Avirulence Factors Research Articles

Failure of RPG1 protein to degrade in high-copy Rpg1 transgenic barley lines results in susceptibility to stem rust

Rpg1 is a valuable resistance gene that has protected barley from serious yield losses due to stem rust (Puccinia graminis f. sp. tritici [Pgt]) for over 60 years in the Upper Midwest region of the United States. In previous research, this gene was cloned from cultivar (cv.) Morex and its function validated by transforming the susceptible barley cv. Golden Promise into a resistant cultivar. A single copy of Rpg1 was sufficient to confer stem rust resistance, but we identified high-copy transgenic lines (with four and five copies of Rpg1) that were susceptible at both the seedling and adult plant stages. To elucidate the basis of these susceptible reactions, we selected six transgenic lines with variable copy numbers of Rpg1 and tested them for level of RPG1 protein accumulation, RPG1 protein degradation upon inoculation with the avirulent pathotype Pgt-MCCF, RPG1 phosphorylation in response to the same avirulent pathotype, and elicitation of a hypersensitive response upon infiltration with Pgt effectors RGD-binding protein and VPS9 protein. The stem rust resistant transgenic lines with one and two copies of Rpg1 (G04-271, G04-273 G04-266, and G03-210) reacted very similar to the positive control of cv. Morex with respect to all of the assays. In contrast, the behavior of the stem rust susceptible high-copy lines (G04-287 with four copies and G04-288 with five copies) was different in several respects. First, the level of RPG1 protein was about 1.5–3.0× higher than in the resistant lines and cv. Morex. Second, the protein failed to degrade, unlike the case with the resistant lines and cv. Morex where RPG1 was completely degraded by 28 hpi. Third, the high-copy lines failed to elicit a hypersensitive response after infiltration with the Pgt effectors, whereas the resistant lines did. RPG1 protein from the high-copy transgenic lines appeared to behave normally with respect to its ability to phosphorylate in vivo. However, these two lines over produced apparently functional RPG1 protein, but failed to degrade it normally. Stem rust susceptibility and failure to respond to avirulence factors by the high-copy Rpg1 transgenic lines G04-287 and G04-288 are probably due to the failure to degrade the RPG1 protein.

Host Resistance and Parasite Virulence in Striga–Host Plant Interactions: A Shifting Balance of Power

The witchweeds, members of the genus Striga, are noxious and persistent pests in farmers' fields and serious constraints to crop productivity throughout Africa, India, and Southeast Asia. Among the primary hosts for Striga are the major cereals (maize, sorghum, rice, and millet) and grain legumes (cowpea) that are important food staples worldwide. The negative impact of parasitic plants on crop productivity increases globally each year, and their potential for affecting domestic agriculture looms larger as the movement of seed resources expands on a global scale. At the present time there is a limited understanding of how Striga and other parasitic plants select a suitable host and overcome the innate defense responses of the host in order to complete their life-cycle. In the grasses most reported resistance to Striga appears to be polygenic with a large genotype by environment interaction. In contrast, resistance to S. gesnerioides in cowpea is conferred by single dominant genes functioning in a race-specific manner suggesting that a gene-for-gene mechanism similar to effector-triggered immunity (ETI) described in other host–pathogen interactions is likely operating in these parasite-host associations. A hallmark of ETI is the direct or indirect recognition of parasite-derived avirulence (Avr) factors and other effectors that interfere with plant innate immunity by host sensors (or R proteins) leading to activation of defense responses. The recent cloning and functional characterization of a race-specific R gene from cowpea encoding a canonical coiled-coil (CC)-nucleotide binding site (NBS)-leucine-rich repeat (LRR) type R-protein opens the door for further exploration of the mechanism of host resistance and provides a focal point for studies aimed at uncovering the molecular and genetic factors underlying parasite virulence and host selection. The potential for the development of novel strategies for parasite control and eradication based on parasite virulence factors is discussed.

Induction of pathogenesis-related proteins in rice bacterial blight resistant gene XA21-mediated interactions with Xanthomonas oryzae pv. oryzae.

