Identification and fine mapping of AvrPi15, a novel avirulence gene of Magnaporthe grisea

2006 ◽  
Vol 113 (5) ◽  
pp. 875-883 ◽  
Author(s):  
Jun-Hong Ma ◽  
Ling Wang ◽  
Shu-Jie Feng ◽  
Fei Lin ◽  
Yi Xiao ◽  
...  
2003 ◽  
Vol 107 (6) ◽  
pp. 1139-1147 ◽  
Author(s):  
R. Berruyer ◽  
H. Adreit ◽  
J. Milazzo ◽  
S. Gaillard ◽  
A. Berger ◽  
...  

2003 ◽  
Vol 93 (11) ◽  
pp. 1452-1459 ◽  
Author(s):  
Yulin Jia ◽  
Gregory T. Bryan ◽  
Leonard Farrall ◽  
Barbara Valent

The resistance gene Pi-ta protects rice crops against the fungal pathogen Magnaporthe grisea expressing the avirulence gene AVR-Pita in a gene-for-gene manner. Pi-ta, originally introgressed into japonica rice from indica origin, was previously isolated by positional cloning. In this study, we report the nucleotide sequence of a 5,113-base pair region containing a japonica susceptibility pi-ta allele, which has overall 99.6% nucleotide identity to the indica Pi-ta allele conferring resistance. The intron region shows the levels of sequence diversity that typically differentiate genes from indica and japonica rices, but the other gene regions show less diversity. Sequences of the Pi-ta allele from resistant cultivars Katy and Drew from the southern United States are identical to the resistance Pi-ta sequence. Sequences from susceptible cultivars El Paso 144 and Cica 9 from Latin America define a third susceptibility haplotype. This brings the total number of Pi-ta haplotypes identified to four, including the resistance allele and three susceptibility alleles. The Pi-ta locus shows low levels of DNA polymorphism compared with other analyzed R genes. Understanding the natural diversity at the Pi-ta locus is important for designing specific markers for incorporation of this R gene into rice-breeding programs.


2005 ◽  
Vol 95 (7) ◽  
pp. 768-772 ◽  
Author(s):  
N. Yasuda ◽  
M. T. Noguchi ◽  
Y. Fujita

A rice isolate of Magnaporthe grisea collected from China was avirulent on rice cvs. Hattan 3 and 13 other Japanese rice cultivars. The rice cv. Hattan 3 is susceptible to almost all Japanese blast fungus isolates from rice. The genetic basis of avirulence in the Chinese isolate on Japanese rice cultivars was studied using a cross between the Chinese isolate and a laboratory isolate. The segregation of avirulence or virulence was studied in 185 progeny from the cross, and monogenic control was demonstrated for avirulence to the 14 rice cultivars. The resistance gene that corresponds to the avirulence gene (Avr-Hattan 3) is thought to be located at the Pik locus. Resistance and susceptibility in response to the Chinese isolate in F3 lines of a cross of resistant and susceptible rice cultivars were very similar to the Pik tester isolate, Ken54-20. Random amplified polymorphic DNA markers and restriction fragment length polymorphism markers from genetic maps of the fungus were used to construct a partial genetic map of Avr-Hattan 3. We obtained several flanking markers and one co-segregated marker of Avr-Hattan 3 in the 144 mapping population.


2015 ◽  
Vol 105 (12) ◽  
pp. 1568-1572 ◽  
Author(s):  
Vu Lan Anh ◽  
Nguyen Tuan Anh ◽  
Analiza Grubanzo Tagle ◽  
Trinh Thi Phuong Vy ◽  
Yoshihiro Inoue ◽  
...  

Blast, caused by Pyricularia oryzae, is one of the major diseases of wheat in South America. We identified a new gene for resistance to Triticum isolates of P. oryzae in common wheat ‘S-615’, and designated it “resistance to Magnaporthe grisea 8” (Rmg8). Rmg8 was assigned to chromosome 2B through molecular mapping with simple-sequence repeat markers. To identify an avirulence gene corresponding to Rmg8, Triticum isolate Br48 (avirulent on S-615) was crossed with 200R29 (virulent on S-615), an F1 progeny derived from a cross between an Eleusine isolate (MZ5-1-6) and Br48. Segregation analysis of their progeny revealed that avirulence of Br48 on S-615 was conditioned by a single gene, which was designated AVR-Rmg8. AVR-Rmg8 was closely linked to AVR-Rmg7, which corresponded to Rmg7 located on chromosome 2A of tetraploid wheat.


2008 ◽  
Vol 21 (5) ◽  
pp. 658-670 ◽  
Author(s):  
Chang Hyun Khang ◽  
Sook-Young Park ◽  
Yong-Hwan Lee ◽  
Barbara Valent ◽  
Seogchan Kang

The avirulence (AVR) gene AVR-Pita in Magnaporthe oryzae prevents the fungus from infecting rice cultivars containing the resistance gene Pi-ta. A survey of isolates of the M. grisea species complex from diverse hosts showed that AVR-Pita is a member of a gene family, which led us to rename it to AVR-Pita1. Avirulence function, distribution, and genomic context of two other members, named AVR-Pita2 and AVR-Pita3, were characterized. AVR-Pita2, but not AVR-Pita3, was functional as an AVR gene corresponding to Pi-ta. The AVR-Pita1 and AVR-Pita2 genes were present in isolates of both M. oryzae and M. grisea, whereas the AVR-Pita3 gene was present only in isolates of M. oryzae. Orthologues of members of the AVR-Pita family could not be found in any fungal species sequenced to date, suggesting that the gene family may be unique to the M. grisea species complex. The genomic context of its members was analyzed in eight strains. The AVR-Pita1 and AVR-Pita2 genes in some isolates appeared to be located near telomeres and flanked by diverse repetitive DNA elements, suggesting that frequent deletion or amplification of these genes within the M. grisea species complex might have resulted from recombination mediated by repetitive DNA elements.


