Publications
NIBIOs employees contribute to several hundred scientific articles and research reports every year. You can browse or search in our collection which contains references and links to these publications as well as other research and dissemination activities. The collection is continously updated with new and historical material.
2012
Authors
Carl Gunnar Fossdal Nina Elisabeth Nagy Ari Hietala Harald Kvaalen Rune Slimestad Steve Woodward Halvor SolheimAbstract
No abstract has been registered
Authors
Igor A. Yakovlev Gustav Vaaje-Kolstad Ari Hietala Emil Stefanczyk Halvor Solheim Carl Gunnar FossdalAbstract
No abstract has been registered
Authors
Åke Olson Andrea Aerts Fred Asiegbu Lassaad Belbahri Ourdia Bouzid Anders Broberg Björn Canback Pedro M. Coutinho Dan Cullen Kerstin Dalman Giuliana Deflorio Linda T.A. van Diepen Christophe Dunand Sébastien Duplessis Mikael Durling Paolo Gonthier Jane Grimwood Carl Gunnar Fossdal David Hansson Bernard Henrissat Ari Hietala Kajsa Himmelstrand Dirk Hoffmeister Nils Högberg Timothy Y. James Magnus Karlsson Annegret Kohler Ursula Kües Yong-Hwan Lee Yao-Cheng Lin Mårten Lind Erika Lindquist Vincent Lombard Susan Lucas Karl Lundén Emmanuelle Morin Claude Murat Jongsun Park Tommaso Raffaello Pierre Rouzé Asaf Salamov Jeremy Schmutz Halvor Solheim Jerry Ståhlberg Heriberto Vélëz Ronald P. de Vries Ad Wiebenga Steve Woodward Igor A. Yakovlev Matteo Garbelotto Francis Martin Igor V. Grigoriev Jan StenlidAbstract
• Parasitism and saprotrophic wood decay are two fungal strategies fundamental for succession and nutrient cycling in forest ecosystems. An opportunity to assess the trade-off between these strategies is provided by the forest pathogen and wood decayer Heterobasidion annosum sensu lato. • We report the annotated genome sequence and transcript profiling, as well as the quantitative trait loci mapping, of one member of the species complex: H. irregulare. Quantitative trait loci critical for pathogenicity, and rich in transposable elements, orphan and secreted genes, were identified. • A wide range of cellulose-degrading enzymes are expressed during wood decay. By contrast, pathogenic interaction between H. irregulare and pine engages fewer carbohydrate-active enzymes, but involves an increase in pectinolytic enzymes, transcription modules for oxidative stress and secondary metabolite production. • Our results show a trade-off in terms of constrained carbohydrate decomposition and membrane transport capacity during interaction with living hosts. Our findings establish that saprotrophic wood decay and necrotrophic parasitism involve two distinct, yet overlapping, processes.
Authors
Nina Elisabeth Nagy Simon Ballance Harald Kvaalen Carl Gunnar Fossdal Halvor Solheim Ari HietalaAbstract
Heterobasidion parviporum, a common pathogenic white-rot fungus in managed Norway spruce forests in northern and central Europe, causes extensive decay columns within stem heartwood of the host tree. Infected trees combat the lateral spread of decay by bordering the heartwood with a fungistatic reaction zone characterized by elevated pH and phenol content. To examine the mode of fungal feeding in the reaction zone of mature Norway spruce trees naturally infected by H. parviporum, we conducted spatial proWling of pectin and hemicellulose composition, and established transcript levels of candidate fungal genes encoding enzymes involved in degradation of the diVerent cell wall components of wood. Colonized inner heartwood showed pectin and hemicellulose concentrations similar to those of healthy heartwood, whereas the carbohydrate proWles of compromised reaction zone, irrespective of the age of fungal activity in the tissue, indicated selective fungal utilization of galacturonic acid, arabinose, xylose and mannose. These data show that the rate of wood decay in the reaction zone is slow. While the up-regulation of genes encoding pectinases and hemicellulases preceded that of the endoglucanase gene during an early phase of fungal interaction with xylem defense, the manganese peroxidase gene showed similar transcript levels during diVerent phases of wood colonization. It seems plausible that the reaction zone components of Norway spruce interfere with both lignin degradation and the associated co-hydrolysis of hemicelluloses and pectin, resulting in a prolonged phase of selective decay.
Authors
Nina Elisabeth Nagy Harald Kvaalen Monica Fongen Carl Gunnar Fossdal Nicholas Clarke Halvor Solheim Ari HietalaAbstract
Pathogen challenge of tree sapwood induces the formation of reaction zones with antimicrobial properties such as elevated pH and cation content. Many fungi lower substrate pH by secreting oxalic acid, its conjugate base oxalate being a reductant as well as a chelating agent for cations. To examine the role of oxalic acid in pathogenicity of white-rot fungi, we conducted spatial quantification of oxalate, transcript levels of related fungal genes, and element concentrations in heartwood of Norway spruce challenged naturally by Heterobasidion parviporum. In the pathogen-compromised reaction zone, upregulation of an oxaloacetase gene generating oxalic acid coincided with oxalate and cation accumulation and presence of calcium oxalate crystals. The colonized inner heartwood showed trace amounts of oxalate. Moreover, fungal exposure to the reaction zone under laboratory conditions induced oxaloacetase and oxalate accumulation, whereas heartwood induced a decarboxylase gene involved in degradation of oxalate. The excess level of cations in defense xylem inactivates pathogen-secreted oxalate through precipitation and, presumably, only after cation neutralization can oxalic acid participate in lignocellulose degradation. This necessitates enhanced production of oxalic acid by H. parviporum. This study is the first to determine the true influence of white-rot fungi on oxalate crystal formation in tree xylem.