In this study, we investigated pathogenesis-related (PR) protein expression in interactions between rice plants with bacterial blight resistant gene Xa21 and Xanthomonas oryzae pv. oryzae (Xoo), the causal agent of bacterial blight. Three PR genes, OsPR1a, OsPR1b, and OsPR10a, were cloned and the fusion proteins were expressed in E. coli to generate polyclonal antibodies. The proteins isolated at 0, 12, 24, 36, 48, 60, 72, and 144 h post-inoculation (hpi) from rice leaves inoculated with incompatible Xoo strains were analyzed using Western blotting. Significant inductions were observed for all three PR proteins in the late stages of inoculation. We also compared the expression of PR proteins among four different modalities: (i) incompatible interactions (R); (ii) compatible interactions in the absence of the Rgene (SR -); (iii) compatible interactions in the absence of the avirulence factor in Xoo (SAvr -); (iv) mock inoculated control treatments (M). Results showed that the three PR proteins are enhanced in the R, SR -, and SAvr - interactions more than in the control treatments. The induction of PR proteins in the R interaction is the highest, suggesting that these proteins are involved in the defense mechanism.

Cloning and Characterization ofR3b; Members of theR3Superfamily of Late Blight Resistance Genes Show Sequence and Functional Divergence

Massive resistance (R) gene stacking is considered to be one of the most promising approaches to provide durable resistance to potato late blight for both conventional and genetically modified breeding strategies. The R3 complex locus on chromosome XI in potato is an example of natural R gene stacking, because it contains two closely linked R genes (R3a and R3b) with distinct resistance specificities to Phytophthora infestans. Here, we report about the positional cloning of R3b. Both transient and stable transformations of susceptible tobacco and potato plants showed that R3b conferred full resistance to incompatible P. infestans isolates. R3b encodes a coiled-coil nucleotide-binding site leucine-rich repeat protein and exhibits 82% nucleotide identity with R3a located in the same R3 cluster. The R3b gene specifically recognizes Avr3b, a newly identified avirulence factor from P. infestans. R3b does not recognize Avr3a, the corresponding avirulence gene for R3a, showing that, despite their high sequence similarity, R3b and R3a have clearly distinct recognition specificities. In addition to the Rpi-mcd1/Rpi-blb3 locus on chromosome IV, the R3 locus on chromosome XI is the second example of an R-gene cluster with multiple genes recognizing different races of P. infestans.

Identification of an amino acid residue required for differential recognition of a viral movement protein by the Tomato mosaic virus resistance gene Tm-22

The Tm-2 gene of tomato and its allelic gene, Tm-2 2 , confer resistance to Tomato mosaic virus (ToMV) and encode a member of the coiled-coil/nucleotide binding-ARC/leucine-rich repeat (LRR) protein class of plant resistance ( R) genes. Despite exhibiting only four amino acid differences between the products of Tm-2 and Tm-2 2 , Tm-2 2 confers resistance to ToMV mutant B7, whereas Tm-2 is broken by ToMV-B7. An Agrobacterium-mediated transient expression system was used to study the mechanism of differential recognition of the movement proteins (MPs), an avirulence factor for ToMV resistance, of ToMV-B7 by Tm-2 and Tm-2 2. Although resistance induced by Tm-2 and Tm-2 2 is not usually accompanied by hypersensitive response (HR), Tm-2 and Tm-2 2 induced HR-like cell death by co-expression with MP of a wild-type ToMV, a strain that causes resistance for these R genes, and Tm-2 2 but not Tm-2 induced cell death with B7-MP in this system. Site-directed amino acid mutagenesis revealed that Tyr-767 in the LRR of Tm-2 2 is required for the specific recognition of the B7-MP. These results suggest that the Tyr residue in LRR contributes to the recognition of B7-MP, and that Tm-2 and Tm-2 2 are involved in HR cell death.

The Evolutionary History of Beet necrotic yellow vein virus Deduced from Genetic Variation, Geographical Origin and Spread, and the Breaking of Host Resistance

Beet necrotic yellow vein virus (BNYVV) is an economically important pathogen of sugar beet and has been found worldwide, probably as the result of recent worldwide spread. The BNYVV genome consists of four or five RNA components. Here, we report analysis of sequence variation in the RNA3-p25, RNA4-p31, RNA2-CP, and RNA5-p26 genes of 73 worldwide isolates. The RNA3-p25 gene encodes virulence and avirulence factors. These four sets of gene sequences each fell into two to four groups, of which the three groups of p25 formed eight subgroups with different geographical distributions. Each of these subgroup isolates (strains) could have arisen from four original BNYVV population and their mixed infections. The genetic diversity for BNYVV was relatively small. Selection pressure varied greatly depending on the BNYVV gene and geographical location. Isolates of the Italy strain, in which p25 was subject to the strongest positive selection, were able to overcome the Rz1-host resistance gene to differing degrees, whereas other geographically limited strains could not. Resistance-breaking variants were generated by p25 amino acid changes at positions 67 and 68. Our studies suggest that BNYVV originally evolved in East Asia and has recently become a pathogen of cultivated sugar beet followed by the emergence of new resistance-breaking variants.

