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Summary

  1. Top of page
  2. Summary
  3. Introduction
  4. Host resistance to S. nodorum is quantitative
  5. S. nodorum produces multiple HSTs
  6. ToxA was laterally transferred from S. nodorum to P. tritici-repentis
  7. Other evidence of lateral gene transfer leading to increased virulence
  8. Concluding remarks
  9. References

Host-specific toxins (HSTs) are defined as pathogen effectors that induce toxicity and promote disease only in the host species and only in genotypes of that host expressing a specific and often dominant susceptibility gene. They are a feature of a small but well-studied group of fungal plant pathogens. Classical HST pathogens include species of Cochliobolus, Alternaria and Pyrenophora. Recent studies have shown that Stagonospora nodorum produces at least four separate HSTs that interact with four of the many quantitative resistance loci found in the host, wheat. Rationalization of fungal phylogenetics has placed these pathogens in the Pleosporales order of the class Dothideomycetes. It is possible that all HST pathogens lie in this order. Strong evidence of the recent lateral gene transfer of the ToxA gene from S. nodorum to Pyrenophora tritici-repentis has been obtained. Hallmarks of lateral gene transfer are present for all the studied HST genes although definitive proof is lacking. We therefore suggest that the Pleosporales pathogens may have a conserved propensity to acquire HST genes by lateral transfer.


Introduction

  1. Top of page
  2. Summary
  3. Introduction
  4. Host resistance to S. nodorum is quantitative
  5. S. nodorum produces multiple HSTs
  6. ToxA was laterally transferred from S. nodorum to P. tritici-repentis
  7. Other evidence of lateral gene transfer leading to increased virulence
  8. Concluding remarks
  9. References

The study of plant–microbe interactions is increasingly having an impact in the broader world of pathogen microbiology. In many cases, full-scale genomic tools are available for both the pathogen and the host. The less onerous regulatory hurdles and lower costs surrounding the use of plants and their viral, bacterial and fungal pathogens have enabled rapid progress. As a result, we now have deep knowledge of some aspects of plant pathogen interactions especially when they involve the direct intracellular delivery of pathogen effectors into the host cytoplasm (Dodds et al., 2006; Jones and Dangl, 2006; Ellis et al., 2007). This aspect of pathogenicity is a feature of pathogens whose interests are served by keeping the invaded host cell alive – the so-called biotrophic class of pathogens (Oliver and Ipcho, 2004). There has been less progress to date about the class of pathogens which benefit from the induction and promotion of host cell death – the necrotrophic pathogens. Recently, a new consensus has emerged about the origin, evolution and biological role of a special class of pathogen effectors, host-specific toxins (HSTs), which are critical for the virulence of a class of necrotrophic fungal pathogens.

Host-specific toxins are an enigmatic group of effectors. As their name suggests, these are molecules that are toxic only to the host of the disease and are innocuous to the great majority of other plants. Furthermore, only specific genotypes of the host are sensitive to the toxin. Genetic analysis of the host shows that in the vast majority of cases, sensitivity to the toxin is a dominant trait, implying that the gene product is the direct or indirect receptor of the toxin. In many cases HSTs have been shown to reproduce, in part or in whole, the symptoms of the disease (Walton, 1996). As the pathogen produces an effector that promotes disease and the host produces a receptor that is required for susceptibility, these HST systems are an obvious mirror image of the classical gene-for-gene systems often found in biotrophic systems where matching products of dominant host and pathogen gene products trigger resistance (Wolpert et al., 2002).

