%D 2003 %0 ARTICLE %T Identification and fine mapping of Pi33 , the rice resistance gene corresponding to the Magnaporthe grisea avirulence gene ACE1 . %J Theor . Appl . Genet . %V 107 ( 6 ) %P 1139-47 %A Berruyer R %A Adreit H %A Milazzo J %A Gaillard S %A Berger A %A Dioh W %A Lebrun MH %A Tharreau D %M pub12838393 %X Rice blast disease is a major constraint for rice breeding . Nevertheless , the genetic basis of resistance remains poorly understood for most rice varieties , and new resistance genes remain to be identified . We identified the resistance gene corresponding to the cloned avirulence gene ACE1 using pairs of isogenic strains of Magnaporthe grisea differing only by their ACE1 allele . This resistance gene was mapped on the short arm of rice chromosome 8 using progenies from the crosses IR64 ( resistant ) x Azucena ( susceptible ) and Azucena x Bala ( resistant ) . The isogenic strains also permitted the detection of this resistance gene in several rice varieties , including the differential isogenic line C101LAC . Allelism tests permitted us to distinguish this gene from two other resistance genes [ Pi11 and Pi-29 ( t ) ] that are present on the short arm of chromosome 8 . Segregation analysis in F ( 2 ) populations was in agreement with the existence of a single dominant gene , designated as Pi33 . Finally , Pi33 was finely mapped between two molecular markers of the rice genetic map that are separated by a distance of 1 . 6 cM . Detection of Pi33 in different semi-dwarf indica varieties indicated that this gene could originate from either one or a few varieties . %D 2004 %0 ARTICLE %T A putative polyketide synthase/peptide synthetase from Magnaporthe grisea signals pathogen attack to resistant rice . %J Plant Cell %V 16 ( 9 ) %P 2499-513 %A Bhnert HU %A Fudal I %A Dioh W %A Tharreau D %A Notteghem JL %A Lebrun MH %M pub15319478 %X Isolates of the rice blast fungus Magnaporthe grisea that carry the gene encoding Avirulence Conferring Enzyme1 ( ACE1 ) are specifically recognized by rice ( Oryza sativa ) cultivars carrying the resistance gene Pi33 . This recognition enables resistant plants to activate a defense response . ACE1 was isolated by map-based cloning and encodes a putative hybrid between a polyketide synthase and a nonribosomal peptide synthetase , enzymes involved in microbial secondary metabolism . ACE1 is expressed exclusively during fungal penetration of host leaves , the time point at which plant defense reactions are triggered . Ace1 appears to be localized in the cytoplasm of the appressorium . Mutation of the putative catalytic site of the beta-ketoacyl synthase domain of Ace1 abolishes recognition of the fungus by resistant rice . This suggests that Ace1 biosynthetic activity is required for avirulence . Our results are consistent with the hypothesis that the fungal signal recognized by resistant rice plants is the secondary metabolite whose synthesis depends on Ace1 . %D 2007 %0 ARTICLE %T Expression of Magnaporthe grisea avirulence gene ACE1 is connected to the initiation of appressorium-mediated penetration . %J Eukaryotic Cell %V 6 ( 3 ) %P 546-54 %A Fudal I %A Collemare J %A Bhnert HU %A Melayah D %A Lebrun MH %M pub17142568 %X 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 delta cpkA and delta mac1 sum1-99 and tetraspanin mutant delta pls1 : : 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 . %D %0 ARTICLE %T Early and specific gene expression triggered by rice resistance gene Pi33 in response to infection by ACE1 avirulent blast fungus . %J New Phytol . %V 174 ( 1 ) %P 159-71 %A Vergne E %A Ballini E %A Marques S %A Sidi Mammar %A B Droc %A G Gaillard %A S Bourot %A S DeRose %A R Tharreau %A D Nottghem %A JL Lebrun %A MH Morel %M pub17335506 %X * Our view of genes involved in rice disease resistance is far from complete . Here we used a gene-for-gene relationship corresponding to the interaction between atypical avirulence gene ACE1 from Magnaporthe grisea and rice resistance gene Pi33 to better characterize early rice defence responses induced during