Spot Of Wheat Research Articles

The sensitivity of Canadian wheat genotypes to the necrotrophic effectors produced by Pyrenophora tritici-repentis

Pyrenophora tritici-repentis (Ptr), the cause of tan spot of wheat, is a foliar pathogen of economic importance worldwide. Tan spot development is associated with the production of necrotrophic effectors (Ptr ToxA, Ptr ToxB and Ptr ToxC) that serve as fungal pathogenicity and/or virulence factors. The objective of this study was to investigate the sensitivity to each of these effectors in a collection of 100 Canadian wheat cultivars representing all wheat classes and developed over a century by various Canadian breeding programmes. Heterologously expressed, His-tagged Ptr ToxA and Ptr ToxB, and spore germination fluids possessing putative Ptr ToxC activity, were produced and used to screen the cultivars for sensitivity. Of the 100 wheat cultivars tested, 92 were sensitive to at least one effector, 68 were sensitive to Ptr ToxA, 63 were sensitive to Ptr ToxC and 24 were sensitive to Ptr ToxB. Only eight cultivars were insensitive to all three effectors. These results reflect the widespread sensitivity in Canadian wheat cultivars to these necrotrophic effectors, with sensitivity to Ptr ToxA and the putative Ptr ToxC found consistently to be more common than Ptr ToxB sensitivity. The predominance of Ptr ToxA and Ptr ToxC sensitivity in Canadian wheat is consistent with the prevalence of races 1 (Ptr ToxA + Ptr ToxC producer) and 2 (Ptr ToxA producer) of Ptr in North America, and could reflect a competitive advantage for Ptr ToxA-producing isolates in the pathogen population.

Characterization of Pyrenophora tritici-repentis (Tan Spot of Wheat) Races in Baltic States and Romania.

Tan spot, caused by the fungus Pyrenophora triticirepentis, is economically important foliar disease in Latvia, Lithuania, and Romania; however, race structure from Baltic States and Romania is not known. In this study, we performed genotypic and phenotypic race characterization of a large collection of P. triticirepentis isolates from these countries to determine race structure and utilize this information for better disease management and breeding wheat for tan spot resistance. We characterized 231 single spore isolates from Latvia (n = 15), Lithuania (n = 107), and Romania (n = 109) for Ptr ToxA and Ptr ToxB genes using two genes specific primers. A subset (139) of 231 isolates were further characterized for their race structure by inoculating them individually on tan spot wheat differentials set. Majority (83%) of the 231 isolates amplified Ptr ToxA gene suggesting prevalence of race 1 and 2. Further, phenotypic characterization of 139 isolates also showed wide prevalence of races 1 (68%), 2 (8%), 3 (11%), and 4 (5%) were also identified from Baltic States as well as Romania. Eighteen of the isolates (13%) did not seem to be of any of the eight known races as they lacked Ptr ToxA gene but they behaved like either race 1 or race 2, suggesting possibility of novel toxins in these isolates as their virulence tools.

Inverse gene-for-gene interactions contribute additively to tan spot susceptibility in wheat.

Tan spot susceptibility is conferred by multiple interactions of necrotrophic effector and host sensitivity genes. Tan spot of wheat, caused by Pyrenophora tritici-repentis, is an important disease in almost all wheat-growing areas of the world. The disease system is known to involve at least three fungal-produced necrotrophic effectors (NEs) that interact with the corresponding host sensitivity (S) genes in an inverse gene-for-gene manner to induce disease. However, it is unknown if the effects of these NE-S gene interactions contribute additively to the development of tan spot. In this work, we conducted disease evaluations using different races and quantitative trait loci (QTL) analysis in a wheat recombinant inbred line (RIL) population derived from a cross between two susceptible genotypes, LMPG-6 and PI 626573. The two parental lines each harbored a single known NE sensitivity gene with LMPG-6 having the Ptr ToxC sensitivity gene Tsc1 and PI 626573 having the Ptr ToxA sensitivity gene Tsn1. Transgressive segregation was observed in the population for all races. QTL mapping revealed that both loci (Tsn1 and Tsc1) were significantly associated with susceptibility to race 1 isolates, which produce both Ptr ToxA and Ptr ToxC, and the two genes contributed additively to tan spot susceptibility. For isolates of races 2 and 3, which produce only Ptr ToxA and Ptr ToxC, only Tsn1 and Tsc1 were associated with tan spot susceptibility, respectively. This work clearly demonstrates that tan spot susceptibility in this population is due primarily to two NE-S interactions. Breeders should remove both sensitivity genes from wheat lines to obtain high levels of tan spot resistance.

