RESUMO
Plant diseases threaten global food security by reducing the production and quality of produce. Identification of disease resistance sources and their utilization in crop improvement is of paramount significance. However, constant evolution and occurrence of new, more aggressive and highly virulent pathotypes disintegrates the resistance of cultivars and hence demanding the steady stream of disease resistance cultivars as the most sustainable way of disease management. In this context, molecular tools and technologies facilitate an efficient and rational engineering of crops to develop cultivars having resistance to multiple pathogens and pathotypes. Puccinia spp. is biotrophic fungi that interrupt crucial junctions for causing infection, thus risking nutrient access of wheat plants and their subsequent growth. Sugar is a major carbon source taken from host cells by pathogens. Sugar transporters (STPs) are key players during wheat-rust interactions that regulate the transport, exchange, and allocation of sugar at plant-pathogen interfaces. Intense competition for accessing sugars decides fate of incompatibility or compatibility between host and the pathogen. The mechanism of transport, allocation, and signaling of sugar molecules and role of STPs and their regulatory switches in determining resistance/susceptibility to rusts in wheat is poorly understood. This review discusses the molecular mechanisms involving STPs in distribution of sugar molecules for determination of rust resistance/susceptibility in wheat. We also present perspective on how detailed insights on the STP's role in wheat-rust interaction will be helpful in devising efficient strategies for wheat rust management.
Assuntos
Basidiomycota , Triticum , Triticum/genética , Triticum/microbiologia , Resistência à Doença/genética , Açúcares , Puccinia , Doenças das Plantas/genética , Doenças das Plantas/microbiologiaRESUMO
Stripe rust (Sr), caused by Puccinia striiformis f. sp. tritici (Pst), is the most devastating disease that poses serious threat to the wheat-growing nations across the globe. Developing resistant cultivars is the most challenging aspect in wheat breeding. The function of resistance genes (R genes) and the mechanisms by which they influence plant-host interactions are poorly understood. In the present investigation, comparative transcriptome analysis was carried out by involving two near-isogenic lines (NILs) PBW343 and FLW29. The seedlings of both the genotypes were inoculated with Pst pathotype 46S119. In total, 1106 differentially expressed genes (DEGs) were identified at early stage of infection (12 hpi), whereas expressions of 877 and 1737 DEGs were observed at later stages (48 and 72 hpi) in FLW29. The identified DEGs were comprised of defense-related genes including putative R genes, 7 WRKY transcriptional factors, calcium, and hormonal signaling associated genes. Moreover, pathways involved in signaling of receptor kinases, G protein, and light showed higher expression in resistant cultivar and were common across different time points. Quantitative real-time PCR was used to further confirm the transcriptional expression of eight critical genes involved in plant defense mechanism against stripe rust. The information about genes are likely to improve our knowledge of the genetic mechanism that controls the stripe rust resistance in wheat, and data on resistance response-linked genes and pathways will be a significant resource for future research.
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Basidiomycota , Triticum , Triticum/genética , Melhoramento Vegetal , Basidiomycota/genética , Genótipo , Perfilação da Expressão Gênica , Doenças das Plantas/genética , Resistência à Doença/genéticaRESUMO
Stem rust is one of the major diseases threatening wheat production globally. To identify novel resistance quantitative trait loci (QTLs), we performed 35K Axiom Array SNP genotyping assays on an association mapping panel of 400 germplasm accessions, including Indian landraces, in conjunction with phenotyping for stem rust at seedling and adult plant stages. Association analyses using three genome wide association study (GWAS) models (CMLM, MLMM, and FarmCPU) revealed 20 reliable QTLs for seedling and adult plant resistance. Among these 20 QTLs, five QTLs were found consistent with three models, i.e., four QTLs on chromosome 2AL, 2BL, 2DL, and 3BL for seedling resistance and one QTL on chromosome 7DS for adult plant resistance. Further, we identified a total of 21 potential candidate genes underlying QTLs using gene ontology analysis, including a leucine rich repeat receptor (LRR) and P-loop nucleoside triphosphate hydrolase, which have a role in pathogen recognition and disease resistance. Furthermore, four QTLs (Qsr.nbpgr-3B_11, QSr.nbpgr-6AS_11, QSr.nbpgr-2AL_117-6, and QSr.nbpgr-7BS_APR) were validated through KASP located on chromosomes 3B, 6A, 2A, and 7B. Out of these QTLs, QSr.nbpgr-7BS_APR was identified as a novel QTL for stem rust resistance which has been found effective in both seedling as well as the adult plant stages. Identified novel genomic regions and validated QTLs have the potential to be deployed in wheat improvement programs to develop disease resistant varieties for stem rust and can diversify the genetic basis of resistance.