Stagonospora nodorum, causal agent of Stagonospora nodorum blotch (SNB), is a necrotrophic fungal pathogen of wheat and is classified in the newly organized Dothideomycete class of Ascomycetes (Schoch et al., 2006). The Dothideomycetes broadly but not precisely replaced the Loculoascomycetes (Winka and Eriksson, 1997). S. nodorum is placed in the order Pleosporales (Eriksson, 2006; Solomon et al., 2006a). Other orders in this group include pathogenic species such as Mycosphaerella spp. and Venturia. The order Pleosporales is predominantly comprised of necrotrophic fungal plant pathogens, many of which have been shown or hypothesized to produce HSTs important to disease development and the successful completion of the pathogenic life cycle. These fungal genera include Alternaria, Cochliobolus, Leptosphaeria, Venturia, Ascochyta and Pyrenophora among others. These pathogens cause major diseases on cereals, legumes, apples and brassicas worldwide. Although many of the pathogens are not well studied, a few of the diseases have attracted significant research. The most prominent of these are Cochliobolus victoriae (Meehan and Murphy, 1947), causal agent of Victoria blight of oat, Cochliobolus heterostrophus, causal agent of southern corn leaf blight (Tatum, 1971), and Pyrenophora tritici-repentis, causal agent of wheat tan spot (Lamari and Bernier, 1991). These three pathogens are dependant on the presence and effectiveness of the HSTs which they produce, which include victorin, T-toxin and ToxA respectively.

Traditionally, S. nodorum was considered an unsophisticated pathogen armed with an effective array of non-specific toxins and cell wall-degrading enzymes. Evidence that it produced HSTs was largely discounted (Keller et al., 1994; Wicki et al., 1999), until several lines of evidence have come together to show that S. nodorum interacts with its host via a specific and complex system of HSTs. Figure 1 illustrates the progress of infection in the interaction and the timing of necrotic reactions.

image

Figure 1. The wheat–S. nodorum interaction illustrated with the use of a GFP-expressing strain fungal and a toxin-sensitive wheat genotype (adapted from Solomon et al., 2006b). Infected leaf cross-sections were viewed using confocal microscopy at 3–6 days post infection (dpi). Invasion of the leaf (3 dpi and 4 dpi) and vascular bundle (5 dpi) occurs prior to obvious host tissue collapse and pycnidiation (6 dpi).

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Host resistance to S. nodorum is quantitative

  1. Top of page
  2. Summary
  3. Introduction
  4. Host resistance to S. nodorum is quantitative
  5. S. nodorum produces multiple HSTs
  6. ToxA was laterally transferred from S. nodorum to P. tritici-repentis
  7. Other evidence of lateral gene transfer leading to increased virulence
  8. Concluding remarks
  9. References

Stagonospora nodorum blotch is an archetypal quantitatively controlled disease trait with resistance/susceptibility loci being identified on almost every chromosome of wheat (Xu et al., 2004). Several groups from around the world have looked at inheritance of resistance/susceptibility to S. nodorum using a plethora of resistance sources. These studies have included classical genetic analysis, monosomic analysis, analysis using chromosome substitution lines, as well as more recently, molecular marker-based quantitative trait locus (QTL) analysis. Resistance to S. nodorum is made additionally complex due to the different genetic control of resistance/susceptibility to the different modes of the disease including seedling leaf blotch, adult plant leaf blotch and glume blotch. Loci associated with resistance/susceptibility to the different modes of the disease have been identified on different chromosomes; however, only a few studies have evaluated both leaf and glume blotch on the same population under the same environment (reviewed by Xu et al., 2004). A few early studies in wheat showed that in some backgrounds resistance/susceptibility was controlled by single genes (Frecha, 1973), but most studies since have described resistance to S. nodorum as being quantitative. As the advent of molecular markers and the broad use of QTL analysis, several of these loci have been delimited to specific regions on chromosome arms and in some cases tightly linked markers have been identified. This quantitative or multigenic inheritance has made the characterization of this system, as well as breeding against the disease, difficult.