Rapid Genetic Diversification and High Fitness Penalties Associated with Pathogenicity Evolution in a Plant Virus

Under the gene-for-gene model of host-pathogen coevolution, recognition of pathogen avirulence factors by host resistance factors triggers host defenses and limits infection. Theory predicts that the evolution of higher levels of pathogenicity will be associated with fitness penalties and that the cost of higher pathogenicity must be much smaller than that of not infecting the host. The analysis of pathogenicity costs is of academic and applied relevance, as these are determinants for the success of resistance genes bred into crops for disease control. However, most previous attempts of addressing this issue in plant pathogens yielded conflicting and inconclusive results. We have analyzed the costs of pathogenicity in pepper-infecting tobamoviruses defined by their ability to infect pepper plants with different alleles at the resistance locus L. We provide conclusive evidence of pathogenicity-associated costs by comparison of pathotype frequency with the fraction of the crop carrying the various resistance alleles, by timescaled phylogenies, and by temporal analyses of population dynamics and selection pressures using nucleotide sequences. In addition, experimental estimates of relative fitness under controlled conditions also provided evidence of high pathogenicity costs. These high pathogenicity costs may reflect intrinsic properties of plant virus genomes and should be considered in future models of host-parasite coevolution.

A Point Mutation in the Polymerase of Potato virus Y Confers Virulence Toward the Pvr4 Resistance of Pepper and a High Competitiveness Cost in Susceptible Cultivar

To understand why the Pvr4 resistance of pepper against Potyvirus spp. remained durable in field conditions while virulent Potato virus Y (PVY) variants could be selected in the laboratory, we studied the molecular mechanisms which generated these variants and the consequences on viral fitness. Using a reverse genetics approach with an infectious cDNA clone of PVY, we found that the region coding for the NIb protein (RNA-dependent RNA polymerase) of PVY was the avirulence factor corresponding to Pvr4 and that a single nonsynonymous nucleotide substitution in that region, an adenosine to guanosine substitution at position 8,424 of the PVY genome (A(8424)G), was sufficient for virulence. This substitution imposed a high competitiveness cost to the virus against an avirulent PVY variant in plants devoid of Pvr4. In addition, during serial passages in susceptible pepper plants, the only observed possibility of the virulent mutant to increase its fitness was through the G(8424)A reversion, strengthening the high durability potential of the Pvr4 resistance. This is in accordance with the fact that the NIb protein is one of the most constrained proteins expressed by the PVY genome and, more generally, by Potyvirus spp., and with a previously developed model predicting the durability of virus resistances as a function of the evolutionary constraint applied on corresponding avirulence factors.

Salmonella typhimurium infection increases p53 acetylation in intestinal epithelial cells

The ability of Salmonella typhimurium to enter intestinal epithelial cells constitutes a crucial step in pathogenesis. Salmonella invasion of the intestinal epithelium requires bacterial type three secretion system. Type three secretion system is a transport device that injects virulence proteins, called effectors, to paralyze or reprogram the eukaryotic cells. Avirulence factor for Salmonella (AvrA) is a Salmonella effector that inhibits the host's inflammatory responses. The mechanism by which AvrA modulates host cell signaling is not entirely clear. p53 is situated at the crossroads of a network of signaling pathways that are essential for genotoxic and nongenotoxic stress responses. We hypothesized that Salmonella infection activates the p53 pathway. We demonstrated that Salmonella infection increased p53 acetylation. Cells infected with AvrA-sufficient Salmonella have increased p53 acetylation, whereas cells infected with AvrA-deficient Salmonella have less p53 acetylation. In a cell-free system, AvrA possessed acetyltransferase activity and used p53 as a substrate. AvrA expression increased p53 transcriptional activity and induced cell cycle arrest. HCT116 p53-/- cells had less inflammatory responses. In a mouse model of Salmonella infection, intestinal epithelial p53 acetylation was increased by AvrA expression. Our studies provide novel mechanistic evidence that Salmonella modulates the p53 pathway during intestinal inflammation and infection.