Plant Disease ◽  
2008 ◽  
Vol 92 (8) ◽  
pp. 1144-1149 ◽  
Author(s):  
N. Yasuda ◽  
M. T. Noguchi ◽  
Y. Fujita

Incompatibility reactions between rice and the blast fungus Magnaporthe grisea produce various degrees of lesions, from large brown flecks to small, nearly invisible lesions. We previously identified four avirulence genes (AvrPia, AvrPii, AvrPit, and Avr-Hattan3) in M. grisea isolates by genetic analysis of progeny from crosses between isolates with differing pathogenicity. Using progeny known to contain a specific avirulence gene, we demonstrated that the type of resistance lesion produced in rice by an avirulent isolate and the degree of leaf blast suppression by preinoculation with that isolate were determined by the combination of avirulence and resistance genes in the isolate and the cultivar. The degree of leaf blast suppression by preinoculation with an avirulent isolate increased with larger resistance lesions. When two genes were involved in an isolate's avirulence, lesions appeared that resembled those expected for the gene that produced the smaller lesion. The degree of leaf blast suppression by the isolate with two avirulence genes was comparable with that induced by the isolate with the avirulence gene that produced the smaller effect. The ability of specific resistance gene combinations that effectively suppress blast disease is discussed for each avirulence gene.


2000 ◽  
Vol 13 (2) ◽  
pp. 217-227 ◽  
Author(s):  
Waly Dioh ◽  
Didier Tharreau ◽  
Jean Loup Notteghem ◽  
Marc Orbach ◽  
Marc-Henri Lebrun

Three genetically independent avirulence genes, AVR1-Irat7, AVR1-MedNoï, and AVR1-Ku86, were identified in a cross involving isolates Guy11 and 2/0/3 of the rice blast fungus, Magnaporthe grisea. Using 76 random progeny, we constructed a partial genetic map with restriction fragment length polymorphism (RFLP) markers revealed by probes such as the repeated sequences MGL/MGR583 and Pot3/MGR586, cosmids from the M. grisea genetic map, and a telomere sequence oligonucleotide. Avirulence genes AVR1-MedNoï and AVR1-Ku86 were closely linked to te-lomere RFLPs such as marker TelG (6 cM from AVR1-MedNoï) and TelF (4.5 cM from AVR1-Ku86). Avirulence gene AVR1-Irat7 was linked to a cosmid RFLP located on chromosome 1 and mapped at 20 cM from the avirulence gene AVR1-CO39. Using bulked segregant analysis, we identified 11 random amplified polymorphic DNA (RAPD) markers closely linked (0 to 10 cM) to the avirulence genes segregating in this cross. Most of these RAPD markers corresponded to junction fragments between known or new transposons and a single-copy sequence. Such junctions or the whole sequences of single-copy RAPD markers were frequently absent in one parental isolate. Single-copy sequences from RAPD markers tightly linked to avirulence genes will be used for positional cloning.


2005 ◽  
Vol 42 (9) ◽  
pp. 761-772 ◽  
Author(s):  
Isabelle Fudal ◽  
Heidi U. Böhnert ◽  
Didier Tharreau ◽  
Marc-Henri Lebrun

2007 ◽  
Vol 6 (3) ◽  
pp. 546-554 ◽  
Author(s):  
Isabelle Fudal ◽  
Jérôme Collemare ◽  
Heidi U. Böhnert ◽  
Delphine Melayah ◽  
Marc-Henri Lebrun

ABSTRACT Magnaporthe grisea is responsible for a devastating fungal disease of rice called blast. Current control of this disease relies on resistant rice cultivars that recognize M. grisea signals corresponding to specific secreted proteins encoded by avirulence genes. The M. grisea ACE1 avirulence gene differs from others, since it controls the biosynthesis of a secondary metabolite likely recognized by rice cultivars carrying the Pi33 resistance gene. Using a transcriptional fusion between ACE1 promoter and eGFP, we showed that ACE1 is only expressed in appressoria during fungal penetration into rice and barley leaves, onion skin, and cellophane membranes. ACE1 is almost not expressed in appressoria differentiated on Teflon and Mylar artificial membranes. ACE1 expression is not induced by cellophane and plant cell wall components, demonstrating that it does not require typical host plant compounds. Cyclic AMP (cAMP) signaling mutants ΔcpkA and Δmac1 sum1-99 and tetraspanin mutant Δpls1::hph differentiate melanized appressoria with normal turgor but are unable to penetrate host plant leaves. ACE1 is normally expressed in these mutants, suggesting that it does not require cAMP signaling or a successful penetration event. ACE1 is not expressed in appressoria of the buf1::hph mutant defective for melanin biosynthesis and appressorial turgor. The addition of hyperosmotic solutes to buf1::hph appressoria restores appressorial development and ACE1 expression. Treatments of young wild-type appressoria with actin and tubulin inhibitors reduce both fungal penetration and ACE1 expression. These experiments suggest that ACE1 appressorium-specific expression does not depend on host plant signals but is connected to the onset of appressorium-mediated penetration.


Sign in / Sign up

Export Citation Format

Share Document