One of the first comprehensive QTL studies of this system using a complete molecular marker map of all 21 wheat chromosomes was performed by Schnurbusch et al. (2003). In this study, several different environments were used to evaluate glume blotch resistance to natural inocula in the field using a winter wheat population derived from the varieties ‘Arina’ and ‘Forno’. A total of seven different single-environment QTL were identified using different field environments consisting of three locations evaluated over 2 years. None of the QTL were significant across all locations but three QTL showed significance in a combined average across all environments. These QTL were identified on chromosome arms 3BS, 4BL and 5BL and accounted for a combined average of 31.9%, 19.1% and 9.0% of the disease variation, respectively, with a multiple regression model accounting for 38.9% (Table 1). Toubia-Rahme and Buerstmayr (2003) identified chromosomes 1B, 2A, 2B, 3A and 5A as having QTL associated with the glume phase of this disease. These five QTL individually accounted for between 6.3% and 14.0% of the disease with a multiple regression model accounting for 30.6% of the phenotypic variation (Table 1). Several similar studies have been conducted that characterize the leaf phase of this disease. Czembor et al. (2003) used a sparsely mapped genome to identify QTL on chromosomes 2B, 3B, 5B and 5D associated with various aspects of leaf disease. The R2 values for these QTL ranged from 13% to 37% (Table 1). Arseniuk et al. (2004) developed a population using the same susceptible parent used by Czembor et al. (2003) in a cross with a different resistant parent. In this study, bulked segregant analysis was used to identify additional QTL associated with leaf disease on chromosomes 6A and 6D accounting for 36% and 8% of the variation in disease respectively; however, the map used was not sufficient for direct comparison with the Czembor et al. (2003) study (Table 1). Aguilar et al. (2005), using a cross of the susceptible winter wheat (Triticum aestivum) variety Forno (Schnurbusch et al., 2003) by the winter spelt (Triticum spelta) ‘Oberkulmer’, identified 10 QTL associated with glume blotch resistance that explained from 0.3% to 35.8% of the variation as well as 11 QTL associated with resistance to leaf blotch that explained from 0.9% to 20.8% of the phenotypic variation. Multiple regression models accounted for 60% and 44.1% of the variation in glume blotch and leaf blotch respectively. Collectively, these QTL studies confirm that this disease is quantitatively inherited with no single QTL accounting for more than 37% of any disease phenotype.

Table 1. Stagonospora nodorum disease analysis studies using mapping populations of wheat and QTL analysis.
ReferenceTotal number of QTLVariation explained (%)Chromosomes with QTLMultiple regression maximum reported (%)Mode of the diseaseHST–host gene interaction
Schnurbusch et al. (2003)79–31.92A, 3B(2), 4B, 5A, 5B, 7B38.9Glume BlotchNone reported
Toubia-Rahme and Buerstmayr (2003)56.3–14.02A, 3A, 5A, 1B, 2B30.6Glume BlotchNone reported
Czembor et al. (2003)413–372B, 3B, 5B, 5DN/ALeaf BlotchNone reported
Arseniuk et al. (2004)28–366A, 6DN/ALeaf BlotchNone reported
Aguilar et al. (2005)100.3–35.81B, 2B, 3A(2), 4A(2), 4D, 5A, 5B, 7A60Glume BlotchNone reported
Aguilar et al. (2005)110.9–20.81B, 2A, 2B(2), 2D, 3B, 4B, 5B, 7B(2), 7S44.1Leaf BlotchNone reported
Liu et al. (2004b)94–581B, 2B, 3A, 3D, 4A, 4B, 5D, 6A, 7B68Leaf BlotchSnTox1–Snn1
Friesen et al. (2006)36–621B, 5B(2)77.0Leaf BlotchSnToxA–Tsn1
Uphaus et al. (2007)22.6–38.12D(2)33.5Glume BlotchNone reported
Friesen et al. (2007)45–471B, 2D, 5B, 5A74Leaf BlotchSnTox2–Snn2
Friesen et al. (2008)313–372D, 5B(2)51Leaf BlotchSnTox3–Snn3

S. nodorum produces multiple HSTs

  1. Top of page
  2. Summary
  3. Introduction
  4. Host resistance to S. nodorum is quantitative
  5. S. nodorum produces multiple HSTs
  6. ToxA was laterally transferred from S. nodorum to P. tritici-repentis
  7. Other evidence of lateral gene transfer leading to increased virulence
  8. Concluding remarks
  9. References

