Rice ESTs with disease-resistance gene- or defense-response gene-like sequences mapped to regions containing major resistance genes or QTLs

2001 ◽  
Vol 265 (2) ◽  
pp. 302-310 ◽  
Author(s):  
Z. Wang ◽  
G. Taramino ◽  
D. Yang ◽  
G. Liu ◽  
S.V. Tingey ◽  
...  
Genetics ◽  
2002 ◽  
Vol 162 (4) ◽  
pp. 1961-1977
Author(s):  
Michelle A Graham ◽  
Laura Fredrick Marek ◽  
Randy C Shoemaker

Abstract PCR amplification was previously used to identify a cluster of resistance gene analogues (RGAs) on soybean linkage group J. Resistance to powdery mildew (Rmd-c), Phytophthora stem and root rot (Rps2), and an ineffective nodulation gene (Rj2) map within this cluster. BAC fingerprinting and RGA-specific primers were used to develop a contig of BAC clones spanning this region in cultivar “Williams 82” [rps2, Rmd (adult onset), rj2]. Two cDNAs with homology to the TIR/NBD/LRR family of R-genes have also been mapped to opposite ends of a BAC in the contig Gm_Isb001_091F11 (BAC 91F11). Sequence analyses of BAC 91F11 identified 16 different resistance-like gene (RLG) sequences with homology to the TIR/NBD/LRR family of disease resistance genes. Four of these RLGs represent two potentially novel classes of disease resistance genes: TIR/NBD domains fused inframe to a putative defense-related protein (NtPRp27-like) and TIR domains fused inframe to soybean calmodulin Ca2+-binding domains. RT-PCR analyses using gene-specific primers allowed us to monitor the expression of individual genes in different tissues and developmental stages. Three genes appeared to be constitutively expressed, while three were differentially expressed. Analyses of the R-genes within this BAC suggest that R-gene evolution in soybean is a complex and dynamic process.


Genome ◽  
1997 ◽  
Vol 40 (5) ◽  
pp. 659-665 ◽  
Author(s):  
Evans S. Lagudah ◽  
Odile Moullet ◽  
Rudi Appels

The Cre3 gene confers a high level of resistance to the root endoparasitic nematode Heterodera avenae in wheat. A DNA marker cosegregating with H. avenae resistance was used as an entry point for map-based cloning of a disease resistance gene family at the Cre3 locus. Two related gene sequences have been analysed at the Cre3 locus. One, identified as a cDNA clone, encodes a polypeptide with a nucleotide binding site (NBS) and a leucine-rich region; this member of the disease resistance gene family is expressed in roots. A second Cre3 gene sequence, cloned as genomic DNA, appears to be a pseudogene, with a frame shift caused by a deletion event. These two genes, related to members of the cytoplasmic NBS – leucine rich repeat class of plant disease resistance genes were physically mapped to the distal 0.06 fragment of the long arm of wheat chromosome 2D and cosegregated with nematode resistance.Key words: cereal cyst nematode, disease resistance genes, nucleotide-binding site, leucine-rich repeat.


1998 ◽  
Vol 11 (10) ◽  
pp. 968-978 ◽  
Author(s):  
N. C. Collins ◽  
C. A. Webb ◽  
S. Seah ◽  
J. G. Ellis ◽  
S. H. Hulbert ◽  
...  

Many of the plant disease resistance genes that have been isolated encode proteins with a putative nucleotide binding site and leucine-rich repeats (NBS-LRR resistance genes). Oligonucleotide primers based on conserved motifs in and around the NBS of known NBS-LRR resistance proteins were used to amplify sequences from maize genomic DNA by polymerase chain reaction (PCR). Eleven classes of non-cross-hybridizing sequences were obtained that had predicted products with high levels of amino acid identity to NBS-LRR resistance proteins. These maize resistance gene analogs (RGAs) and one RGA clone obtained previously from wheat were used as probes to map 20 restriction fragment length polymorphism (RFLP) loci in maize. Some RFLPs were shown to map to genomic regions containing virus and fungus resistance genes. Perfect co-segregation was observed between RGA loci and the rust resistance loci rp1 and rp3. The RGA probe associated with rp1 also detected deletion events in several rp1 mutants. These data strongly suggest that some of the RGA clones may hybridize to resistance genes.