Assuntos
Basidiomycota , Plântula , Mapeamento Cromossômico , Plântula/genética , Triticum/genética , Estudo de Associação Genômica Ampla , Locos de Características Quantitativas/genética , Basidiomycota/genética , Resistência à Doença/genética , Doenças das Plantas/genéticaRESUMO
MAIN CONCLUSION: The outcome of different host-pathogen interactions is influenced by both genetic and epigenetic systems, which determine the response of plants to pathogens and vice versa. This review highlights key molecular mechanisms and conceptual advances involved in epigenetic research and the progress made in epigenetics of wheat-rust interactions. Epigenetics implies the heritable changes in the way of gene expression as a consequence of the modification of DNA bases, histone proteins, and/or non-coding-RNA biogenesis without disturbing the underlying nucleotide sequence. The changes occurring between DNA and its surrounding chromatin without altering its DNA sequence and leading to significant changes in the genome of any organism are called epigenetic changes. Epigenetics has already been used successfully to explain the mechanism of human pathogens and in the identification of pathogen-induced modifications within various host plants. Wheat rusts are one of the most vital fungal diseases throughout the major wheat-growing areas of the world. The epigenome in plant pathogens causing diseases such as wheat rusts is mysterious. The investigations of host and pathogen epigenetics in the wheat rusts system can offer a piece of suitable evidence for elucidation of the molecular basis of host-pathogen interaction. Besides, the information on the epigenetic regulation of the genes involved in resistance or pathogenicity will provide better insights into the complex resistance signaling pathways and could provide answers to certain key questions, such as whether epigenetic regulation of certain genes is imparting resistance to host in response of certain pathogen elicitors or not. In the last few years, there has been an upsurge in research on the host as well as pathogen epigenetics and its outcome in plant-pathogen interactions. This review summarizes the progress made in the areas related to the epigenetic control of host-pathogen interaction with particular emphasis on wheat rusts.
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Basidiomycota , Triticum , Epigênese Genética , Interações Hospedeiro-Patógeno/genética , Doenças das Plantas/genética , Triticum/genéticaRESUMO
Leaf rust is one of the important diseases limiting global wheat production and productivity. To identify quantitative trait nucleotides (QTNs) or genomic regions associated with seedling and adult plant leaf rust resistance, multilocus genome-wide association studies (ML-GWAS) were performed on a panel of 400 diverse wheat genotypes using 35 K single-nucleotide polymorphism (SNP) genotyping assays and trait data of leaf rust resistance. Association analyses using six multi-locus GWAS models revealed a set of 201 significantly associated QTNs for seedling and 65 QTNs for adult plant resistance (APR), explaining 1.98-31.72% of the phenotypic variation for leaf rust. Among these QTNs, 51 reliable QTNs for seedling and 15 QTNs for APR were consistently detected in at least two GWAS models and were considered reliable QTNs. Three genomic regions were pleiotropic, each controlling two to three pathotype-specific seedling resistances to leaf rust. We also identified candidate genes, such as leucine-rich repeat receptor-like (LRR) protein kinases, P-loop containing nucleoside triphosphate hydrolase and serine-threonine/tyrosine-protein kinases (STPK), which have a role in pathogen recognition and disease resistance linked to the significantly associated genomic regions. The QTNs identified in this study can prove useful in wheat molecular breeding programs aimed at enhancing resistance to leaf rust and developing next-generation leaf rust-resistant varieties.