More recently, the underlying mechanism of this disease has been a point of investigation. The presence of multiple HSTs encoded on separate genes has been demonstrated. The first S. nodorum-produced HST identified was designated SnTox1. SnTox1 was shown to be a proteinaceous HST produced by isolate Sn 2000 and in the size range of 10–30 kDa. Liu et al. (2004a) showed that it interacted with a corresponding host gene designated Snn1. The dominant allele of the host gene conferred sensitivity to SnTox1 and susceptibility to leaf blotch caused by isolate Sn 2000. This is in contrast to classical resistance genes that are most frequently dominant for resistance. In parallel, Liu et al. (2004b) used the International Triticeae Mapping Initiative (ITMI) population to identify nine QTL significantly associated with seedling disease. Similar to previous studies, these QTL explained from 4% to 58% of the variation in disease, but only two QTL maintained significance in a multiple regression model. These two QTL resided on chromosome arms 1BS and 4BL with the toxin sensitivity gene Snn1 defining the peak of the 1BS QTL (Liu et al., 2004a).

In successive work, a new recombinant inbred population, BR34 × Grandin (BG), developed by Dr James Anderson (University of Minnesota) for the characterization of resistance effective against tan spot of wheat, was mapped (Liu et al., 2005) and used for the characterization of SNB resistance/susceptibility. The same isolate used in the SnTox1–Snn1 study was used to evaluate the BG population. QTL explaining 6%, 10% and 62% of the variation were identified on chromosome arms 5BL, 1BS and 5BL, respectively, and a multiple regression model consisting of these three loci together accounted for 77% of the disease phenotype. This study showed that the same isolate used in the SnTox1–Snn1 study produced an additional toxin that was interacting with a wheat gene on the long arm of chromosome 5B in the vicinity of the P. tritici-repentis (Ptr)ToxA sensitivity gene Tsn1 (Faris et al., 1996; Haen et al., 2004) Analysis of Tsn1-disrupted mutants indicated that the same gene responsible for sensitivity to Ptr ToxA was also responsible for sensitivity to a toxin being produced by S. nodorum (Liu et al., 2006). Due to the release of the S. nodorum genomic sequence, it was soon discovered that S. nodorum harboured a gene almost identical to PtrToxA (Friesen et al., 2006). Subsequent work showed that this gene had all the characteristics of a gene which had been transferred laterally from S. nodorum to P. tritici-repentis (discussed below).

Additional isolates which were shown to vary in their virulence were also evaluated using the BG population. Isolate Sn6 was inoculated onto the BG population and four QTL significantly associated with seedling disease were detected and explained from 5% to 47% of the phenotypic variation. Of these four QTL, one on the long arm of chromosome 5B associated with Tsn1 (SnToxA sensitivity) accounted for 20% of the disease variation, and relatively minor QTL on chromosome arms 1BS and 5AL accounted for 5% and 10% of the variation respectively. In addition, a major QTL on chromosome arm 2DS was highly associated with disease and accounted for 47% of the variation in disease. The effects of the 2DS QTL were due to a novel HST–host sensitivity gene interaction. In this case, the toxin was designated as SnTox2 and the corresponding host gene as Snn2. The SnTox2–Snn2 interaction was the third significant HST–host sensitivity gene interaction identified in this system (Friesen et al., 2007). SnTox2 was shown to be a small protein with a mass of approximately 7 kDa. Interestingly, compatible Tsn1–SnToxA and Snn2–SnTox2 interactions were shown to be additive in their effects for susceptibility, indicating that in contrast to the classical gene-for-gene model, the presence of two HST–host sensitivity gene interactions, that is, the production of two HSTs by a single strain of the pathogen, in the presence of two corresponding host sensitivity gene products, incurs more disease than that of one interaction alone (Friesen et al., 2007).

