Does a cognate receptor know its own effector?

Introduction to a Virtual Special Issue on cell biology at the plant-microbe interface.

The coming of age of EvoMPMI: evolutionary molecular plant–microbe interactions across multiple timescales

Powdery mildews, obligate biotrophic fungal parasites on a wide range of important crops, can be controlled by plant resistance (R) genes, but these are rapidly overcome by parasite mutants evading recognition. It is unknown how this rapid evolution occurs without apparent loss of parasite fitness. R proteins recognize avirulence (AVR) molecules from parasites in a gene-for-gene manner and trigger defense responses. We identify AVR(a10) and AVR(k1) of barley powdery mildew fungus, Blumeria graminis f sp hordei (Bgh), and show that they induce both cell death and inaccessibility when transiently expressed in Mla10 and Mlk1 barley (Hordeum vulgare) varieties, respectively. In contrast with other reported fungal AVR genes, AVR(a10) and AVR(k1) encode proteins that lack secretion signal peptides and enhance infection success on susceptible host plant cells. AVR(a10) and AVR(k1) belong to a large family with >30 paralogues in the genome of Bgh, and homologous sequences are present in other formae speciales of the fungus infecting other grasses. Our findings imply that the mildew fungus has a repertoire of AVR genes, which may function as effectors and contribute to parasite virulence. Multiple copies of related but distinct AVR effector paralogues might enable populations of Bgh to rapidly overcome host R genes while maintaining virulence.

The common wheat cultivar 'Chancellor' and its near-isogenic lines carrying resistance genes to Erysiphe graminis f.sp. tritici were inoculated with 240 F1 cultures derived from a cross between E. graminis f.sp. agropyri, Ak-1, and E. graminis f.sp. tritici, Tk-1. Segregation patterns of avirulent and virulent cultures suggested that the F1 population carries avirulence genes corresponding to Pm1, Pm2, Pm3a, and Pm3b. These avirulence genes were considered to be derived from Ak-1. It was therefore concluded that Pm1, Pm2, Pm3a, and Pm3b, resistance genes to E. graminis f.sp. tritici, operate against E. graminis f.sp. agropyri.Key words: powdery mildew, Erysiphe graminis, resistance, wheat, wheatgrass.

Preparatory work for the pest categorisation of three bacteria listed in the annexes of the Council directive 2000/29/EC Erwinia amylovora Winslow et al. Xylophilus ampelinus (Panagopoulos) Willems et al. Clavibacter michiganensis subsp. insidiosus(McCulloch) Davis et al

A Genetic Map of Blumeria graminis Based on Functional Genes, Avirulence Genes, and Molecular Markers

Plant disease resistance (R) gene products recognize pathogen avirulence (Avr) gene products and induce defense responses. It is not known if an R gene can function in different plant families, however. The Arabidopsis thaliana R genes RPW8.1 and RPW8.2 confer resistance to the powdery mildew pathogens Erysiphe orontii, E. cichoracearum, and Oidium lycopersici, which also infect plants from other families. We produced transgenic Nicotiana tabacum, N. benthamiana, and Lycopersicon esculentum plants containing RPW8.1 and RPW8.2. Transgenic N. tabacum plants had increased resistance to E. orontii and O. lycopersici, transgenic N. benthamiana plants had increased resistance to E. cichoracearum, but transgenic L. esculentum plants remained susceptible to these pathogens. The defense responses induced in transgenic N. tabacum and N. benthamiana were similar to those mediated by RPW8.1 and RPW8.2 in Arabidopsis. Apparently, RPW8.1 and RPW8.2 could be used to control powdery mildew diseases of plants from other families.

We try to mimic the unidirectional sliding-type movement of the PP-tRNA . mRNA complex with respect to the ribosome by looking at the effect of different combinations of cognate tRNAs on the stability of the 70S-AUGUn complex. The association constant for the binary complex 70S-AUGU3 was determined as 6.8 x 10(5) M-1. Addition of tRNAfMet resulted in a 67-fold increase in the association constant, which with both cognate tRNAs is revised to Kassoc = 2.2 x 10(8) M-1. Increasing the chain length of the oligonucleotide from AUGU3 to AUGU13 did not further raise the association constant. The data indicate that the stability of the 70S ribosome . mRNA interaction is governed by the presence of the cognate tRNAs and is topographically restricted to the decoding domains. Since a peptidyl group in the tRNA increases the affinity of AUGU3 for the ribosome by up to 15-fold, we conclude that the affinity of the peptidyl transfer center for the peptidyl moiety pulls the PP-tRNA . mRNA complex from the A (aminoacyl-tRNA) site to the P (peptidyl-tRNA) site. EF-G . GTP or EF-G . GMPPCP 5'-(beta, gamma-methylene)triphosphate] displace tRNAfMet from the quaternary complex 70S . AUGUn . tRNAfMet . tRNAPhe (n = 3 and 6) at Mg2+ less than 25 mM. From the amount of EF-G . GTP bound to a 70S ribosome, it follows that the elongation factor replaces the deacylated tRNA in a stoichiometric way. These data indicate that the EF-G . GTP-dependent release of the deacylated tRNA from the P site, followed by removal of EF-G . GDP from the 50S subunit, is sufficient to trigger the translocation of the mRNA . PP-tRNA complex.

