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Pathogenicity Determinants (pathogenicity + determinant)
Selected AbstractsGaeumannomyces graminis, the take-all fungus and its relativesMOLECULAR PLANT PATHOLOGY, Issue 4 2004JACQUELINE FREEMAN SUMMARY Take-all, caused by the fungus Gaeumannomyces graminis var. tritici, is the most important root disease of wheat worldwide. Many years of intensive research, reflected by the large volume of literature on take-all, has led to a considerable degree of understanding of many aspects of the disease. However, effective and economic control of the disease remains difficult. The application of molecular techniques to study G. graminis and related fungi has resulted in some significant advances, particularly in the development of improved methods for identification and in elucidating the role of the enzyme avenacinase as a pathogenicity determinant in the closely related oat take-all fungus (G. graminis var. avenae). Some progress in identifying other factors that may be involved in determining host range and pathogenicity has been made, despite the difficulties of performing genetic analyses and the lack of a reliable transformation system. [source] Ambient pH controls the expression of endopolygalacturonase genes in the necrotrophic fungus Sclerotinia sclerotiorumFEMS MICROBIOLOGY LETTERS, Issue 2 2003Pascale Cotton Abstract In the necrotrophic fungus Sclerotinia sclerotiorum, secretion of polygalacturonases (PGs) and decrease of the environmental pH via oxalic acid production are considered as the main pathogenicity determinants. In order to evaluate the relationship between these two aspects of the infection process, we analyzed the expression of the endoPG-encoding genes pg1,3. Transcription of pg1,3 was not carbon regulated but was strictly controlled by pH and highly favored in a narrow range of acidic pH. During plant infection, a pH gradient was established in relation to oxalic acid secretion. Transcripts of pg1,3 were localized to the zone of colonization of healthy tissues while transcripts of genes encoding other lytic enzymes were restricted to the more acidic zones of the infected tissues. Our results show that progressive acidification of the ambient medium by the fungus is a major strategy for the sequential expression of pathogenicity factors. [source] The Lmgpi15 gene, encoding a component of the glycosylphosphatidylinositol anchor biosynthesis pathway, is required for morphogenesis and pathogenicity in Leptosphaeria maculansNEW PHYTOLOGIST, Issue 4 2008Estelle Remy Summary ,,Random insertional mutagenesis was used to investigate pathogenicity determinants in Leptosphaeria maculans. One tagged nonpathogenic mutant, termed m20, was analysed in detail here. ,,The mutant phenotype was investigated by microscopic analyses of infected plant tissues and in vitro growth assays. Complementation and silencing experiments were used to identify the altered gene. Its function was determined by bioinformatics analyses, cell biology experiments and functional studies. ,,The mutant was blocked at the invasive growth phase after an unaffected initial penetration stage, and displayed a reduced growth rate and an aberrant hyphal morphology in vitro. The T-DNA insertion occurred in the intergenic region between two head-to-tail genes, leading to a complex deregulation of their expression. The unique gene accounting for the mutant phenotype was suggested to be the orthologue of the poorly conserved Saccharomyces cerevisiae gpi15, which encodes for one component of the glycosylphosphatidylinositol (GPI) anchor biosynthesis pathway. Consistent with this predicted function, a functional translational fusion with the green fluorescent protein (GFP) was targeted to the endoplasmic reticulum. Moreover, the mutant exhibited an altered cell wall and addition of glucosamine relieved growth defects. ,,It is concluded that the GPI anchor biosynthetic pathway is required for morphogenesis, cell wall integrity and pathogenicity in Leptosphaeria maculans. [source] Recent developments in effector biology of filamentous plant pathogensCELLULAR MICROBIOLOGY, Issue 6 2010Ricardo Oliva Summary Filamentous pathogens, such as plant pathogenic fungi and oomycetes, secrete an arsenal of effector molecules that modulate host innate immunity and enable parasitic infection. It is now well accepted that these effectors are key pathogenicity determinants that enable parasitic infection. In this review, we report on the most interesting features of a representative set of filamentous pathogen effectors and highlight recent findings. We also list and describe all the linear motifs reported to date in filamentous pathogen effector proteins. Some of these motifs appear to define domains that mediate translocation inside host cells. [source] Host,pathogen interplay and the evolution of bacterial effectorsCELLULAR MICROBIOLOGY, Issue 2 2008John Stavrinides Summary Many bacterial pathogens require a type III secretion system (T3SS) and suite of type III secreted effectors (T3SEs) to successfully colonize their hosts, extract nutrients and consequently cause disease. T3SEs, in particular, are key components of the bacterial arsenal, as they function directly inside the host to disrupt or suppress critical components of the defence network. The development of host defence and surveillance systems imposes intense selective pressures on these bacterial virulence factors, resulting in a host,pathogen co-evolutionary arms race. This arms race leaves its genetic signature in the pattern and structure of natural genetic variation found in T3SEs, thereby permitting us to infer the specific evolutionary processes and pressures driving these interactions. In this review, we summarize our current knowledge of T3SS-mediated host,pathogen co-evolution. We examine the evolution of the T3SS and the T3SEs that traverse it, in both plant and animal pathosystems, and discuss the processes that maintain these important pathogenicity determinants within pathogen populations. We go on to examine the possible origins of T3SEs, the mechanisms that give rise to new T3SEs and the processes that underlie their evolution. [source] | ||||||||||||||||||||||