Antagonism of Aspergillus terreus to Sclerotinia sclerotiorum.

An Aspergillus terreus strain showed in vitro antagonistic activity against tha plant pathogens Sclerotinia sclerotiorum (Lib.) de Bary.The interacton between A. terreus and sclerotia revealed that the mycoparasite sporulated abundantly on the sclerotial surface. Cell breakdown due to host cell wall disruption was observed in inner rind cells, by a scanning electron microscopy

Mycoparasitic nature of Bionectria sp. strain 6.21.

Abstract: In this study, a Bionectria sp. strain isolated from citrus rhizosphere was evaluated for its potential in inhibiting the growth of Rhizoctonia solani and Pythium aphanidermatum. It was demonstrated that Bionectria sp. 6.21 inhibited the growth of P. aphanidermatum and R. solani. In dual cultures, however, the antagonist only parasitised R. solani. Regarding the assay involving P. aphanidermatum, a lack of mycoparasitic ability was demonstrated. Crude extract of Bionectria completely inhibited the mycelial growth of both fungi. It appears that the main mechanism involved in the antagonism of Pythium by Bionectria is through antibiotic production. The antagonistic fungus released extracellular secondary metabolites. The metabolites were found to be inhibitory to both plant pathogenic fungi. From the crude extract, eleven fractions were obtained and tested for their antifungal properties. Two of them showed very strong activity against P. aphanidermatum. The obtained results indicated that this biocontrol agent has both antibiotic and mycoparasitic properties. On the other hand, evidence obtained from Scanning Electron Microscopy (SEM) suggests the involvement of an enzymatic process, with enzymatic digestion playing a major role in the parasitism of Bionectria sp. 6.21. In conclusion, these results provide evidence that mainly due to mycoparasitism, this strain has the potential to become a good candidate for biological control

Cell loss in the motor and cingulate cortex correlates with symptomatology in Huntington's disease

Huntington's disease is an autosomal dominant inherited neurodegenerative disease with motor symptoms that are variably co-expressed with mood and cognitive symptoms, and in which variable neuronal degeneration is also observed in the basal ganglia and the cerebral cortex. We have recently shown that the variable symptomatology in Huntington's disease correlates with the variable compartmental pattern of GABAA receptor and cell loss in the striatum. To determine whether the phenotypic variability in Huntington's disease is also related to variable neuronal degeneration in the cerebral cortex, we undertook a double-blind study using unbiased stereological cell counting methods to determine the pattern of cell loss in the primary motor and anterior cingulate cortices in the brains of 12 cases of Huntington's disease and 15 controls, and collected detailed data on the clinical symptomatology of the patients with Huntington's disease from family members and clinical records. The results showed a significant association between: (i) pronounced motor dysfunction and cell loss in the primary motor cortex; and (ii) major mood symptomatology and cell loss in the anterior cingulate cortex. This association held for both total neuronal loss (neuronal N staining) and pyramidal cell loss (SMI32 staining), and also correlated with marked dystrophic changes in the remaining cortical neurons. There was also an association between cortical cell loss and striatal neuropathological grade, but no significant association with CAG repeat length in the Huntington's disease gene. These findings suggest that the heterogeneity in clinical symptomatology that characterizes Huntington's disease is associated with variation in the extent of cell loss in the corresponding functional regions of the cerebral cortex whereby motor dysfunction correlates with primary motor cortex cell loss and mood symptomatology is associated with cell loss in the cingulate corte

Tracking extra-celullar enzyme production by Trichoderma harzianum in the rhizosphere.

The exact role of extracellular enzyme production in the activities of Trichoderma harzianum as a biological control agent are much debated. Production of such enzymes as cellulase, proteinase, endoglucanase, (glucosidase and chitinase has been linked to biological control in vitro experiments (Elad et al, 1982, Ahmad & Baker, 1988 a,b) bur it has been difficult to prove that these enzymes are important in vivo. Baker (1991) demonstrated that mutant strains of Trichoderma with improved rhizosphere competence had higher extracellular cellulase production than wild types strains, and he speculated that enhanced cellulase production might lead to better utilisation of rhizosphere substrates and thus improved colonisation of the resource. However, it has been recently shown that rhizosphere competence of Trichoderma strains is not always associated with improved in vitro production of extracellular enzymes (de Melo, Faull, J, L, and Graeme-Cook, 1997). In order to extend this work to the soil environment we have developed a sensitive, quantifiable assay for extracellular enzymes that uses a fluorescent substrate to detect enzyme activity in soil. Using a number of different strains of Trichoderma with known in vitro extra-cellular enzyme production patterns (both high and low) we will demonstrate differences in the production of enzymes in the rhizosphere with varying soil depth. We will attempt to relate these differences to the root colonisation ability of the Trichoderma strain

