Microbes, however, have developed their own strategies to counteract plant defence responses.
Recent research on plant—microbe interactions has revealed that an important part of the infection strategies of a diverse range of plant pathogens, including bacteria, fungi and oomycetes, is the production of effector proteins that are secreted by the pathogen and that promote successful infection by manipulating plant structure and metabolism, including interference in plant defence mechanisms.
Pathogen effector proteins may function either in the extracellular spaces within plant tissues or within the plant cell cytoplasm. Extracellular effectors include cell wall degrading enzymes and inhibitors of plant enzymes that attack invading pathogens. This article presents a brief overview of our current understanding of the nature and function of effectors produced by oomycete plant pathogens.
About this book
Very little information is known about the biology of this pathogen, its interaction with host plant. Large genetic variation and lack of well defined resistance citrus plants makes it a challenging pathosystem to work with. We will explore the biology of this pathogen by molecular genetics studies which will elucidate new virulence functions in this pathogen.
About Us. Group Leaders. Web Mail. Subhadeep Chatterjee.
Research Projects Plants are non motile but they constantly encounters both abiotic and biotic stress. There is a constant war between the pathogenic microbes and the host plants-the outcome of which determines resistance or disease. The phenomena called as quorum sensing Fig. Host-selective toxins HSTs are effectors produced by some necrotrophic pathogenic fungi that typically confer the ability to cause disease.
Often, diseases caused by pathogens that produce HSTs follow an inverse gene-for-gene model where toxin production is required for the ability to cause disease and a single locus in the host is responsible for toxin sensitivity and disease susceptibility.
Pyrenophora tritici-repentis represents an ideal pathogen for studying the biological significance of such inverse gene-for-gene interactions, because it displays a complex race structure based on its production of multiple HSTs. This review will summarize the current knowledge of how these two dissimilar HSTs display distinct modes of action, yet each confers pathogenicity to P.
This root pathogen is an attractive model to investigate the question of host adaptation as it exhibits a remarkably broad host range, being able to infect numerous plant species belonging to different botanical families. Several effector proteins transiting through the type III secretion system have been shown to restrict or extend specifically the host range of the bacterium.
Recent investigations on the mechanisms that coordinate changes in gene expression during the passage between saprophytism and life within host tissues have allowed the identification of other molecular determinants implicated in the adaptation of R. Among these determinants are genes involved in chemotaxis, secondary metabolic pathways and the detoxification of various antimicrobial compounds, and genes directing the biosynthesis of phytohormones or adherence factors.
The regulation of many of these genes is coordinated by the master pathogenicity regulator HrpG. These hrpG-dependent genes control major steps during the interaction with plant cells, and probably determine the ecological behaviour of the microorganism, being required for the establishment of pathogenesis or mutualism. Research review Molecular traits controlling host range and adaptation to plants in Ralstonia solanacearum Author for correspondence: R.
Pathogen—plant host coevolutionary interactions exert strong natural selection on both organisms, specifically on the genes coding for effectors pathogens , as well as on those coding for effector targets and R proteins plant hosts.
Natural selection leaves behind DNA sequence signatures on such genes and on linked genomic regions. These signatures can readily be detected by studying the patterns of intraspecies polymorphisms and interspecies divergence of the DNA sequences. Recent developments in DNA sequencing technology have made whole-genome studies on patterns of DNA polymorphisms : divergence possible. Here, we provide an overview of the statistical tools used for population genomics and their applications.
This is followed by a brief review of evolutionary studies on plant genes involved in host—pathogen interactions.
Finally we provide an example from our study on Magnaporthe oryzae. Pseudomonas syringae effectors AvrB and AvrRpm1 are recognized by phylogenetically distinct resistance R proteins in Arabidopsis thaliana Brassicaceae and soybean Glycine max, Fabaceae. In soybean, these resistances are encoded by two tightly linked R genes, Rpg1-b and Rpg1-r. To study the evolution of these specific resistances, we investigated AvrB- and AvrRpm1-induced responses in common bean Phaseolus vulgaris, Fabaceae.
By contrast, multiple genotypes responded to AvrRpm1, and two independent R genes conferring AvrRpm1specific resistance were mapped to the ends of linkage group B11 Rpsar-1, for resistance to Pseudomonas syringae effector AvrRpm1 number 1 and B8 Rpsar Rpsar-1 is located in a region syntenic with the soybean Rpg1 cluster. However, mapping of specific Rpg1 homologous genes suggests that AvrRpm1 recognition evolved independently in common bean and soybean.
Table of contents : Plant–microbe interactions
Lupas and Regine Kahmann. Summary Author for correspondence: R.
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Because of the limited number of selectable markers, the ability to carry out sequential gene deletions has limited the analysis of effector gene families that may have redundant functions. To avoid genome rearrangements via FRT sites remaining in the genome after excision, different mutated FRT sites were introduced.
We showed that expression of all 11 genes is up-regulated during the biotrophic phase. Strains carrying deletions of 9 or all 11 genes showed a significant reduction in virulence, and this phenotype could be partially complemented by the introduction of differentmembers from the gene family, demonstrating redundancy.