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Basidiomycota , Triticum , Basidiomycota/genética , Pão , Mapeamento Cromossômico , Resistência à Doença/genética , Estudo de Associação Genômica Ampla , Genômica , Doenças das Plantas/genética , Proteínas Quinases , Plântula/genética , Triticum/genéticaRESUMO
Wheat is the second most cultivated cereal crop in the world and is an important crop in India. Leaf (brown) rust, caused by Puccinia triticina, was the most prevalent among the three rusts found in all the wheat-growing areas of India, Bhutan, and Nepal during 2016 to 2019. Leaf rust samples from wheat crops in these countries were pathotyped using the wheat differential genotypes and binomial Indian system of nomenclature. To facilitate international communication, each pathotype identified was also tested using the North American differentials. A total of 33 pathotypes were identified from 1,086 samples, including three new pathotypes: 61R47 (162-5 = KHTPM) and 93R49 (49 = NHKTN) from India and 93R57 (20-1 = NHKTN) from Nepal. Two pathotypes, 121R60-1 (77-9/52 = MHTKL) and 121R63-1 (77-5 = THTTM), accounted for 79.46% of the population. Virulence on Lr19 was identified in 0.27% of the samples from Nepal only. The proportion of pathotype 121R60-1 (77-9 = MHTKL) increased to 57.55% during these years. Virulence was not observed on Lr9, Lr24, Lr25, Lr28, Lr32, Lr39, Lr45, and Lr47 in the population of the Indian subcontinent. Eighteen polymorphic simple sequence repeat (SSR) primer pairs tested on the isolates amplified 48 alleles with an average of 2.66 alleles per primer pair. Based on SSR genotyping, these pathotypes could be grouped into two clades with another two subclades each. Many of the Lr genes present in Indian wheat germplasm (Lr1, Lr3a, Lr10, Lr11, Lr14a, Lr15, Lr16, Lr17, Lr20, Lr23, and Lr26) were ineffective for a majority of pathotypes. Most of these varieties possessed a high degree of leaf rust resistance. The field resistance of wheat varieties could be attributed to the interaction of genes, unknown resistance, or adult plant resistance.
Assuntos
Basidiomycota , Triticum , Basidiomycota/genética , Doenças das Plantas , Puccinia , Triticum/genética , VirulênciaRESUMO
MAIN CONCLUSION: Identification and functional characterization of plant pathogen effectors promise to ameliorate future research and develop effective and sustainable strategies for controlling or containing crop diseases. Wheat is the second most important food crop of the world after rice. Rust pathogens, one of the major biotic stresses in wheat production, are capable of threatening the world food security. Understanding the molecular basis of plant-pathogen interactions is essential for devising novel strategies for resistance breeding and disease management. Now, it has been established that effectors, the proteins secreted by pathogens, play a key role in plant-pathogen interactions. Therefore, effector biology has emerged as one of the most important research fields in plant biology. Recent advances in genomics and bioinformatics have allowed identification of a large repertoire of candidate effectors, while the evolving high-throughput tools have continued to assist in their functional characterization. The repertoires of effectors have become an important resource for better understanding of effector biology of pathosystems and resistance breeding of crop plants. In recent years, a significant progress has been made in the field of rust effector biology. This review describes the recent advances in effector biology of obligate fungal pathogens, identification and functional analysis of wheat rust pathogens effectors and the potential applications of effectors in molecular plant biology and rust resistance breeding in wheat.