Evaluation of spray nozzles for fungicidal control of tan spot in wheat

Tan spot, caused by Pyrenophora tritici-repentis (Died.) Drechs, is a serious constraint on wheat yields in the Southern Cone region of South America. A 2-year experiment was conducted to evaluate fungicide deposition, disease development and grain yield. Three spray nozzles were evaluated: an air-induction flat fan (AI), a wide-angle flat fan (TT), and an extended-range flat fan (XR). A systemic fungicide containing azoxystrobin and cyproconazole was used in both years. Tan spot severity and the area under non-green leaf area disease progress curve (AUNGLA) were analysed. There were no significant differences in deposition among nozzles, and no significant interactions between nozzles and leaf layers in the first year. In both years, AUNGLAs were similar for the three nozzles types, and the tan spot severity in untreated plots was significantly higher than in fungicide-applied plots. Grain yield was higher in the fungicide-applied plots, and there were no significant differences among nozzles in both years. Droplet size had no effect on the fungicide’s efficacy for tan spot control in Uruguay across three susceptible wheat cultivars. The use of drift-reducing nozzles and a systemic fungicide in these trials led to satisfactory performance for spray deposition, canopy penetration and control of the tan spot disease of wheat in the same way as expected from conventional nozzles.

New Insights into the Roles of Host Gene-Necrotrophic Effector Interactions in Governing Susceptibility of Durum Wheat to Tan Spot and Septoria nodorum Blotch.

Tan spot and Septoria nodorum blotch (SNB) are important diseases of wheat caused by the necrotrophic fungi Pyrenophora tritici-repentis and Parastagonospora nodorum, respectively. The P. tritici-repentis necrotrophic effector (NE) Ptr ToxB causes tan spot when recognized by the Tsc2 gene. The NE ToxA is produced by both pathogens and has been associated with the development of both tan spot and SNB when recognized by the wheat Tsn1 gene. Most work to study these interactions has been conducted in common wheat, but little has been done in durum wheat. Here, quantitative trait loci (QTL) analysis of a segregating biparental population indicated that the Tsc2-Ptr ToxB interaction plays a prominent role in the development of tan spot in durum. However, analysis of two biparental populations indicated that the Tsn1-ToxA interaction was not associated with the development of tan spot, but was strongly associated with the development of SNB. Pa. nodorum expressed ToxA at high levels in infected Tsn1 plants, whereas ToxA expression in P. tritici-repentis was barely detectable, suggesting that the differences in disease levels associated with the Tsn1-ToxA interaction were due to differences in pathogen expression of ToxA. These and previous results together indicate that: (1) the effects of Tsn1-ToxA on tan spot in common wheat can range from nonsignificant to highly significant depending on the host genetic background; (2) Tsn1-ToxA is not a significant factor for tan spot development in durum wheat; and (3) Tsn1-ToxA plays a major role in SNB development in both common and durum wheat. Durum and common wheat breeders alike should strive to remove both Tsc2 and Tsn1 from their materials to achieve disease resistance.

Resistance to yellow spot in wheat grown under accelerated growth conditions

Yellow spot, also known as tan spot (YS), is a serious fungal foliar disease of wheat worldwide. The introduction of resistance to YS in wheat cultivars offers the most durable, economic, and environmentally safe management strategy. Adult plant resistance (APR) is preferred over seedling resistance to control other diseases in wheat and has the potential to offer non-race specific resistance to YS. The search for APR currently relies on screening vast numbers of wheat genotypes in the field, where expression is affected by environmental factors. We report a rapid phenotyping method for APR to YS that combines use of constant light and controlled temperatures to achieve accelerated growth conditions (AGC). A panel comprising 20 spring wheat genotypes was evaluated in four separate experiments: (1) seedling stage under regular greenhouse conditions; (2) adult-plant (AP) stage under AGC; (3) integrated seedling and AP disease assessment; and (4) AP stage in the field. Phenotypes from all AP experiments conducted under controlled and field conditions correlated well (r = 0.71–0.84), but correlations between AP and seedling phenotypes were weaker (r = 0.30–0.62). Moderate to high levels of APR were displayed by some genotypes (e.g. CIMMYT line ‘ZWW10-50’) that were equivalent to levels attained by seedling resistant cultivar ‘Leichhardt’. An integrated cycle requires only seven weeks to complete, and provides a useful tool for breeders and pathologists to efficiently phenotype APR to YS under controlled conditions.