Cell loss in the motor and cingulate cortex correlates with symptomatology in Huntington's disease

Huntington's disease is an autosomal dominant inherited neurodegenerative disease with motor symptoms that are variably co-expressed with mood and cognitive symptoms, and in which variable neuronal degeneration is also observed in the basal ganglia and the cerebral cortex. We have recently shown that the variable symptomatology in Huntington's disease correlates with the variable compartmental pattern of GABA(A) receptor and cell loss in the striatum. To determine whether the phenotypic variability in Huntington's disease is also related to variable neuronal degeneration in the cerebral cortex, we undertook a double-blind study using unbiased stereological cell counting methods to determine the pattern of cell loss in the primary motor and anterior cingulate cortices in the brains of 12 cases of Huntington's disease and 15 controls, and collected detailed data on the clinical symptomatology of the patients with Huntington's disease from family members and clinical records. The results showed a significant association between: (i) pronounced motor dysfunction and cell loss in the primary motor cortex; and (ii) major mood symptomatology and cell loss in the anterior cingulate cortex. This association held for both total neuronal loss (neuronal N staining) and pyramidal cell loss (SMI32 staining), and also correlated with marked dystrophic changes in the remaining cortical neurons. There was also an association between cortical cell loss and striatal neuropathological grade, but no significant association with CAG repeat length in the Huntington's disease gene. These findings suggest that the heterogeneity in clinical symptomatology that characterizes Huntington's disease is associated with variation in the extent of cell loss in the corresponding functional regions of the cerebral cortex whereby motor dysfunction correlates with primary motor cortex cell loss and mood symptomatology is associated with cell loss in the cingulate cortex

The structural basis for Z α1-antitrypsin polymerization in the liver

The serpinopathies are among a diverse set of conformational diseases that involve the aberrant self-association of proteins into ordered aggregates. α1-Antitrypsin deficiency is the archetypal serpinopathy and results from the formation and deposition of mutant forms of α1-antitrypsin as “polymer” chains in liver tissue. No detailed structural analysis has been performed of this material. Moreover, there is little information on the relevance of well-studied artificially induced polymers to these disease-associated molecules. We have isolated polymers from the liver tissue of Z α1-antitrypsin homozygotes (E342K) who have undergone transplantation, labeled them using a Fab fragment, and performed single-particle analysis of negative-stain electron micrographs. The data show structural equivalence between heat-induced and ex vivo polymers and that the intersubunit linkage is best explained by a carboxyl-terminal domain swap between molecules of α1-antitrypsin

mTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype

Senescent cells secrete a combination of factors collectively known as the senescence-associated secretory phenotype (SASP). The SASP reinforces senescence and activates an immune surveillance response, but it can also show pro-tumorigenic properties and contribute to age-related pathologies. In a drug screen to find new SASP regulators, we uncovered the mTOR inhibitor rapamycin as a potent SASP suppressor. Here we report a mechanism by which mTOR controls the SASP by differentially regulating the translation of the MK2 (also known as MAPKAPK2) kinase through 4EBP1. In turn, MAPKAPK2 phosphorylates the RNA-binding protein ZFP36L1 during senescence, inhibiting its ability to degrade the transcripts of numerous SASP components. Consequently, mTOR inhibition or constitutive activation of ZFP36L1 impairs the non-cell-autonomous effects of senescent cells in both tumour-suppressive and tumour-promoting contexts. Altogether, our results place regulation of the SASP as a key mechanism by which mTOR could influence cancer, age-related diseases and immune responses

Cornish identities and migration: a multi-scalar approach

The definitive version is available at www.blackwell-synergy.com. 24 month embargo by the publisher. Article will be released July 2009.In this article we argue that theories of transnationalism have value in exploring the historical context of migration and that historical contexts help to shape such theoretical conceptualizations. Historians of migration have now begun to engage more directly with the literature of transnationalism, focusing on the networks that linked settler and home communities. Here we add to this by examining a nineteenth-century migrant community from a British region through the lens of transnationalism, applying the concept to the case of the Cornish, whose economic specialization produced culturally distinct Cornish communities on the mining frontiers of North America, Australia and South Africa. In doing so, we bring together the issues of scale and time. We review the multiple levels of the Cornish transnational space of the late nineteenth century, which exhibited aspects of both core transnationalism and translocalism. This waned, but in the later twentieth century, a renewed interest in a transnational Cornish identity re-emerged, articulating with changing identity claims in Cornwall itself. To capture better the experience of the Cornish over these two very different phases of transnationalism we identify another subset of transnationalism - that of transregionalism.Leverhulme Trus