A third study using the BG mapping population was performed using different isolates, two of which were identical except for the presence of the SnToxA gene and the other being a wild-type isolate that did not contain the ToxA gene but did produce HSTs including SnTox2 as well as others (Friesen et al., 2008). Analysis of the BG population inoculated with the three isolates revealed three QTL that explained from 8% to 34% of the variation depending on the isolate or strain used (Table 1). The toxin sensitivity genes Tsn1 and Snn2 defined the peaks of two of the QTL, and the third QTL was underlain by a fourth S. nodorum toxin sensitivity locus on chromosome arm 5BS, which was designated Snn3. The corresponding HST involved in the interaction with Snn3 was designated SnTox3 and was once again shown to be a proteinaceous necrosis inducing toxin in the 10–30 kDa range (Friesen et al., 2008). However unlike the SnToxA–Tsn1 and SnTox2–Snn2 interactions, which had largely additive effects relative to each other, both the SnToxA–Tsn1 and SnTox2–Snn2 interactions were epistatic to the SnTox3–Snn3 interaction indicating that this system, however, simple on the surface, has underlying complexities that will need in-depth investigation.

Collectively the genetic characterization of disease resistance/susceptibility in the host via QTL analysis clearly shows that S. nodorum has an abundance of weapons to induce disease. Accordingly, resistance/susceptibility, unless isolated as a single gene in a segregating population, appears in the form of multiple quantitatively inherited loci. Research performed on the underlying mechanism of the resistance/susceptibility has shown that four of these QTL are associated with toxin sensitivity loci. Preliminary data have also shown that numerous other HST–host gene interactions are present (T.L. Friesen and J.D. Faris, unpubl. data). Each of the HST–host sensitivity gene interactions in the S. nodorum–wheat system has been shown to act in an inverse gene-for-gene manner where multiple HSTs produced by the pathogen interact either directly or indirectly with dominant host sensitivity/susceptibility gene products to induce disease.

ToxA was laterally transferred from S. nodorum to P. tritici-repentis

  1. Top of page
  2. Summary
  3. Introduction
  4. Host resistance to S. nodorum is quantitative
  5. S. nodorum produces multiple HSTs
  6. ToxA was laterally transferred from S. nodorum to P. tritici-repentis
  7. Other evidence of lateral gene transfer leading to increased virulence
  8. Concluding remarks
  9. References

The discovery of a gene identical to ToxA in the genome of S. nodorum not only confirmed that SNB was induced at least in part by HSTs, it also suggested the origin of the gene. ToxA was well known and characterized from the related Pleosporales wheat pathogen, P. tritici-repentis (Ciuffetti et al., 1997; Sarma et al., 2005). Several lines of evidence strongly suggested that the gene had been laterally transferred from S. nodorum to P. tritici-repentis in the recent past (Friesen et al., 2006). The gene was present in both organisms but absent from all others including more closely related species in both genera. An 11 kb region containing the gene, a transposase sequence and several kilo base pairs of anonymous DNA was found in both species. A survey of 600 isolates of S. nodorum revealed a very high level of sequence polymorphism in the gene. In contrast, only one haplotype was found in 57 P. tritici-repentis isolates, consistent with a recent arrival of a founder gene. This suggests that P. tritici-repentis is the recipient and S. nodorum is the donor. Although direct proof is lacking, the data are consistent with a lateral transfer some time before 1941 being responsible for the emergence of tan spot as a wheat disease in the 1940s and 1950s.

The pattern of sequence variation in S. nodorum isolates is also consistent with the acquisition of ToxA in this organism in South Africa somewhat further back in history, perhaps when wheat was first imported by European colonizers (Stukenbrock and McDonald, 2007). The evidence is based on a comparison of geographic sequence variation in anonymous simple sequence repeats, which are consistent with the pathogen having arisen in the Fertile Crescent region when wheat was domesticated, with sequence variation in ToxA that is consistent with an origin in South Africa. Thus it appears that S. nodorum can participate in lateral gene transfer as both a donor and a recipient, while we currently have evidence that P. tritici-repentis can act as a recipient only so far.