Authors
Carl Gunnar Fossdal Ari M. Hietala Igor A. Yakovlev Gustav Vaaje-Kolstad Emil Stefaczyk Halvor SolheimAbstract
The GH61 represents the most enigmatic Glycoside Hydrolase Family (GH) regarding putative enzymatic activity and importance in cellulose degradation. Heterobasidion irregulare is a necrotizing pathogen and white rot fungus, causing enormous damages in conifer forests.The genome of H. irregulare allowed identification of ten HiGH61 genes. qRT-PCR analysis separate the HiGH61 members into two groups; one that show up regulation on lignocellulosic substrates and another that show either down regulation or constitutive expression. This grouping suggests that the fungus relates different sets of GH61s for different substrates, like in the various stages of necrotizing and saprophytic growth on the host.One HiGH61 showed up to 17000 fold increase on spruce heartwood suggesting a pivotal role in cellulose decomposition during saprophytic growth. Sequence analysis of these genes reveals that all GH61s but one possess the conserved metal binding motif predicted to be essential for activity.The sequences also divide into groups having either an insert near the N-terminus or an insert near the second catalytic histidine, which both may represent extensions of the substrate binding surface. Three HiGH61s encode cellulose-binding modules (CBM1), indicating direct targeting of crystalline cellulose, two being up regulated on pure cellulose.There was a common substrate-specific induction patterns of the HiGH61s with several reference cellulolytic and hemicellulolytic GHs, this taken together with their low levels on media lacking lignocellulose, reflect the concerted nature of cell wall polymer degradation.
2011
Abstract
Twenty cypress accessions were tested for freezing tolerance. After freezing to −15°C, differences among cypress accessions were tested by measuring electrolyte leakage and chlorophyll fluorescence. Based on these data, cypress accessions showing contrasting freezing tolerance were subjected to transcript profiling of candidate genes upon the development of cold hardening, with the ultimate goal of providing a scientific basis for selecting/breeding cypress genotypes with higher tolerance to low temperature. Nine different cypress genes were selected: a heat shock protein, a putative chaperonin, a chlorophyll-binding protein, a serine/threonine protein kinase, a putative exonuclease, a dehydrin, and three senescenceassociated proteins. Transcript levels of these genes were profiled during cold hardening under controlled conditions using real-time reverse-transcription-polymerase chain reaction. While the genes showed regulation patterns common to both cypress accessions, in the case of chaperonin, exonuclease, and some senescence-associated proteins, clonal differences in gene regulation were found. The potential relationship of these differences with cold tolerance is discussed.
Abstract
The causative agent of dieback on European ash (Fraxinus excelsior) was first described as Chalara fraxinea based on cultural morphology because no sexual stage of the fungus was known. Later, based on culturing of ascospores of a candidate teleomorph, morphological comparison and nuclear ribosomal internal transcribed spacer sequencing, the sexual stage of C. fraxinea was assigned as Hymenoscyphus albidus, a native and widespread species in Europe. Recently, the morphological species concept of H. albidus was shown to cover two species that cannot be separated from each other based on teleomorph characters, but which can be distinguished by several DNA markers. As a result, the strains causing ash dieback were reassigned as H. pseudoalbidus. The closely related H. albidus is presumably a non-pathogenic endophyte, but pathogenicity tests to confirm this hypothesis have not yet been performed. Genotyping of herbarium specimens has shown that H. pseudoalbidus was present in Switzerland for at least a decade prior to the epidemic outbreak in Europe. The origin of the ash dieback pathogen, and the general importance of correct pathogen identification to development of effective disease control, are discussed.
Abstract
No abstract has been registered
Abstract
Dieback of European ash (Fraxinus excelsior), caused by the ascomycete Hymenoscyphus pseudoalbidus (anamorph Chalara fraxinea), started around 1992 in Poland and has since then spread over large geographical areas. By November 2010, the disease had been recorded in 22 European countries. The gradual expansion and high intensity of the ash dieback epidemic in Europe may suggest that H. pseudoalbidus is an invasive alien organism. In Norway, ash dieback was first reported in spring 2008, and a survey in early summer of the same year revealed that the disease had spread over large parts of the southern and eastern regions of the country. The distance from the southernmost to the northernmost infected stands was, at that time, about 400 km. Some old necrotic lesions were also observed, indicating that the ash dieback pathogen is likely to have been present in Norway since at least 2006. In 2009, a spore sampler was installed in a diseased ash stand at Ås, South-Eastern Norway. Sampling started in late July and continued until late September. Large numbers of ascospores resembling those of H. pseudoalbidus were observed, with the maximum number of spores occurring from the end of July to mid-August. The deposition of ascospores occurred mainly between 6 and 8 a.m. Ascospores are most likely to be the primary source initiating host infections and responsible for the rapid recent spread of H. pseudoalbidus in Europe.