such interaction . * Rice genes differentially expressed during early stages of Pi33/ACE1 interaction were identified using DNA chip-based differential hybridization and QRT-PCR survey of the expression of known and putative regulators of disease resistance . * One hundred genes were identified as induced or repressed during rice defence response , 80% of which are novel , including resistance gene analogues . Pi33/ACE1 interaction also triggered the up-regulation of classical PR defence genes and a massive down-regulation of chlorophyll a/b binding genes . Most of these differentially expressed genes were induced or repressed earlier in Pi33/ACE1 interaction than in the gene-for-gene interaction involving Nipponbare resistant cultivar . * Besides demonstrating that an ACE1/Pi33 interaction induced classical and specific expression patterns , this work provides a list of new genes likely to be involved in rice disease resistance . %D 2007 %0 MEDLINE %T Modern elite rice varieties of the Green Revolution have retained a large introgression from wild rice around the Pi33 rice blast resistance locus . %J New Phytol %V 175 %P 340-50 %A Ballini E %A Berruyer R %A Morel JB %A Lebrun MH %A Notteghem JL %A Tharreau D %M pub17587382 %X During the breeding process of cultivated crops , resistance genes to pests and diseases are commonly introgressed from wild species . The size of these introgressions is predicted by theoretical models but has rarely been measured in cultivated varieties . By combining resistance tests with isogenic strains , genotyping and sequencing of different rice accessions , it was shown that , in the elite rice variety IR64 , the resistance conferring allele of the rice blast resistance gene Pi33 was introgressed from the wild rice Oryza rufipogon ( accession IRGC101508 ) . Further characterization of this introgression revealed a large introgression at this locus in IR64 and the related variety IR36 . The introgressed fragment represents approximately half of the short arm of rice chromosome 8 . This is the first report of a large introgression in a cultivated variety of rice . Such a large introgression is likely to have been maintained during backcrossing only if a selection pressure was exerted on this genomic region . The possible traits that were selected are discussed . %D 2008 %0 In-Process %T Magnaporthe grisea avirulence gene ACE1 belongs to an infection-specific gene cluster involved in secondary metabolism . %J New Phytol %V 179 %P 196-208 %A Collemare J %A Pianfetti M %A Houlle AE %A Morin D %A Camborde L %A Gagey MJ %A Barbisan C %A Fudal I %A Lebrun MH %A Bohnert HU %M pub18433432 %X The avirulence gene ACE1 from the rice blast fungus Magnaporthe grisea encodes a polyketide synthase ( PKS ) fused to a nonribosomal peptide synthetase ( NRPS ) probably involved in the biosynthesis of a secondary metabolite recognized by Pi33 resistant rice ( Oryza sativa ) cultivars . Analysis of the M grisea genome revealed that ACE1 is located in a cluster of 15 genes , of which 14 are potentially involved in secondary metabolism as they encode enzymes such as a second PKS-NRPS ( SYN2 ) , two enoyl reductases ( RAP1 and RAP2 ) and a putative Zn ( II ) ( 2 ) Cys ( 6 ) transcription factor ( BC2 ) . These 15 genes are specifically expressed during penetration into the host plant , defining an infection-specific gene cluster . A pORF3-GFP transcriptional fusion showed that the highly expressed ORF3 gene from the ACE1 cluster is only expressed in appressoria , as is ACE1 . Phenotypic analysis of deletion or disruption mutants of SYN2 and RAP2 showed that they are not required for avirulence in Pi33 rice cultivars , unlike ACE1 . Inactivation of other genes was unsuccessful because targeted gene replacement and disruption were inefficient at this locus . Overall , the ACE1 gene cluster displays an infection-specific expression pattern restricted to the penetration stage which is probably controlled at the transcriptional level and reflects regulatory networks specific to early stages of infection .