Assuntos
Basidiomycota/fisiologia , Resistência à Doença/genética , Doenças das Plantas/imunologia , Triticum/genética , Biologia Computacional , Produtos Agrícolas , Genômica , Melhoramento Vegetal , Doenças das Plantas/microbiologia , Triticum/imunologiaRESUMO
Wheat stem rust, caused by Puccinia graminis f. sp. tritici (Pgt), has re-emerged as one of the major concerns for global wheat production since the evolution of Ug99 and other virulent pathotypes of Pgt from East Africa, Europe, Central Asia, and other regions. Host resistance is the most effective, economic, and eco-friendly approach for managing stem rust. Understanding the virulence nature, genetic diversity, origin, distribution, and evolutionary pattern of Pgt pathotypes over time and space is a prerequisite for effectively managing newly emerging Pgt isolates through host resistance. In the present study, we monitored the occurrence of stem rust of wheat in India and neighboring countries from 2016 to 2022, collected 620 single-pustule isolates of Pgt from six states of India and Nepal, analyzed them on Indian stem rust differentials, and determined their virulence phenotypes and molecular genotypes. The Ug99 type of pathotypes did not occur in India. Pathotypes 11 and 40A were most predominant during these years. Virulence phenotyping of these isolates identified 14 Pgt pathotypes, which were genotyped using 37 Puccinia spp.-specific polymorphic microsatellites, followed by additional phylogenetic analyses using DARwin. These analyses identified three major molecular groups, demonstrating fewer lineages, clonality, and long-distance migration of Pgt isolates in India. Fourteen of the 40 recently released Indian wheat varieties exhibited complete resistance to all 23 Pgt pathotypes at the seedling stage. Twelve Sr genes were postulated in 39 varieties based on their seedling response to Pgt pathotypes. The values of slow rusting parameters i.e. coefficient of infection, area under disease progress curve, and infection rates, assessed at adult plant stage at five geographically different locations during two crop seasons, indicated the slow rusting behavior of several varieties. Six Sr genes (Sr2, Sr57, Sr58, Sr24, Sr31, and Sr38) were identified in 24 wheat varieties using molecular markers closely linked to these genes. These findings will guide future breeding programs toward more effective management of wheat stem rust.
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Annual surveys of pathogen populations have monitored the changing pathotype situation of Puccinia triticina that causes leaf (brown) rust of wheat, to release and deploy rust-resistant cultivars of wheat in India. In surveys during 2009 to 2010, samples of leaf rust infecting wheat were collected from the Solan district of Himachal Pradesh. The samples were established on susceptible wheat cv. Agra Local and pathotypes were identified on three differentials following binomial nomenclature (3). Based on the infection types on sets of differentials, this sample was found different to all the known pathotypes of P. triticina from India. This report records a new pathotype of race group 104 of P. triticina from India. Unique feature of this pathotype is its avirulence to Lr3 (Democrat) and virulence to Lr10, Lr13, Lr23, Lr26. These genes are the most common resistance genes in Indian wheat material (1). It appears to be a result of reverse mutation on Lr3 in pathotype 21R63 (104-3). In 2012, this pathotype was detected in 5% of samples from northern India. The new pathotype produces susceptible infection type on Lr10 to which 104 groups gives mesothetic response (4). When compared to other pathotypes of the 104 group, it was different to pathotype 29R23 (104B) in avirulence to Lr26, to which pathotype 93R57 (104-4) is virulent. All the other pathotypes of the 104 group are virulent to Lr3, to which new pathotypes are avirulent. The new pathotype produces resistant response on Lr2a, Lr3, Lr9, Lr15, Lr19, Lr24, Lr25, Lr28, Lr32, Lr39, Lr45, Lr47, and susceptible response on Lr1, Lr2b, Lr2c, Lr10, Lr11, Lr12, Lr13, Lr14a, Lr14b, Lr14ab, Lr16, Lr17a, Lr17b, Lr18, Lr20, Lr21, Lr22a, Lr22b, Lr23, Lr26, Lr27+31, Lr29, Lr30, Lr33, Lr34, Lr35, Lr36, Lr37, Lr38, Lr40, Lr44, Lr46, Lr48, Lr49, Lr51, and Lr57. It is designated as NHKSP on international differentials. A live culture is being maintained as well as cryo-preserved in the National Repository of Pathotypes at the Regional Station of Directorate of Wheat Research, Shimla. Initial evaluation of 