Other evidence of lateral gene transfer leading to increased virulence

  1. Top of page
  2. Summary
  3. Introduction
  4. Host resistance to S. nodorum is quantitative
  5. S. nodorum produces multiple HSTs
  6. ToxA was laterally transferred from S. nodorum to P. tritici-repentis
  7. Other evidence of lateral gene transfer leading to increased virulence
  8. Concluding remarks
  9. References

As mentioned above, the other species with well-characterized HSTs are from the related genera Alternaria, Cochliobolus and Pyrenophora. In each case, the possibility that the genes for the HST were laterally transferred has been raised and is still tenable.

A major epidemic in maize occurred in 1970 and 1971 which was caused by Race T of C. heterostrophus (Ullstrup, 1972). This race had acquired the ability to severely infect maize carrying the Texas CMS cytoplasm. The new virulence was shown to be due to a polyketide toxin called T-toxin (Yoder, 1980). Race T isolates appeared to harbour an extra 1.2 Mb of DNA compared with the relatively innocuous Race 0 isolates that predated Race T (Chang and Bronson, 1996). The idea that this was a simple case of lateral gene transfer was not supported, and a more complex picture emerged. The Tox1 locus that encodes T-toxin biosynthesis was found to be a bipartite genetic element which induces a reciprocal translocation in crosses with race O (Turgeon and Baker, 2007).

Northern corn leaf spot is caused by Cochliobolus carbonum and pathogenicity is largely due to HC-toxin, a cyclic tetrapeptide, encoded at the locus TOX2 (Walton, 1996). The locus is complex with at least five genes present in multiple copies (Ahn and Walton, 1998). The absence of the genes in strains that do not make HC-toxin is suggestive of lateral gene transfer, but no supporting evidence is available (Walton, 2000).

Different pathotypes of Alternaria alternata produce one of at least 12 HSTs that enable them to cause disease on a range of dicotyledonous hosts (Hayashi et al., 1990; Thomma, 2003) and these toxins are all the products of gene clusters (Ito et al., 2004). The AKT, AMT and ALT toxin biosynthesis clusters are all located on small conditionally dispensable chromosomes (Hatta et al., 2002). Phylogenetic analysis based on housekeeping nuclear genes indicates that all the strains have a common origin, but that each strain has a unique toxin biosynthesis cluster. The incongruity of the toxin gene phylogenetic trees and the bulk genome trees is the primary evidence for lateral transfer of these genes. The presence of the genes on small CD chromosomes provides a means by which the genes could transfer between the isolates (Tanaka et al., 1999).

There are a few other examples of HST for which even preliminary evidence of lateral gene transfer has not been sought to our knowledge and thus remains a clear research priority. These include C. victoriae causal agent of Victoria blight of oats and producer of the HST victorin (Meehan and Murphy, 1947; Wolpert et al., 2002; Sweat and Wolpert, 2007), Phyllosticta maydis (syn. Mycosphaerella zeae-maydis) causing Yellow blight of maize (Arny and Nelson, 1971) a disease ascribed to PM toxin (Yun et al., 1998) and Corynespora cassiicola, the cause of Corynespora leaf fall of rubber (Barthe et al., 2007) caused by the toxin cassiicolin.

All the pathogens mentioned above are in the order Pleosporales with the exception of M. zeae-maydis, which is placed in the related Capnodiales order. However the only DNA sequence available for this pathogen is the PKS encoding PM toxin and until more phylogenetic studies have been performed, it remains a possibility that it should be placed in the Pleosporales. With this potential exception remaining, all HST fungi are from one order, the Pleosporales. We thus propose that Pleosporales have retained an unusual ability to acquire genes laterally and to express them as HSTs. Presumably these HST effectors interact with host genes whose evolved role is the detection and response to effectors from other pathogens as has been shown for victorin at least in Arabidopsis (Sweat and Wolpert, 2007; Sweat et al., 2008). It seems that these HST subvert the host response to induce cell death and thus disease.