2001 ◽  
Vol 14 (2) ◽  
pp. 181-188 ◽  
Author(s):  
Michael J. Axtell ◽  
Timothy W. McNellis ◽  
Mary Beth Mudgett ◽  
Caroline S. Hsu ◽  
Brian J. Staskawicz

Plants have evolved a large number of disease resistance genes that encode proteins containing conserved structural motifs that function to recognize pathogen signals and to initiate defense responses. The Arabidopsis RPS2 gene encodes a protein representative of the nucleotide-binding site-leucine-rich repeat (NBS-LRR) class of plant resistance proteins. RPS2 specifically recognizes Pseudomonas syringae pv. tomato strains expressing the avrRpt2 gene and initiates defense responses to bacteria carrying avrRpt2, including a hypersensitive cell death response (HR). We present an in planta mutagenesis experiment that resulted in the isolation of a series of rps2 and avrRpt2 alleles that disrupt the RPS2-avrRpt2 gene-for-gene interaction. Seven novel avrRpt2 alleles incapable of eliciting an RPS2-dependent HR all encode proteins with lesions in the C-terminal portion of AvrRpt2 previously shown to be sufficient for RPS2 recognition. Ten novel rps2 alleles were characterized with mutations in the NBS and the LRR. Several of these alleles code for point mutations in motifs that are conserved among NBS-LRR resistance genes, including the third LRR, which suggests the importance of these motifs for resistance gene function.


Genome ◽  
1999 ◽  
Vol 42 (4) ◽  
pp. 735-743 ◽  
Author(s):  
A Joyeux ◽  
M G Fortin ◽  
R Mayerhofer ◽  
A G Good

Genetic mapping of plants traditionally involves the analysis of large segregating populations. However, not all individuals in a population contribute equal amounts of genetic information. It is thus possible to achieve rough mapping using a subset of the most informative individuals in the population. We have designed a minimal Brassica napus mapping population of 23 doubled-haploid plants and have tested this method using this population in the mapping of disease resistance gene homologues in B. napus. Several groups have identified such homologues in soybean and potato by amplifying sequences corresponding to conserved nucleotide-binding sites from known resistance genes. However, the sequence conservation in the leucine-rich repeat domain that is present in most of the disease resistance genes isolated has not been exploited via the polymerase chain reaction (PCR). We present the genetic mapping of Brassica napus DNA sequences amplified with primers corresponding to both the nucleotide-binding site and the leucine rich-repeat domain of the Arabidopsis thaliana RPS2 gene. We also describe a method for the quick mapping of resistance gene homologues using the polymerase chain reaction.Key words: Brassica napus, disease resistance genes, minimal mapping population, RFLP markers.


Genome ◽  
2000 ◽  
Vol 43 (1) ◽  
pp. 86-93 ◽  
Author(s):  
Michelle A Graham ◽  
Laura Fredrick Marek ◽  
David Lohnes ◽  
Perry Cregan ◽  
Randy C Shoemaker

Sequence analysis of cloned plant disease-resistance genes reveals a number of conserved domains. Researchers have used these domains to amplify analogous sequences, resistance gene analogs (RGAs), from soybean and other crops. Many of these RGAs map in close proximity to known resistance genes. While this technique is useful in identifying potential disease resistance loci, identifying the functional resistance gene from a cluster of homologs requires sequence information from outside of these conserved domains. To study RGA expression and to determine the extent of their similarity to other plant resistance genes, two soybean cDNA libraries (root and epicotyl) were screened by hybridization with RGA class-specific probes. cDNAs hybridizing to RGA probes were detected in each library. Two types of cDNAs were identified. One type was full-length and contained several disease-resistance gene (R-gene) signatures. The other type contained several deletions within these signatures. Sequence analyses of the cDNA clones placed them in the Toll-Interleukin-1 receptor, nucleotide binding domain, and leucine-rich repeat family of disease-resistance genes. Using clone-specific primers from within the 3' end of the LRRs, we were able to map two cDNA clones (LM6 and MG13) to a BAC contig that is known to span a cluster of disease-resistance genes. Key words: expression, R-genes, contig, RGAs, soybean.


1995 ◽  
Vol 73 (S1) ◽  
pp. 468-474 ◽  
Author(s):  
G. S. Johal ◽  
J. Gray ◽  
D. Gruis ◽  
S. P. Briggs

In this review, an attempt has been made to scrutinize mechanisms controlling disease or resistance from the perspective of biological forces and constraints affecting co-evolution of a fungal pathogen with its plant host. We reckon that plants are naturally resistant to almost all potentially pathogenic organisms. Defense mechanisms responsible for this default resistance, also termed nonhost or general resistance, are many and include both physical and chemical factors triggered rapidly in response to attempted infection. Pathogenic organisms have to contend with these mechanisms before they can succeed in colonizing a plant. It appears that two different strategies, biotrophic and necrotrophic, have evolved in fungi for this purpose. In the former, defenses are not allowed to be triggered, and in the latter these mechanisms are suppressed or nullified. Consequently, two different kinds of resistance mechanisms have evolved in plants. Against biotrophs, resistance genes function to ensure that normal plant defenses are triggered in time to keep the plant resistant to the pathogen. Against necrotrophs, resistance genes operate to negate the key pathogenic strategy of the invader. Further evolution between the host and the pathogen, and hence durability of a disease resistance gene, is governed by the importance of the fungal target of a disease resistance gene in plant pathogenesis. Key words: disease resistance, plant–fungal interaction, plant pathogenesis, gene-for-gene interaction, defense mechanisms.


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