700 Indian and exotic wheat lines revealed that more than 500 lines possesses resistance to this pathotype. The identity of the pathotype was also confirmed by sequencing the internal transcribed spacer region of the rDNA with the primers ITS1/ITS4 (GenBank Accession No. JX020949) (2). Analysis of rDNA sequence identified this pathotype as a variant of P. triticina. The strain was most similar to ANK9538 of P. triticina (Accession No. DQ 147418, 98%) and 77-5 strain of P. triticina (Accession No. JQ360856, 93%). Identification of pathotypes from wheat growing areas in the initial stages is a prime effort that helps in developing ecologically safe, economic, and effective ways to manage wheat rusts. References: (1) S. C. Bhardwaj et al. Indian Phytopathol. 63:174, 2010. (2) M. A. Innis et al. PCR Protocols: A Guide to Methods and Applications. Academic Press. San Diego, CA, 1990. (3) S. Nagarajan et al. Curr. Sci. 52:413, 1983. (4) S. K. Nayar et al. Indian Phytopathol. 51:290, 1998.
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Stripe rust disease of wheat, caused by Puccinia striiformis f. sp. tritici, (Pst) is one of the most serious diseases of wheat worldwide. In India, virulent stripe rust races have been constantly evolving in the North-Western Plains Zone leading to the failure of some of the most widely grown resistant varieties in the region. With the goal of studying the recent evolution of virulent races in this region, we conducted whole-genome re-sequencing of three prevalent Indian Pst pathotypes Pst46S119, Pst78S84 and Pst110S119. We assembled 58.62, 58.33 and 55.78 Mb of Pst110S119, Pst46S119 and Pst78S84 genome, respectively and found that pathotypes were highly heterozygous. Comparative phylogenetic analysis indicated the recent evolution of pathotypes Pst110S119 and Pst78S84 from Pst46S119. Pathogenicity-related genes classes (CAZyme, proteases, effectors, and secretome proteins) were identified and found to be under positive selection. Higher rate of gene families expansion were also observed in the three pathotypes. A strong association between the effector genes and transposable elements may be the source of the rapid evolution of these strains. Phylogenetic analysis differentiated the Indian races in this study from other known United States, European, African, and Asian races. Diagnostic markers developed for the identification of three Pst pathotypes will help tracking of yellow rust at farmers field and strategizing resistance gene deployment.
Assuntos
Basidiomycota , Doenças das Plantas , Estados Unidos , Filogenia , Doenças das Plantas/genética , Basidiomycota/genética , PucciniaRESUMO
Leaf rust (also called brown rust) in wheat, caused by fungal pathogen Puccinia triticina Erikss. (Pt) is one of the major constraints in wheat production worldwide. Pt is widespread with diverse population structure and undergoes rapid evolution to produce new virulent races against resistant cultivars that are regularly developed to provide resistance against the prevailing races of the pathogen. Occasionally, the disease may also take the shape of an epidemic in some wheat-growing areas causing major economic losses. In the recent past, substantial progress has been made in characterizing the sources of leaf rust resistance including non-host resistance (NHR). Progress has also been made in elucidating the population biology of Pt and the mechanisms of wheat-Pt interaction. So far, â¼80 leaf rust resistance genes (Lr genes) have been identified and characterized; some of them have also been used for the development of resistant wheat cultivars. It has also been shown that a gene-for-gene relationship exists between individual wheat Lr genes and the corresponding Pt Avr genes so that no Lr gene can provide resistance unless the prevailing race of the pathogen carries the corresponding Avr gene. Several Lr genes have also been cloned and their products characterized, although no Avr gene corresponding a specific Lr gene has so far been identified. However, several candidate effectors for Pt have been identified and functionally characterized using genome-wide analyses, transcriptomics, RNA sequencing, bimolecular fluorescence complementation (BiFC), virus-induced gene silencing (VIGS), transient expression and other approaches. This review summarizes available information on different aspects of the pathogen Pt, genetics/genomics of leaf rust resistance in wheat including cloning and characterization of Lr genes and epigenetic regulation of disease resistance.