Fine genetic mapping of spot blotch resistance gene Sb3 in wheat (Triticum aestivum).

Spot blotch disease resistance gene Sb3 was mapped to a 0.15 centimorgan (cM) genetic interval spanning a 602 kb physical genomic region on chromosome 3BS. Wheat spot blotch disease, caused by B. sorokiniana, is a devastating disease that can cause severe yield losses. Although inoculum levels can be reduced by planting disease-free seed, treatment of plants with fungicides and crop rotation, genetic resistance is likely to be a robust, economical and environmentally friendly tool in the control of spot blotch. The winter wheat line 621-7-1 confers immune resistance against B. sorokiniana. Genetic analysis indicates that the spot blotch resistance of 621-7-1 is controlled by a single dominant gene, provisionally designated Sb3. Bulked segregant analysis (BSA) and simple sequence repeat (SSR) mapping showed that Sb3 is located on chromosome arm 3BS linked with markers Xbarc133 and Xbarc147. Seven and twelve new polymorphic markers were developed from the Chinese Spring 3BS shotgun survey sequence contigs and 3BS reference sequences, respectively. Finally, Sb3 was mapped in a 0.15 cM genetic interval spanning a 602 kb physical genomic region of Chinese Spring chromosome 3BS. The genetic and physical maps of Sb3 provide a framework for map-based cloning and marker-assisted selection (MAS) of the spot blotch resistance.

Efeito de temperaturas na expansão, número de lesões e severidade da mancha-amarela da folha do trigo

RESUMOA mancha-amarela da folha do trigo, causada pelo fungo Pyrenophora tritici-repentis, forma anamórfica Drechslera tritici-repentis, é uma das principais doenças da cultura. A expansão da lesão é um importante componente dessa epidemia, e assim como os demais, podem ser influenciados pela temperatura. Por isso, objetivou-se a realização do trabalho para avaliar o efeito da temperatura na expansão e no número de lesões, bem como na severidade da mancha-amarela do trigo. O trabalho foi conduzido em câmaras climatizadas, sob cinco temperaturas (10, 15, 20, 25 e 30 oC), com as cultivares de trigo Mirante e Fundacep Horizonte. As plantas foram inoculadas no estádio de três folhas expandidas, com 3x103 conídios/mL de suspensão em água. As lesões foram medidas a cada três dias a partir do aparecimento dos sintomas. Contou-se as lesões por folha e deram-se notas de severidade estimada. O delineamento utilizado foi de blocos casualizados com quatro repetições, sendo cada vaso uma repetição. A temperatura influenciou positivamente o aumento da doença, sendo que, a 30 °C o número e crescimento das lesões, bem como, a severidade da doença foram maiores.

Mendelization and fine mapping of a bread wheat spot blotch disease resistance QTL

The wheat (Triticum aestivum L.) quantitative trait locus (QTL) QSb.bhu-5B, which determines resistance to spot blotch (causative pathogen Bipolaris sorokiniana), was mapped to an interval of 0.62 cM on chromosome arm 5BL via the analysis of a recombinant inbred line population bred from a cross between ‘YS116’ and ‘Sonalika.’ ‘YS116’ is an F12 selection from the cross ‘Yangmai 6’ (source of resistance) × ‘Sonalika,’ which contains only one spot blotch resistance QTL. Lines tested from F3 to F5 were inoculated in the field with B. sorokiniana over three consecutive seasons. Measurements of both disease severity and the area under the disease progress curve were used to assess each line’s disease response. In the present population, QSb.bhu-5B, which is flanked by the SSR loci Xgwm639 (0.28 cM) and Xgwm1043, behaved as a single Mendelian gene and was given the gene symbol Sb2. The physical location of Sb2 is within the 5BL1-0.55-0.75 deletion bin. Both Xgwm1043 and Xgwm639 were effective as indirect selection tools in various genetic backgrounds.

