scholarly journals Direct protein interaction underlies gene-for-gene specificity and coevolution of the flax resistance genes and flax rust avirulence genes

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


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.


2020 ◽  
Vol 33 (7) ◽  
pp. 996-1006
Author(s):  
Jing Wang ◽  
Fengsheng Hao ◽  
Kunfeng Song ◽  
Weihuan Jin ◽  
Bo Fu ◽  
...  

Tobacco mosaic virus (TMV) infection can causes serious damage to tobacco crops. To explore the approach of preventing TMV infection of plants, two tobacco cultivars with different resistances to TMV were used to analyze transcription profiling before and after TMV infection. The involvement of biological pathways differed between the tolerant variety (Yuyan8) and the susceptible variety (NC89). In particular, the plant–virus interaction pathway was rapidly activated in Yuyan8, and specific resistance genes were enriched. Liquid chromatography tandem mass spectrometry analysis detected large quantities of antiviral substances in the tolerant Yuyan8. A novel Nicotiana tabacum leucine-rich repeat receptor kinase (NtLRR-RLK) gene was identified as being methylated and this was verified using bisulfite sequencing. Transient expression of TMV-green fluorescent protein in pRNAi-NtLRR-RLK transgenic plants confirmed that NtLRR-RLK was important for susceptibility to TMV. The specific protein interaction map generated from our study revealed that levels of BIP1, E3 ubiquitin ligase, and LRR-RLK were significantly elevated, and all were represented at node positions in the protein interaction map. The same expression tendency of these proteins was also found in pRNAi-NtLRR-RLK transgenic plants at 24 h after TMV inoculation. These data suggested that specific genes in the infection process can activate the immune signal cascade through different resistance genes, and the integration of signal pathways could produce resistance to the virus. These results contribute to the overall understanding of the molecular basis of plant resistance to TMV and in the long term could identify new strategies for prevention and control virus infection.


2017 ◽  
Vol 38 (SI 2 - 6th Conf EFPP 2002) ◽  
pp. 612-614
Author(s):  
N. Mironenko ◽  
O. Filatova ◽  
O. Afanasenko

Ascospore progeny of cross of Pyrenophora teres f. teres isolates was evaluated on virulence to three barley genotypes. Monogenic inheritance of virulence (26 a:17 v and 31 a:18 v) was shown to cultivar Harbin and accession c 21272 and supported by results of two fungal backcrosses. The existence of three unlinked avirulence genes to CI 4922 is suggested (37 a:7 v). The model of interaction between barley resistance genes and avirulence genes with postulated fungal genotypes is proposed.


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