Assuntos
Genes Fúngicos , Genes de Plantas , Doenças das Plantas/microbiologia , Puccinia , Triticum/genética , Triticum/microbiologia , Evolução Biológica , Resistência à Doença/genética , Epigênese Genética , Genoma Fúngico , Genoma de Planta , Interações Hospedeiro-Patógeno , Doenças das Plantas/imunologia , Puccinia/genética , Puccinia/patogenicidade , Puccinia/fisiologia , Característica Quantitativa Herdável , Triticum/fisiologiaRESUMO
Stem (black) rust, caused by Puccinia graminis Pers. f. sp. tritici Eriks. & Henn., is one of the most destructive diseases of wheat. It could be controlled through introgression of race-specific resistance genes. However, such kind of resistance is mostly short lived due to emergence of new virulences. For example, resistance genes Sr11, Sr24, Sr30, and Sr31 are no longer effective (2,4). Detection of new virulences has remained vital in the evaluation and identification of new sources of resistance. We report here the detection of virulence to Sr25, a gene from Thinopyrum elongatum (4), which had been effective or partially effective against stem rust worldwide, including race Ug99 (TTKSK) (4). A stem rust isolate collected in 2006 from Karnataka (southern India) produced susceptible reactions (infection type [IT] 3+ to 4) on the primary leaves of differential genotype 'Agatha' carrying Sr25 and susceptible check 'Agra Local' at 22 ± 2°C. To verify virulence to Sr25, single-pustule isolates from this sample were inoculated onto seedlings of 'Agrus', 'Agatha', 'RL6040' ('Thatcher' + Sr25), 'Superseri#1', 'Wheatear', and 'Morocco' + Sr25 (obtained from CIMMYT), which all carry Sr25. All these accessions were found susceptible (IT 3+ to 4) to this isolate, except Wheatear which expressed resistance (IT ;1), indicating the presence of additional gene(s). These genotypes are resistant (ITs ;1 to 2+) to Sr25-avirulent pathotypes. The new pathotype is avirulent to Sr11, 13, 14, 21, 22, 23, 24, 26, 27, 29, 31, 32, 33, 35, 37, 38, 39, 40, 43, and Tmp and virulent to Sr5, 6, 7a, 7b, 8a, 9a, 9b, 9d, 9e, 9f, 9g, 10, 12, 15, 16, 17, 18, 19, 20, 25, 28, 30, 34, 36, 42, Wld-1, and Gt at 22 ± 2°C. This pathotype has been designated as 58G13-3 and PKTSC according to the Indian nomenclature (1) and the North American system (3), respectively. It represents race 40 based on Stakman's differentials. It may have arisen from race 40 through mutation. The type culture of the pathotype has been added to the culture collection at Flowerdale, Shimla. Interestingly, 'Festiguay' (Sr30) was found resistant to this pathotype, indicating the presence of additional gene(s), whereas 'Webster' (Sr30) was susceptible. Adult plants of Agrus, Agatha, RL6040, Superseri#1, and Morocco+Sr25 also were susceptible, producing 20S to 60S responses. Sr25-avirulent pathotype 62G29 produced a TR (flecking in traces) response on these lines except Morocco + Sr25 that showed 20 to 40MR (moderately resistant) responses. In the same study however, adult plants of Thatcher showed a resistant reaction (10R to MR) at low (16 ± 2°C) and susceptible (20S) at high (22 ± 2°C) temperatures. Agatha and RL6040, having Thatcher as one of the parents, had similar responses. The detection of Sr25 virulence is significant since Sr25 is an important gene to be targeted for breeding wheat cultivars resistant to Ug99. We should use either adult plant resistance and/or pyramiding two or more genes for seedling resistance to enhance the field life of wheat cultivars. References: (1) P. Bahadur et al. Proc. Indian Acad. Sci. 95:29, 1985. (2) S. C. Bhardwaj et al. J. Wheat Res. 1:51, 2007. (3) Y. Jin et al. Plant Dis. 92:923, 2008. (4) R. P. Singh et al. CAB Rev. No. 054:1, 2006.
