aβ and subsequently regulates Aβ toxicity in the CNS. In addition, previous studies have shown that iron is involved in the aggravation of insulin resistance. Considering these effects of iron metabolism in CNS, we expect that iron metabolism may play crucial roles in diabetic AD brain. Thus, we review the recent evidence regarding the relationship between diabetes-induced AD and iron metabolism.     

Genetic differentiation between populations of swimming crab <Emphasis Type="Italic">Portunus trituberculatus</Emphasis> along the coastal waters of the East China Sea

Portunus trituberculatus is a commercially important species widely spread in the East China Sea. Intraspecific variation of the mitochondrial DNA cytochrome oxidase subunit I (mtDNA COI) gene was investigated in 213 individuals from six localities (Changjiang Estuary, Shengsi Islands, Zhoushan Islands, Dongtou Islands, Dinghai Bay, and Quanzhou Bay) ranging from north (31°21′N) to south (24°55′N) coastal waters of the East China Sea. Overall, a total of 27 mtDNA haplotypes and 21 variable sites were detected in the 787 bp segment of COI gene. Analysis of mtDNA COI sequence data revealed that crabs from the six localities were characterized by moderately high haplotypic diversity (h = 0.787 ± 0.026), while sequence divergence values between haplotypes were relatively low (π = 0.00241 ± 0.00098). Each population was characterized by a single most frequent haplotype, shared among all six localities, and a small number of rare ones, typically present in only one or two individuals and representative of a specific population. However, neither the neighbor-joining tree nor the minimum spanning network (MSN) based on the haplotype data exhibited geographical patterns of the six populations. Mismatch distribution analysis of P. trituberculatus individuals sampled from the six localities suggested that sudden population expansion might have occurred in CJ and SS population that might be consistent with over-exploitation of the swimming crab. Analysis of molecular variance (AMOVA) and F _ST statistics showed that significant genetic differentiation existed among the SS, ZS, DT, DH, and QZ populations, suggesting that gene flow might be reduced, even between the geographically close sites, despite the high potential of dispersal. The possible causes of the observed genetic heterogeneity among the P. trituberculatus populations and the potential applications of the mtDNA COI marker in the artificial breeding and fisheries management are discussed. Handling editor: C. Sturmbauer     

Targeting IFN-alpha to B cell lymphoma by a tumor-specific antibody elicits potent antitumor activities

IFN-alpha, a cytokine crucial for the innate immune response, also demonstrates antitumor activity. However, use of IFN-alpha as an anticancer drug is hampered by its short half-life and toxicity. One approach to improving IFN-alpha's therapeutic index is to increase its half-life and tumor localization by fusing it to a tumor-specific Ab. In the present study, we constructed a fusion protein consisting of anti-HER2/neu-IgG3 and IFN-alpha (anti-HER2/neu-IgG3-IFN-alpha) and investigated its effect on a murine B cell lymphoma, 38C13, expressing human HER2/neu. Anti-HER2/neu-IgG3-IFN-alpha exhibited potent inhibition of 38C13/HER2 tumor growth in vivo. Administration of three daily 1-microg doses of anti-HER2/neu-IgG3-IFN-alpha beginning 1 day after tumor challenge resulted in 88% of the mice remaining tumor free. Remarkably, anti-HER2/neu-IgG3-IFN-alpha demonstrated potent activity against established 38C13/HER2 tumors, with complete tumor remission observed in 38% of the mice treated with three daily doses of 5 microg of the fusion protein (p = 0.0001). Ab-mediated targeting of IFN-alpha induced growth arrest and apoptosis of lymphoma cells contributing to the antitumor effect. The fusion protein also had a longer in vivo half-life than rIFN-alpha. These results suggest that IFN-alpha Ab fusion proteins may be effective in the treatment of B cell lymphoma.     

Endostatin gene therapy enhances the efficacy of paclitaxel to suppress breast cancers and metastases in mice

Chemotherapy combined with antiangiogenic therapy is more effective than chemotherapy alone. The aim of this study was to investigate whether endostatin, a potent anti-angiogenic agent, could enhance the efficacy of paclitaxel to combat breast cancer. An expression plasmid encoding mouse endostatin (End-pcDNA3.1) was constructed, which produced intense expression of endostatin and inhibited angiogenesis in the chorioallantoic membrane assay. 4T1 breast tumors were established in BALB/c mice by subcutaneous injection of 1 × 10⁵ 4T1 cells. The End-pcDNA3.1 plasmid diluted in the transfection reagent FuGENE^TM was injected into the tumors (around 100 mm²), and paclitaxel was injected i.p. into the mice. Endostatin gene therapy synergized with paclitaxel in suppressing the growth of 4T1 tumors and their metastasis to the lung and liver. Both endostatin and paclitaxel inhibited tumor angiogenesis and induced cell apoptosis. Despite the finding that endostatin was superior to paclitaxel at inhibiting tumor angiogenesis, paclitaxel was nevertheless more effective at inducing tumor apoptosis. The combination of paclitaxel and endostatin was more effective in suppressing tumor growth, metastases, angiogenesis, and inducing apoptosis than the respective monotherapies. The combinational therapy with endostatin and paclitaxel warrants future investigation as a therapeutic strategy to combat breast cancer.