Host-pathogen Interactions (host-pathogen + interaction)

Distribution by Scientific Domains


Selected Abstracts


Attraction of ambrosia and bark beetles to coast live oaks infected by Phytophthora ramorum

AGRICULTURAL AND FOREST ENTOMOLOGY, Issue 4 2008
Brice A. McPherson
Abstract 1,Sudden oak death is caused by the apparently introduced oomycete, Phytophthora ramorum. We investigated the role of bark and ambrosia beetles in disease progression in coast live oaks Quercus agrifolia. 2,In two Marin County, California sites, 80 trees were inoculated in July 2002 with P. ramorum and 40 were wounded without inoculation. Half of the trees in each group were sprayed with the insecticide permethrin [cyclopropanecarboxylic acid, 3-(2,2-dichloroethenyl)-2,2-dimethyl-(3-phenoxyphenyl) methyl ester] to prevent ambrosia and bark beetle attacks, and then were sprayed twice per year thereafter. After each treatment, sticky traps were placed on only the permethrin-treated trees. Beetles were collected periodically in 2003. 3,Inoculated trees accounted for 95% of all beetles trapped. The ambrosia beetles Monarthrum scutellare and Xyleborinus saxeseni and the western oak bark beetle Pseudopityophthorus pubipennis were the most abundant of the seven species trapped. 4,Permethrin treatment delayed initiation of beetle attacks and significantly reduced the mean number of attacks per tree. Beetles did not attack any wounded or noncankered inoculated trees. 5,Trees with larger cankers trapped more beetles early in the disease. Once permethrin lost effectiveness, the number of beetle entrance tunnels was a more reliable predictor of subsequent trap catch than was canker size. 6,Beetles were initially attracted to P. ramorum cankers in response to kairomones generated in the host-pathogen interaction. After beetles attacked the permethrin-treated trees, aggregation pheromones most probably were the principal factor in beetle colonization behaviour. [source]


The Plant's Capacity in Regulating Resource Demand

PLANT BIOLOGY, Issue 6 2005
R. Matyssek
Abstract: Regulation of resource allocation in plants is the key to integrate understanding of metabolism and resource flux across the whole plant. The challenge is to understand trade-offs as plants balance allocation between different and conflicting demands, e.g., for staying competitive with neighbours and ensuring defence against parasites. Related hypothesis evaluation can, however, produce equivocal results. Overcoming deficits in understanding underlying mechanisms is achieved through integrated experimentation and modelling the various spatio-temporal scaling levels, from genetic control and cell metabolism towards resource flux at the stand level. An integrated, interdisciplinary research concept on herbaceous and woody plants and its outcome to date are used, while drawing attention to currently available knowledge. This assessment is based on resource allocation as driven through plant-pathogen and plant-mycorrhizosphere interaction, as well as competition with neighbouring plants in stands, conceiving such biotic interactions as a "unity" in the control of allocation. Biotic interaction may diminish or foster effects of abiotic stress on allocation, as changes in allocation do not necessarily result from metabolic re-adjustment but may obey allometric rules during ontogeny. Focus is required on host-pathogen interaction under variable resource supply and disturbance, including effects of competition and mycorrhization. Cost/benefit relationships in balancing resource investments versus gains turned out to be fundamental in quantifying competitiveness when related to the space, which is subject to competitive resource exploitation. A space-related view of defence as a form of prevention of decline in competitiveness may promote conversion of resource turnover across the different kinds of biotic interaction, given their capacity in jointly controlling whole plant resource allocation. [source]


Mapping polygenes for tuber resistance to late blight in a diploid Solanum phureja × S. stenotomum hybrid population

PLANT BREEDING, Issue 4 2006
I. Simko
Abstract Potato tuber blight is a disease caused by the oomycete Phytophthora infestans (Mont.) de Bary. Due to the significant economic impact of this disease, introgression of durable resistance into the cultivated potato is one of the top priorities of breeding programmes worldwide. Though numerous resistance loci against this devastating disease have already been mapped, most of the detected loci are contributing towards foliar resistance while specific information on tuber resistance is limited. To identify the genetic components of tuber resistance and its relationship to foliar resistance and plant maturity we have investigated the host-pathogen interaction in a segregating diploid hybrid Solanum phureja × S. stenotomum family. Mature tubers from this mapping family were inoculated with a sporangial suspension of P. infestans (US-8 clonal lineage) and evaluated for lesion expansion. No significant correlation was detected between late blight resistance in foliage and tubers, and between plant maturity and tuber resistance. Four chromosomal regions were significantly associated with tuber resistance to the disease. The largest effect was detected near the marker locus PSC (LOD 10.7) located on chromosome 10. This locus explained about 63% of the total phenotypic variation of the trait. The other three resistance-related loci were mapped on chromosomes 8 (GP1282, LOD 4.4), 6 (CP18, LOD 4.0) and 2 (CP157, LOD 3.8). None of the four tuber resistance loci coincides with the foliage resistance loci detected in this same family. Tuber blight resistance quantitative trait loci (QTL) on chromosomes 2, 8 and 10 are distinct from the maturity QTLs and have an additive effect on tuber resistance. These results indicate that different genes are involved in foliar and tuber resistance to P. infestans in the present family and that some of the resistance genes might be associated with late maturity. [source]