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Lr19, a resistance gene originally transferred from Agropyron elongatum to wheat (Triticum aestivum L.), has remained effective worldwide against leaf rust (Puccinia triticina Eriks.) except in Mexico (1). This report records a new pathotype of P. triticina virulent on Lr19 from India. From 2003 to 2004, 622 wheat leaf rust samples from 14 states were subjected to pathotype analysis. Samples were established on susceptible wheat cv. Agra Local, and pathotypes were identified on three sets of differentials following binomial nomenclature (3). Virulence on Lr19 (Agatha T4 line) was observed in approximately 2% of samples. These samples were picked from Lr19 (NIL), cvs. Ajit, Lal Bahadur, Local Red, Lok1, and Nirbhay from Karnataka and Gujarat states. All Lr19 virulent isolates were identical. The reference culture is being maintained on susceptible wheat cv. Agra Local and has also been put under long-term storage in a national repository at Flowerdale. From 2004 to 2005, this pathotype was detected in 6.3% of samples from central and peninsular India. There is no wheat variety with Lr19 under cultivation in India, however, it is being used in wheat breeding programs targeted at building resistance against leaf and stem rusts. NIL's Lr19/Sr25 (LC25) and Lr19/Sr25 (82.2711) were also susceptible to this isolate, whereas Lr19/Sr25 (spring accession) was resistant. The new isolate, designated as 253R31 (77-8), appears to be close to the pathotype 109R31 (4) with additional virulence for Lr19. The avirulence/virulence formula of pathotype 253R31 is Lr9, 23, 24, 25, 26, 27+31, 28, 29, 32, 36, 39, 41, 42, 43, 45/Lr1, 2a, 2b, 2c, 3, 10, 11, 12, 13, 14a, 14b, 14ab, 15, 16, 17, 18, 20, 21, 22a, 22b, 30, 33, 34, 35, 37, 38, 40, 44, 48, and 49. To our knowledge, this is the first report of virulence on Lr19 from two states of India. On international rust differentials, it is designated as TGTTQ (2), and is different from CBJ/QQ (1), the other isolate reported virulent on Lr19 from Mexico. The Mexican isolate is avirulent on Lr1, 2a, 2b, 2c, 3ka, 16, 21, and 30 to which the Indian isolate is virulent. However, both isolates are avirulent on Lr9, 24, 26, 36, and Lr42. Among the wheat cultivars identified during the last 6 years, HD2824, HD2833, HD2864, HI1500, HS375, HUW 510, HW 2044, HW 5001, Lok 45, MACS 6145, MP4010, NW 2036, PBW 443, PBW 498, PBW 502, PBW 524, Raj 4037, UP 2565, VL 804, VL 829, and VL 832 and lines of wheat possessing Lr9, Lr23, Lr24, and Lr26 showed resistance to this pathotype. PBW 343, which occupies more than 5 million ha in India, is also resistant to this pathotype along with PBW 373. An integrated strategy using a combination of diverse resistance genes, deployment of cultivars by using pathotype distribution data, slow rusting, and adult plant resistance is in place to curtail selection of new pathotypes and prevent rust epiphytotics. References: (1) J. Huerta-Espino and R. P. Singh. Plant Dis. 78:640,1994. (2) D. V. Mc Vey et al. Plant Dis. 88:271, 2004. (3) S. Nagarajan et al. Curr. Sci. 52:413, 1983. (4) S. K. Nayar et al. Curr. Sci. 44:742, 1975.