Constraints on evolution of virus avirulence factors predict the durability of corresponding plant resistances

SUMMARY Understanding the factors driving pathogen emergence and re-emergence is a major challenge, particularly in agriculture, where the use of resistant plant cultivars imposes strong selective pressures on plant pathogen populations and leads frequently to 'resistance breakdown'. Presently, durable resistances are only identified after a long period of large-scale cultivation of resistant cultivars. We propose a new predictor of the durability of plant resistance. Because resistance breakdown involves modifications in the avirulence factors of pathogens, we tested for correlations between the evolutionary constraints acting on avirulence factors or their diversity and the durability of the corresponding resistance genes in the case of plant-virus interactions. An analysis performed on 20 virus species-resistance gene combinations revealed that the selective constraints applied on amino acid substitutions in virus avirulence factors correlate with the observed durability of the corresponding resistance genes. On the basis of this result, a model predicting the potential durability of resistance genes as a function of the selective constraints applied on the corresponding avirulence factors is proposed to help breeders to select the most durable resistance genes.

Host–pathogen warfare at the plant cell wall

Plants have evolved sensory mechanisms to detect pathogen attack and trigger signalling pathways that induce rapid defence responses. These mechanisms include not only direct detection of pathogen-derived elicitors (e.g. pathogen-associated molecular patterns (PAMPs) and avirulence factors or effectors) but also indirect sensing of pathogens' impact on the host plant. Among the first plant barriers to pathogen ingress are the cell wall and the cuticle. For those pathogens that penetrate the plant cell wall to gain access to water and nutrients of the plant protoplast, small wounds at penetration sites are created by enzymatic or physical disruption of the plant cell wall. Thus, cell wall integrity sensing is one mechanism by which plants may detect pathogen attack. Some plant cell wall fragments, notably oligogalacturonic acids, elicit similar defence responses in plants as the non-specific PAMP elicitors (e.g. production of reactive oxygen species, elevated expression of defence-associated genes), suggesting that PAMP signalling may provide a good model for studying cell wall integrity sensing in plants. However, much remains to be discovered about this sensing mechanism.

Characterisation of mjap genes encoding novel secreted proteins from the root-knot nematode, Meloidogyne javanica

AbstractTwo homologues of map-1, which encodes a putative avirulence factor, were found in a single egg mass line of the root-knot nematode Meloidogyne javanica that was virulent to the Mi-resistant gene. The main difference between the two encoded proteins of these homologues, MJ-MAP-1 and MJ-MAP-2, was the position of a 13 amino acid repeat region. Genes encoding two related but novel proteins, MJAP-1 and MJAP-2 (290 and 283 amino acids, respectively, including a potential signal secretion peptide), were also isolated from M. javanica. They have high similarity to MAP at the C-terminus. MJAP-1 and MJAP-2 differ from each other in the number and position of a seven-amino-acid repeat and in five other amino acids. The mjap genes are expressed in the subventral pharyngeal glands of second-stage juveniles of M. javanica, and transcription analysis in different developmental stages showed expression in the juvenile stage but not in eggs or adult females. Both mjap-1 and mjap-2 were expressed in both Mi-virulent and avirulent lines of M. javanica.

CRT1, an Arabidopsis ATPase that Interacts with Diverse Resistance Proteins and Modulates Disease Resistance to Turnip Crinkle Virus

Plant immunity frequently involves the recognition of pathogen-encoded avirulence (avr) factors by their corresponding plant resistance (R) proteins. This triggers the hypersensitive response (HR) where necrotic lesions formed at the site(s) of infection help restrict pathogen spread. HRT is an Arabidopsis R protein required for resistance to turnip crinkle virus (TCV). In a genetic screen for mutants compromised in the recognition of TCV's avr factor, we identified crt1 (compromised recognition of TCV), a mutant that prematurely terminates an ATPase protein. Following TCV infection, crt1 developed a spreading HR and failed to control viral replication and spread. crt1 also suppressed HR-like cell death induced by ssi4, a constitutively active R protein, and by Pseudomonas syringae carrying avrRpt2. Furthermore, CRT1 interacts with HRT, SSI4, and two other R proteins, RPS2 and Rx. These data identify CRT1 as an important mediator of defense signaling triggered by distinct classes of R proteins.