Visualization of Helicobacter Species Within the Murine Cecal Mucosa Using Specific Fluorescence In Situ Hybridization

HELICOBACTER, Issue 2 2005
Vivian Chan
ABSTRACT Background., Members of the genus Helicobacter have been associated with colitis development in a number of immunodeficient animal models. While it is known that these organisms can initiate colitis development, the location and spatial distribution of these bacteria within the intestinal tract is currently unknown. In this study, we developed and optimized fluorescence in situ hybridization (FISH) probes specifically for Helicobacter species. Materials and Methods., Based on 16S-RNA gene alignments, two probes specific for the entire family Helicobacteraceae and two probes specific for Helicobacter ganmani and Helicobacter hepaticus were designed. Evaluation of these probes was determined using ATCC reference strains and cecum samples from ten IL-10 knockout mice. The presence of Helicobacter species was determined using FISH and verified using PCR-DGGE and microscopic examination of silver stained sections. Results., Analysis of the ATCC reference strains revealed that the probes HEL274/HEL717 were specific for the family Helicobacteraceae, while HEP642 was specific for H. hepaticus and GAN1237 for H. ganmani. Using these probes, a pattern of spatial localization of the two different Helicobacter species was observed in the cecum tissues of IL-10 knockout mice. This consistently showed that H. ganmani was localized to the lower regions and H. hepaticus to the mid-upper regions of the crypts. Conclusion., We have developed FISH probes specific for the family Helicobacteraceae as well as two individual Helicobacter species. This study will allow the future use of the FISH to better understand host-pathogen interactions in vitro. [source]


Innate immunity in Drosophila: Pathogens and pathways

INSECT SCIENCE, Issue 1 2008
Shubha Govind
Abstract Following in the footsteps of traditional developmental genetics, research over the last 15 years has shown that innate immunity against bacteria and fungi is governed largely by two NF-,B signal transduction pathways, Toll and IMD. Antiviral immunity appears to stem from RNA interference, whereas resistance against parasitoids is conferred by Toll signaling. The identification of these post-transcriptional regulatory mechanisms and the annotation of most Drosophila immunity genes have derived from functional genomic studies using "model" pathogens, intact animals and cell lines. The D. melanogaster host has thus provided the core information that can be used to study responses to natural microbial and metazoan pathogens as they become identified, as well as to test ideas of selection and evolutionary change. These analyses are of general importance to understanding mechanisms of other insect host-pathogen interactions and determinants of variation in host resistance. [source]


Molecular, ecological and evolutionary approaches to understanding Alternaria diseases of citrus

MOLECULAR PLANT PATHOLOGY, Issue 6 2003
Kazuya Akimitsu
SUMMARY Alternaria fungi cause four different diseases of citrus: Alternaria brown spot of tangerines, Alternaria leaf spot of rough lemon, Alternaria black rot of several citrus fruits and Mancha foliar of Mexican lime. The first three diseases are caused by the small-spored species, Alternaria alternata and the causal agents can only be differentiated using pathogenicity tests, toxin assays or genetic markers. Mancha foliar is caused by the morphologically distinct, large-spored species A. limicola. Substantial progress has been made in understanding the biology, ecology, population biology, systematics, molecular biology and biochemistry of the interactions between these pathogens and citrus. Epidemiological studies have focused on brown spot of tangerines and their hybrids and have contributed to the development of a model of disease development which has improved control and reduced fungicide use. Studies of the population genetics, host specificity and ecology of A. alternata from different ecological niches on citrus have revealed host specific forms of the pathogen which cause disease on different citrus species, the existence of three phylogenetic lineages of the fungus which cause brown spot world-wide, and closely related non-pathogenic isolates which colonize healthy citrus tissue. The role of host-specific toxins in Alternaria diseases of citrus has been extensively studied for over 20 years, and these pathosystems have become model systems for host-pathogen interactions. Recent molecular research has started to unravel the genetic basis of toxin production and the host susceptibility to toxin, and the role of extracellular, degradative enzymes in disease. [source]


Meeting report: Imaging host-pathogen interactions

BIOTECHNOLOGY JOURNAL, Issue 6 2009
Freddy Frischknecht
No abstract is available for this article. [source]


Illuminating the host , How RNAi screens shed light on host-pathogen interactions

BIOTECHNOLOGY JOURNAL, Issue 6 2009
Miguel Prudêncio
Abstract Over millions of years pathogens have coevolved with their respective hosts utilizing host cell functions for survival and replication. Despite remarkable progress in developing antibiotics and vaccination strategies in the last century, infectious diseases still remain a severe threat to human health. Meanwhile, genomic research offers a new era of data-generating platforms that will dramatically enhance our knowledge of pathogens and the diseases they cause. Improvements in gene knockdown studies by RNA interference (RNAi) combined with recent developments in instrumentation and image analysis enable the use of high-throughput screening approaches to elucidate host gene functions exploited by pathogens. Although only a few RNAi-based screens focusing on host genes have been reported so far, these studies have already uncovered hundreds of genes not previously known to be involved in pathogen infection. This review describes recent progress in RNAi screening approaches, highlighting both the limitations and the tremendous potential of RNAi-based screens for the identification of essential host cell factors during infection. [source]