Effector-triggered immunity (ETI) can be defined as immune responses activated upon specific recognition of a pathogen effector protein by its cognate plant immune receptor protein. This classic gene-for-gene model of the interaction of one pathogen effector, also known as an Avirulence (Avr) gene, with one plant immune receptor gene, known as a Resistance (R) gene has been documented since the 1950s. Since then, different types of recognition that deviate from the gene-for-gene model, for example, immune receptor pairs and immune receptor networks, have been identified. In addition, while many R genes encode NLR (nucleotide binding, leucine rich repeat) proteins, R genes that encode only parts of NLR domains, and non-NLR encoding R genes such as tandem kinases have been identified, broadening the immune receptor repertoire in plants. In recent years, there have been significant advances in understanding the molecular mechanisms of NLR intracellular immune receptors in plants, including how they are inhibited, activated, and regulated. This review covers recent developments in ETI initiation mechanisms and in plant NLR biology.

SummaryChitin, a major component of fungal cell walls, is a well‐known pathogen‐associated molecular pattern (PAMP) that triggers defense responses in several mammal and plant species. Here, we show that two chitooligosaccharides, chitin and chitosan, act as PAMPs in grapevine (Vitis vinifera) as they elicit immune signalling events, defense gene expression and resistance against fungal diseases. To identify their cognate receptors, the grapevine family of LysM receptor kinases (LysM‐RKs) was annotated and their gene expression profiles were characterized. Phylogenetic analysis clearly distinguished three V. vinifera LysM‐RKs (VvLYKs) located in the same clade as the Arabidopsis CHITIN ELICITOR RECEPTOR KINASE1 (AtCERK1), which mediates chitin‐induced immune responses. The Arabidopsis mutant Atcerk1, impaired in chitin perception, was transformed with these three putative orthologous genes encoding VvLYK1‐1, ‐2, or ‐3 to determine if they would complement the loss of AtCERK1 function. Our results provide evidence that VvLYK1‐1 and VvLYK1‐2, but not VvLYK1‐3, functionally complement the Atcerk1 mutant by restoring chitooligosaccharide‐induced MAPK activation and immune gene expression. Moreover, expression of VvLYK1‐1 in Atcerk1 restored penetration resistance to the non‐adapted grapevine powdery mildew (Erysiphe necator). On the whole, our results indicate that the grapevine VvLYK1‐1 and VvLYK1‐2 participate in chitin‐ and chitosan‐triggered immunity and that VvLYK1‐1 plays an important role in basal resistance against E. necator.

Powdery mildew of Arabidopsis thaliana: a pathosystem for exploring the role of silicon in plant–microbe interactions

The genetics of avirulence were studied in crosses of the barley powdery mildew fungus Erysiphe graminis f. sp. hordei (synamorph Blumeria graminis f. sp. hordei). The number of genes controlling avirulence on 10 near-isogenic lines of Pallas carrying different resistance genes were determined, as were the incompatible infection types (ITs) they conferred. Four crosses were made between isolates of different origins, and one cross, CC52 x DH14, was analyzed further with backcrosses and sibcrosses. Avirulence on P11 (Mla13) was controlled by two genes giving different ITs: Avr a13 1 with ITs 0 or 0-1 and Avr a13 2 with ITs 1-2 or 2. Two hypotheses can be suggested: (i) P11 carries a second gene, Mla(Ru3), in addition to Mla13, and each resistance gene matches one avirulence gene; or (ii) P11 carries the single resistance gene Mla13, which matches the two avirulence genes. Avirulences on P01 (Mlal), P08B (Mla9), P09 (Mla10), P10 (Mla12), P12 (Mla22), P16 (Mlkl), and P21 (Mlg) were controlled by one gene in all crosses in which phenotypes segregated. It could not be concluded whether avirulence on P04B (Mla7) and P23 (MlLa) was controlled by one or two genes. One linkage group, including Avr a9 , Avr a10 , Avr a22 , Avr k1 , and probably Avr a13 1, was detected.

Ultrastructural comparison of a compatible and incompatible interaction triggered by the presence of an avirulence gene during early infection of the smut fungus, Ustilago hordei, in barley

RNA Splicing: A Novel Pathogen Effector Target

Chloroplasts isolated from powdery mildew-infected (Erysiphe polygoni DC) sugar beet leaves (Beta vulgaris L) showed a reduction in the rate of electron transport and in the accompanying ATP formation in noncyclic photophosphorylation (water as electron donor, NADP as electron acceptor) and little or no change in the rate of ATP formation in cyclic photophosphorylation catalyzed by phenazine methosulfate. The inhibition of noncyclic photophosphorylation appeared to lead in the parent leaves to a decreased rate of photosynthetic CO(2) assimilation and a shift in products resulting in a relative increase of amino acids. These changes were accompanied by alterations in chloroplast ultrastructure and by a reduction in the activity of enzymes necessary for the formation of organic acids (phosphoenolpyruvate carboxylase and malate dehydrogenase). These results are similar to the findings of Montalbini and Buchanan (1974 Physiol. Plant Pathol. 4: 191-196) with chloroplasts from rust-infected Vicia faba leaves.