The N-terminus of the Begomovirus Nuclear Shuttle Protein (BV1) Determines Virulence or Avirulence in Phaseolus vulgaris

The BV1 gene of the bipartite Begomovirus genome encodes a nuclear shuttle protein (NSP) that is also an avirulence determinant in common bean. The function of the NSP of two common bean-infecting bipartite begomoviruses, Bean dwarf mosaic virus (BDMV) and Bean golden yellow mosaic virus (BGYMV), was investigated using a series of hybrid DNA-B components expressing chimeric BDMV and BGYMV NSP, and genotypes of the two major common bean gene pools: Andean (cv. Topcrop) and Middle American (cvs. Alpine and UI 114). BDMV DNA-A coinoculated with HBDBG4 (BDMV DNA-B expressing the BGYMV NSP) and HBDBG9 (BDMV DNA-B expressing a chimeric NSP with the N-terminal 1 to 42 amino acids from BGYMV) overcame the BDMV resistance of UI 114. This established that the BDMV NSP is an avirulence determinant in UI 114, and mapped the domain involved in this response to the N-terminus, which is a variable surface-exposed region. BDMV DNA-A coinoculated with HBDBG10, expressing a chimeric NSP with amino acids 43 to 92 from BGYMV, was not infectious, revealing an essential virus-specific domain. In the BGYMV background, the BDMV NSP was a virulence factor in the Andean cv. Topcrop, whereas it was an avirulence factor in the Middle American cultivars, particularly in the absence of the BGYMV NSP. The capsid protein (CP) also played a gene pool-specific role in viral infectivity; it was dispensable for infectivity in the Andean cv. Topcrop, but was required for infectivity of BDMV, BGYMV, and certain hybrid viruses in the Middle American cultivars. Redundancy of the CP and NSP, which are nuclear proteins involved directly or indirectly in viral movement, provides a masking effect that may allow the virus to avoid host defense responses.

The rules of engagement

The rules of engagement

Strain-Ecotype Specificity in Sinorhizobium meliloti - Medicago truncatula Symbiosis Is Correlated to Succinoglycan Oligosaccharide Structure

Molecular signals, including Nod factors and succinoglycan, are necessary for the establishment of nitrogen-fixing nodules (Fix+) in Medicago truncatula-Sinorhizobium meliloti symbiosis. This report shows that M. truncatula-S. meliloti interactions involve ecotype-strain specificity, as S. meliloti Rm41 and NRG247 are Fix+ (compatible) on M. truncatula A20 and Fix- (incompatible) on M. truncatula A17, the Fix phenotypes are reversed with S. meliloti NRG185 and NRG34, and there is a correlation between the host specificity and succinoglycan oligosaccharide structure. S. meliloti NRG185 produces oligosaccharides that are almost fully succinylated, with two succinate groups per subunit, whereas the oligosaccharides produced by S. meliloti Rm41 include many nonsuccinylated subunits, as well as subunits with a single succinate group and others with malate. The results of this study demonstrated the following: (i) incompatibility is not a consequence of an avirulence factor or lack of Nod factor activity; (ii) the Fix+ phenotypes are succinoglycan dependent; (iii) there is structural variability in the succinoglycan oligosaccharide populations between S. meliloti strains; (iv) the structural nature of the succinoglycan oligosaccharides is correlated to compatibility; most importantly, (v) an S. meliloti Rm41 derivative, carrying exo genes from an M. truncatula A17-compatible strain, produced a modified population of succinoglycan oligosaccharides (similar to the donor strain) and was Fix+ on A17.

The bifunctional effector AvrXccC of Xanthomonas campestris pv. campestris requires plasma membrane‐anchoring for host recognition

Bacterial pathogens use type III secretion systems (TTSS) to deliver effector proteins into eukaryotic cells for pathogenesis. In bacterial-plant interactions, one effector may function as an avirulence factor to betray the pathogen to the plant surveillance system and induce the hypersensitive response (HR) in the resistant host carrying a corresponding resistance (R) gene. However, the same effector can also sustain the growth of the pathogen by acting as a virulence factor to modulate plant physiology in the susceptible host lacking the corresponding R gene. Here, we identified and characterized a bifunctional TTSS effector AvrXccC belonging to the AvrB effector family in Xanthomonas campestris pv. campestris 8004. This effector is required for full bacterial virulence in the susceptible host cabbage (Brassica oleracea) and avirulence in the resistant host mustard (Brassica napiformis L.H. Baily). Expressing avrXccC in mustard-virulent strain Xcc HRI 3849A converts its virulence to avirulence. The effector AvrXccC is anchored to the plant plasma membrane, and the N-terminal myristoylation site (amino acids 2-7: GLcaSK) is essential for its localization. In addition, the avirulence function of AvrXccC for host recognition depends on its plasma membrane localization. Promoter activity assays showed that the expression of avrXccC is hrpG/hrpX-dependent. Moreover, the secretion of AvrXccC displayed hrp-dependency and the core sequence for AvrXccC translocation was defined to the N-terminal 40 amino acids.