Endophytes from wheat as biocontrol agents against tan spot disease

Endophytes from wheat cultivars isolated in Buenos Aires province, Argentina, were assessed for their potential as biocontrol agents against Pyrenophora tritici-repentis (Died.) Drechsler (anamorph Drechslera tritici-repentis) (Died.) Shoem (Dtr), the causal agent of tan spot of wheat. Endophytes were screened using dual culture techniques and examining the effect on growth, sporulation and the antifungal activity in greenhouse assays. The most of endophytes tested significantly reduced Dtr growth compared to the control except Rhodotorula rubra from 11 to 15days post inoculation. Trichoderma hamatum, Penicillium sp., Bacillus sp. and Paecilomyces lilacinus significantly reduced the colony diameter of the pathogen. Most of the endophytes evaluated showed morphological changes in the conidia and/or the mycelia of D. tritici-repentis. In addition, two endophytes, Bacillus sp. and Fusarium sp., reduced significantly the percent spore germination of Dtr compared to the control by 82% and 52% respectively. In greenhouse experiment T. hamatum, Chaetomium globosum and Fusarium sp. significantly (P⩽0.05) reduced the average disease severity on all three leaves compared to the control. However, the best antagonistic effect was shown with T. hamatum as it resulted in the greatest suppression in the greenhouse and in the dual-plate assays. Likewise, Bacillus sp. was other highlighted microorganism that antagonized the pathogen in in vitro assays. From our promising results, we conclude that endophytes have potential in the biological control of tan spot of wheat caused by D. tritici-repentis, particularly T. hamatum and Bacillus sp.

Persistence of the Host-Selective Toxin Ptr ToxB in the Apoplast.

The necrotrophic fungus Pyrenophora tritici-repentis is responsible for the disease tan spot of wheat. Ptr ToxB (ToxB), a proteinaceous host-selective toxin, is one of the effectors secreted by P. tritici-repentis. ToxB induces chlorosis in toxin-sensitive wheat cultivars and displays characteristics common to apoplastic effectors. We addressed the hypothesis that ToxB exerts its activity extracellularly. Our data indicate that hydraulic pressure applied in the apoplast following ToxB infiltration can displace ToxB-induced symptoms. In addition, treatment with a proteolytic cocktail following toxin infiltration results in reduction of symptom development and indicates that ToxB requires at least 8 h in planta to induce maximum symptom development. In vitro assays demonstrate that apoplastic fluids extracted from toxin-sensitive and -insensitive wheat cultivars cannot degrade ToxB. Additionally, ToxB can be reisolated from apoplastic fluid after toxin infiltration. Furthermore, localization studies of fluorescently labeled ToxB indicate that the toxin remains in the apoplast in toxin-sensitive and -insensitive wheat cultivars. Our findings support the hypothesis that ToxB acts as an extracellular effector.

Reaction of Five Non-cereal Grasses to Five Races and Two Host Selective Toxins of Pyrenophora tritici-repentis.

Alternative hosts increase the difficulty of disease management in crops because these alternate hosts provide additional sources of primary inoculum or refuges for diversity in the pathogen gene pool. Agropyron cristatum (crested wheatgrass), Bromus inermis (smooth bromegrass), Pascopyrum smithii (western wheatgrass), Stipa viridula (green needlegrass), and Thinopyrum intermedium (intermediate wheatgrass), commonly identified in range, prairie, verge, and soil reclamation habitats, serve as additional hosts for Pyrenophora tritici-repentis, the cause of tan spot in wheat (Triticum aestivum L.). A. cristatum (five lines), B. inermis (seven lines), P. smithii (four lines), S. viridula (two lines), and T. intermedium (six lines) were tested for their reactions to 30 representative P. tritici-repentis isolates from races 1–5. Plants were grown until the two-three-leaf stage in a greenhouse, inoculated individually with the 30 isolates, held at high humidity for 24 h, and rated after 7 days. All lines developed lesion types 1–2 (resistant) based on a 1–5 rating scale. Also, leaves from an additional plant set were infiltrated with two host selective toxins, Ptr ToxA as a pure preparation and Ptr ToxB as a dilute crude culture filtrate. All lines were insensitive to the toxins. Results indicate that these grass hosts have a limited or nonsignificant role in tan spot epidemiology on wheat in the northern Great Plains. Additionally, the resistant reactions demonstrated by the grass species in this research indicate the presence of resistance genes that can be valuable to wheat breeding programs for improving wheat resistance to P. tritici-repentis.

