Fungal Avirulence Genes and Plant Resistance Genes: Unraveling the Molecular Basis of Gene-for-gene Interactions

1995 ◽  
pp. 147-185 ◽  
Author(s):  
Pierre J.G.M. De Wit
1995 ◽  
Vol 73 (S1) ◽  
pp. 490-494 ◽  
Author(s):  
Pierre J. G. M. de Wit ◽  
Matthieu H. A. J. Joosten ◽  
Guy Honée ◽  
Paul J. M. J. Vossen ◽  
Ton J. Cozijnsen ◽  
...  

Host genotype specificity in interactions between biotrophic fungal pathogens and plants in most cases complies with the gene-for-gene model. Success or failure of infection is determined by the absence or presence of complementary genes, avirulence and resistance genes, in the pathogen and the host plant, respectively. Resistance, expressed by the induction of a hypersensitive response followed by other defence responses in the host, is envisaged to be based on recognition of the pathogen, mediated through direct interaction between products of avirulence genes of the pathogen (the so-called race-specific elicitors) and receptors in the host plant, the putative products of resistance genes. The interaction between the biotrophic fungus Cladosporium fulvum and its only host, tomato, is a model system to study fungus–plant gene-for-gene relationships. Here we review research on isolation, characterization, and biological function of two race-specific elicitors AVR4 and AVR9 of C. fulvum and cloning and regulation of their encoding genes. Key words: avirulence genes, race-specific elicitors, resistance genes, hypersensitive response, host defense responses.


2006 ◽  
Vol 103 (23) ◽  
pp. 8888-8893 ◽  
Author(s):  
P. N. Dodds ◽  
G. J. Lawrence ◽  
A.-M. Catanzariti ◽  
T. Teh ◽  
C.-I. A. Wang ◽  
...  

2018 ◽  
Author(s):  
Sandeep R. Marla ◽  
Kevin Chu ◽  
Satya Chintamanani ◽  
Dilbag Multani ◽  
Antje Klempien ◽  
...  

ABSTRACTAdult plant resistance (APR) is an enigmatic phenomenon in which resistance genes are ineffective in protecting seedlings from disease but confer robust resistance at maturity. Maize has multiple cases in which genes confer APR to northern leaf spot, a lethal disease caused byCochliobolus carbonumrace 1 (CCR1). The first identified case of APR in maize is encoded by a hypomorphic allele,Hm1A, at thehm1locus. In contrast, wild type alleles ofhm1provide complete protection at all developmental stages and in every part of the maize plant.Hm1encodes an NADPH-dependent reductase, which inactivates HC-toxin, a key virulence effector of CCR1. Cloning and characterization ofHm1Aruled out differential transcription or translation for its APR phenotype and identified an amino acid substitution that reduced HC-toxin reductase (HCTR) activity. The possibility of a causal relationship between the weak nature ofHm1Aand its APR phenotype was confirmed by the generation of two new APR alleles ofHm1by mutagenesis. The HCTRs encoded by these new APR alleles had undergone relatively conservative missense changes that partially reduced their enzymatic activity similar to HM1A. No difference in accumulation of HCTR was observed between adult and juvenile plants, suggesting that the susceptibility of seedlings derives from a greater need for HCTR activity, not reduced accumulation of the gene product. Conditions and treatments that altered the photosynthetic output of the host had a dramatic effect on resistance imparted by the APR alleles, demonstrating a link between the energetic or metabolic status of the host and disease resistance affected by HC-toxin catabolism by the APR alleles of HCTR.AUTHOR SUMMARYAdult plant resistance (APR) is a phenomenon in which disease resistance genes are able to confer resistance at the adult stages of the plant but somehow fail to do so at the seedling stages. Despite the widespread occurrence of APR in various plant diseases, the mechanism underlying this trait remains obscure. It is not due to the differential transcription of these genes, and here we show that it is also not due to the differential translation or activity of the APR alleles of the maizehm1gene at different stages of development. Using a combination of molecular genetics, biochemistry and physiology, we present multiple lines of evidence that demonstrate that APR is a feature or symptom of weak forms of resistance. While the mature parts of the plant are metabolically robust enough to manifest resistance, seedling tissues are not, leaving them vulnerable to disease. Growth conditions that compromise the photosynthetic output of the plant further deteriorate the ability of the seedlings to protect themselves from pathogens.One sentence summaryCharacterization of adult plant resistance in the maize-CCR1 pathosystem reveals a causal link between weak resistance and APR.


2011 ◽  
Vol 77 (20) ◽  
pp. 7147-7150 ◽  
Author(s):  
Kristina Kadlec ◽  
Ellen von Czapiewski ◽  
Heike Kaspar ◽  
Jürgen Wallmann ◽  
Geovana Brenner Michael ◽  
...  

ABSTRACTSulfonamide-trimethoprim-resistantAeromonas salmonicidaand motileAeromonasspp. from diseased fish of the GERM-Vet study carried thesul1gene together with mostly cassette-borne trimethoprim resistance genes, including the novel genedfrA28. The sevendfrAanddfrBgenes identified were located mostly in class 1 integrons which commonly harbored other gene cassettes.


2016 ◽  
Vol 83 (4) ◽  
Author(s):  
V. Chellappan Biju ◽  
Like Fokkens ◽  
Petra M. Houterman ◽  
Martijn Rep ◽  
Ben J. C. Cornelissen

ABSTRACT Race 1 isolates of Fusarium oxysporum f. sp. lycopersici (FOL) are characterized by the presence of AVR1 in their genomes. The product of this gene, Avr1, triggers resistance in tomato cultivars carrying resistance gene I. In FOL race 2 and race 3 isolates, AVR1 is absent, and hence they are virulent on tomato cultivars carrying I. In this study, we analyzed an approximately 100-kb genomic fragment containing the AVR1 locus of FOL race 1 isolate 004 (FOL004) and compared it to the sequenced genome of FOL race 2 isolate 4287 (FOL4287). A genomic fragment of 31 kb containing AVR1 was found to be missing in FOL4287. Further analysis suggests that race 2 evolved from race 1 by deletion of this 31-kb fragment due to a recombination event between two transposable elements bordering the fragment. A worldwide collection of 71 FOL isolates representing races 1, 2, and 3, all known vegetative compatibility groups (VCGs), and five continents was subjected to PCR analysis of the AVR1 locus, including the two bordering transposable elements. Based on phylogenetic analysis using the EF1-α gene, five evolutionary lineages for FOL that correlate well with VCGs were identified. More importantly, we show that FOL races evolved in a stepwise manner within each VCG by the loss of function of avirulence genes in a number of alternative ways. IMPORTANCE Plant-pathogenic microorganisms frequently mutate to overcome disease resistance genes that have been introduced in crops. For the fungus Fusarium oxysporum f. sp. lycopersici, the causal agent of Fusarium wilt in tomato, we have identified the nature of the mutations that have led to the overcoming of the I and I-2 resistance genes in all five known clonal lineages, which include a newly discovered lineage. Five different deletion events, at least several of which are caused by recombination between transposable elements, have led to loss of AVR1 and overcoming of I. Two new events affecting AVR2 that led to overcoming of I-2 have been identified. We propose a reconstruction of the evolution of races in FOL, in which the same mutations in AVR2 and AVR3 have occurred in different lineages and the FOL pathogenicity chromosome has been transferred to new lineages several times.


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