Evidence That the Nonstructural Protein ofTomato spotted wilt virusIs the Avirulence Determinant in the Interaction with Resistant Pepper Carrying theTswGene

All known pepper cultivars resistant to Tomato spotted wilt virus (TSWV) possess a single dominant resistance gene, Tsw. Recently, naturally occurring resistance-breaking (RB) TSWV strains have been identified, causing major concerns. We used a collection of such strains to identify the specific genetic determinant that allows the virus to overcome the Tsw gene in Capsicum spp. A reverse genetic approach is still not feasible for TSWV; therefore, we analyzed reassortants between wild-type (WT) and RB strains. Our results confirmed that the S RNA, which encodes both the nucleocapsid protein (N) and a nonstructural protein (NSs), carries the genetic determinant responsible for Tsw resistance breakdown. We then used full-length S RNA segments or the proteins they encode to compare the sequences of WT and related RB strains, and obtained indirect evidence that the NSs protein is the avirulence factor in question. Transient expression of NSs protein from WT and RB strains showed that they both can equally suppress post-transcriptional gene silencing (PTGS). Moreover, biological characterization of two RB strains carrying deletions in the NSs protein showed that NSs is important in maintaining TSWV infection in newly emerging leaves over time, preventing recovery. Analysis of another RB strain phenotype allowed us to conclude that local necrotic response is not sufficient for resistance in Capsicum spp. carrying the Tsw gene.

The PTI1-like kinase ZmPti1a from maize (Zea maysL.) co-localizes with callose at the plasma membrane of pollen and facilitates a competitive advantage to the male gametophyte

BackgroundThe tomato kinase Pto confers resistance to bacterial speck disease caused by Pseudomonas syringae pv. tomato in a gene for gene manner. Upon recognition of specific avirulence factors the Pto kinase activates multiple signal transduction pathways culminating in induction of pathogen defense. The soluble cytoplasmic serine/threonine kinase Pti1 is one target of Pto phosphorylation and is involved in the hypersensitive response (HR) reaction. However, a clear role of Pti1 in plant pathogen resistance is uncertain. So far, no Pti1 homologues from monocotyledonous species have been studied.ResultsHere we report the identification and molecular analysis of four Pti1-like kinases from maize (ZmPti1a, -b, -c, -d). These kinase genes showed tissue-specific expression and their corresponding proteins were targeted to different cellular compartments. Sequence similarity, expression pattern and cellular localization of ZmPti1b suggested that this gene is a putative orthologue of Pti1 from tomato. In contrast, ZmPti1a was specifically expressed in pollen and sequestered to the plasma membrane, evidently owing to N-terminal modification by myristoylation and/or S-acylation. The ZmPti1a:GFP fusion protein was not evenly distributed at the pollen plasma membrane but accumulated as an annulus-like structure which co-localized with callose (1,3-β-glucan) deposition. In addition, co-localization of ZmPti1a and callose was observed during stages of pollen mitosis I and pollen tube germination. Maize plants in which ZmPti1a expression was silenced by RNA interference (RNAi) produced pollen with decreased competitive ability. Hence, our data provide evidence that ZmPti1a plays an important part in a signalling pathway that accelerates pollen performance and male fitness.ConclusionZmPti1a from maize is involved in pollen-specific processes during the progamic phase of reproduction, probably in crucial signalling processes associated with regions of callose deposition. Pollen-sporophyte interactions and pathogen induced HR show certain similarities. For example, HR has been shown to be associated with cell wall reinforcement through callose deposition. Hence, it is hypothesized that Pti1 kinases from maize act as general components in evolutionary conserved signalling processes associated with callose, however during different developmental programs and in different tissue types.

Cereal rust fungi genomics and the pursuit of virulence and avirulence factors

Rust diseases cause significant reductions annually in yield of cereal crops worldwide. Traditional monoculture cropping systems apply significant selection pressure on the pathogen to cause rapid shifts in pathotypes. Plant breeders strive to stay ahead of the evolving pathogens by releasing new crop genotypes with new rust resistance genes or gene combinations. Owing to the limited number of known resistance genes and the lack of molecular understanding of the plant-pathogen interaction, rusts remain challenging organisms to study, both at organismal and molecular levels. This review discusses recent progress by a number of laboratories towards better understanding the molecular component of rust disease resistance.