English

The purpose of this paper is twofold: First, we look at the fundamentals of spot prices of corn and wheat and analyse several measures of dispersion, arguing that the use of the standard deviation of prices is more instructive for regulators and world food organisations than volatility, that is, standard deviation of returns. Second, we look at alternative predictors of corn and wheat spot prices and exhibit that the average value of the forward curve introduced by Borovkova and Geman (2006) performs better than individual forward prices to forecast spot prices at future dates.

Dose e taxa de aplicação de fungicida no controle da ferrugem da folha (Puccinia triticina) e da mancha amarela (Pyrenophora tritici repentis) do trigo

The aim of this paper was to study the role of dose and rate of application, and the effect of concentration of fungicide in the spray solution resulted from the interaction of these factors, in the control of leaf rust and yellow spot of wheat. It was conducted two experiments, the first used the CD 104 cultivar (susceptible to lead rust and yellow spot). The experimental design was an factorial 3 x 3 + untreated control, that involve the factors dose (0,25, 0,30 and 0,35 L.ha-1) and application rate (143, 286 and 429 L.ha-1). The second experiment used the BRS 208 cultivar (resistant to leaf rust and moderately resistant to yellow spot). The experimental design was an factorial 2 x 2 + untreated control, consisting the factors dose (0,2 and 0,3 L.ha-1) and application rate (143 and 286 L.ha-1). The applications were made with a coastal sprayer by CO2, pressure of 250 kPa, XR 110-02 nozzle, which generated an application rate of 143 L.ha-1. The respective rates of each treatment were changed by the number of sprayers per area. It was also used a spore trap denominated Siga, associated with meteorological data and weather forecast, which detected spores of rust and yellow spot before the symptoms in the plants, helping in the identification of disease and in the timing of application. There wasn´t any interaction between dose and rate of application for any of the experiments, therefore, there wasn´t effect of concentration of fungicide in control. The dose and rate of application just influenced in the control of the yellow spot. Higher doses and rates were more effective. However, no difference was observed for yield and hectolitre weight among treatments, except untreated control.

The control of tan spot of wheat (caused by <i>Pyrenophora triticirepentis</i> a possible emerging disease in New Zealand

Pyrenophora triticirepentis the cause of tan spot of wheat was first recorded in New Zealand in 1979 but only on wheat seed However this pathogen has recently been recorded as causing possible yield losses in isolated crops A small plot trial set up in a central Canterbury crop of cv Saracen tested several fungicides alone or in mixtures Control was not entirely effective since tan spot infection was well established when the first applications were made at GS33 (third node detectible) Nevertheless two triazoles (propiconazole and prothioconazole) and three SDHI fungicides (isopyrazam bixafen plus prothioconazole and fluxapyroxad plus epoxiconazole) all gave similar levels of control either when applied alone or in mixtures Two triazoles (epoxiconazole and difenoconazole) were less effective alone while addition of strobilurin (pyraclostrobin) to mixtures gave little extra control Several treatments showed significant increases in green leaf retention and final grain yield The life cycle of the pathogen dictates that management of the overwintering inoculum in stubble is a probable essential step in control of the disease

Dissection of wheat spot blotch disease resistance QTLs in to single Mendelian genes

Two QTLs imparting spot blotch resistance and located on chromosomes 2BS and 5BL were dissected in to a single Mendelian gene using 341 single seed descent (SSD) derived F3 and F4 lines of YS102 × Sonalika and 335 F3, F4 and F5 lines of YS116 × Sonalika cross. The resistant parental lines YS102 and YS116 were selected on the basis of phenotypic and genotyping data of base mapping population (Yangmai 6 × Sonalika in F12 generation) used for QTL mapping. Both the populations were tested for spot blotch resistance under artificial epiphytotic conditions in the field. Disease severity (%) and AUDPC values of each line were calculated. The parent YS116 was known to possess a single major QTL on chromosome 5BL, while YS102 possess QTL on chromosome 2BS. The test for goodness of fit (1: 2: 1 in F3, 3: 2: 3 in F4 and 7: 2: 7 in F5 generations) confirmed segregation at one locus in both the crosses. These SSD derived lines from both the crosses may further be used for fine mapping and map based cloning of the QTLs of spot blotch resistance OTLs.

Simple Method to Produce in vitro Pyrenophora tritici-repentis Teleomorph.