Concluding remarks

  1. Top of page
  2. Summary
  3. Introduction
  4. Host resistance to S. nodorum is quantitative
  5. S. nodorum produces multiple HSTs
  6. ToxA was laterally transferred from S. nodorum to P. tritici-repentis
  7. Other evidence of lateral gene transfer leading to increased virulence
  8. Concluding remarks
  9. References

Until recently, evidence of HSTs was limited to a few well-studied examples: Cochliobolus, Alternaria and Pyrenophora. We can now add S. nodorum to that list. We must ask ourselves why the presence of HSTs in S. nodorum took so long to be recognized. The answer lies in the complex pattern of multiple HSTs present variably in pathogen populations and of the multiple susceptibility genes present variably in host populations. Each interaction contributes only marginally to overall disease susceptibility and was thus not recognized as being a specific phenomenon. The breakthrough came with the use of well-structured host populations, the use of culture filtrates and the presence of ToxA in the genome sequence.

The presence of multiple HST interactions in this disease immediately suggests a route to improve disease resistance. Isolated HSTs can be used to assay wheat genotypes for the presence of the corresponding sensitivity locus. Resistance alleles can be stacked in adapted genotypes.

Many other Pleosporales pathogens closely resemble S. nodorum in exhibiting foliar necrotrophic symptoms and toxic culture filtrates (Strange, 2007). Examples include Pyrenophora teres (Sarpeleh et al., 2007) and the legume pathogens in the Ascochyta group (Hernandez-Bello et al., 2006; Muehlbauer and Chen, 2007). A critical search for HSTs using the techniques of subfractionation of culture filtrates and genome sequencing is surely warranted. It remains to be seen how widespread the presence of HSTs is in this class.

Critical evidence of lateral gene transfer is hard to come by. In the past, incongruent phylogenetic trees of individual genes and the organisms harbouring them were taken at face value to indicate lateral gene transfer. We now know that complex processes of gene duplication, loss and diversification can combine to explain many apparent incongruities. It is only with the advent of whole genome sequences from multiple species that such evidence is rendered credible (Richards et al., 2006a). Within the Pleosporales, current evidence of lateral gene transfer of HST genes ranges from strong to neutral; in no cases has it been ruled out (Oliver and Solomon, 2008). We therefore suggest as a working model that Pleosporales have an unusual ability to acquire genes laterally; expression of such genes enables virulence on new hosts. This idea can be tested both experimentally [by co-infecting putative donor and recipient organisms (He et al., 1998)] and by examination of the flood of fungal genome sequences that can be expected to be deposited (Richards et al., 2006b; Khaldi et al., 2008).

References

  1. Top of page
  2. Summary
  3. Introduction
  4. Host resistance to S. nodorum is quantitative
  5. S. nodorum produces multiple HSTs
  6. ToxA was laterally transferred from S. nodorum to P. tritici-repentis
  7. Other evidence of lateral gene transfer leading to increased virulence
  8. Concluding remarks
  9. References
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  • Ahn, J.H., and Walton, J.D. (1998) Regulation of cyclic peptide biosynthesis and pathogenicity in Cochliobolus carbonum by TOXEp, a novel protein with a bZIP basic DNA-binding motif and four ankyrin repeats. Mol Gen Genet 260: 462469.
  • Arny, D., and Nelson, R. (1971) Phyllostiicta maydis species nova, the incitant of yellow blight of maize. Phytopathology 61: 11701172.
  • Arseniuk, E., Czembor, P.C., Czaplicki, A., Song, Q.J., Cregan, P.B., Hoffman, D.L., and Ueng, P.P. (2004) QTL controlling partial resistance to Stagonospora nodorum leaf blotch in winter wheat cultivar Alba. Euphytica 137: 225231.
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