A fungus Pyrenophora tritici-repentis induces tan spot of wheat which is a foliar disease that causes yield loss to wheat crops worldwide. In this study, a new, simple and non-costly technique was performed to produce the sexual stage of this fungus in culture, within 9 weeks using wheat straw. This protocol will be helpful to researchers studying the biology of sexual stage development, disease epidemiology and genetics of this fungus.

Transformation of a Ptr ToxB Nonproducing Isolate of Pyrenophora tritici‐repentis with the ToxB Gene Confers Pathogenicity on a Toxin‐Sensitive Wheat Genotype

ABSTRACTThe causal agent of tan spot of wheat, Pyrenophora tritici‐repentis, is a necrotrophic ascomycete that produces multiple host‐selective toxins (HSTs) responsible for the development of destructive foliar lesions. Ptr ToxB, a small proteinaceous HST produced by some races of P. tritici‐repentis, causes extensive chlorosis on toxin‐sensitive wheat genotypes. To investigate the role of Ptr ToxB in the pathogenicity and virulence of P. tritici‐repentis, the open reading frame of the encoding gene, ToxB, was cloned from a wild‐type race 5 isolate of the fungus and transferred into a Ptr ToxB nonproducing isolate of race 2. Ectopic integration of ToxB was confirmed by Southern blotting analysis with a digoxigenin (DIG)‐labeled DNA probe, while the abundance of ToxB transcript in culture was evaluated by quantitative reverse transcriptase polymerase chain reaction (qRT‐PCR). The production and secretion of Ptr ToxB were assessed by Western blotting analysis of the transformed fungal strains. The pathogenicity of the transformants was tested by inoculation on Ptr ToxB‐sensitive and insensitive wheat genotypes. The Ptr ToxB‐producing transformants were able to induce chlorosis in a host‐specific manner only on the toxin‐sensitive host genotype, resulting in significantly higher levels of disease than those caused by the nontransformed isolate. The extent of chlorosis was well correlated with the amount of Ptr ToxB produced. These results demonstrate that the acquisition of Ptr ToxB‐producing ability is a sufficient condition for pathogenicity in P. tritici‐repentis and confirm the role of this toxin in mediating the compatibility between the fungus and different genotypes of its wheat host.

Solution NMR Structures of Pyrenophora tritici-repentis ToxB and Its Inactive Homolog Reveal Potential Determinants of Toxin Activity

Pyrenophora tritici-repentis Ptr ToxB (ToxB) is a proteinaceous host-selective toxin produced by Pyrenophora tritici-repentis (P. tritici-repentis), a plant pathogenic fungus that causes the disease tan spot of wheat. One feature that distinguishes ToxB from other host-selective toxins is that it has naturally occurring homologs in non-pathogenic P. tritici-repentis isolates that lack toxic activity. There are no high-resolution structures for any of the ToxB homologs, or for any protein with >30% sequence identity, and therefore what underlies activity remains an open question. Here, we present the NMR structures of ToxB and its inactive homolog Ptr toxb. Both proteins adopt a β-sandwich fold comprising three strands in each half that are bridged together by two disulfide bonds. The inactive toxb, however, shows higher flexibility localized to the sequence-divergent β-sandwich half. The absence of toxic activity is attributed to a more open structure in the vicinity of one disulfide bond, higher flexibility, and residue differences in an exposed loop that likely impacts interaction with putative targets. We propose that activity is regulated by perturbations in a putative active site loop and changes in dynamics distant from the site of activity. Interestingly, the new structures identify AvrPiz-t, a secreted avirulence protein produced by the rice blast fungus, as a structural homolog to ToxB. This homology suggests that fungal proteins involved in either disease susceptibility such as ToxB or resistance such as AvrPiz-t may have a common evolutionary origin.

Price Discovery Dynamics of Wheat in Indian Futures and Spot Market

In an agriculture dominated economy like India farmers face yield risk as well as price risk. Commodity futures and derivatives have a crucial role to play in the price risk management process especially in agriculture. The present study analyses the price discovery of wheat in Futures and Spot market in India. The data collected from the Multi Commodity Exchange (MCX). The study considers agri commodity of Futures and spot prices of wheat samples for twenty six months (Jan 2005 to Feb 2007). Correlation Analysis has been used to analyze the relationship between futures and spot price of wheat. The main finding of the study shows that there is high significant correlation between Wheat Futures and Wheat Spot market.