Critical period of weed interference in chickpea

The critical period of weed interference in one variety of chickpea was determined in field experiments carried out at two sites, Tabriz 2002 and Kermanshah 2003, Iran. Chickpea culture was either kept free of weeds for 0, 12, 24, 36, 48 and 60 days after crop emergence (DAE) or weeds were allowed to grow for 0, 12, 24, 36, 48 and 60 DAE. In these experiments, chickpea yield increased with increasing duration of weed-free period and was reduced by increasing duration of weed-infested period. Unweeded conditions for the entire growing season caused 66.4% and 48.3% seed yield reduction when compared with the treatment that was weed-free throughout the growing season, at Tabriz 2002 and Kermanshah 2003, respectively. The results indicated that chickpea must be kept weed-free between the five-leaf and full flowering stages (24–48 DAE) and from the four-leaf to beginning of flowering stages (17–49 DAE) at the two sites, respectively, in order to prevent >10% seed yield loss. At both sites, reduction in seed yield, because of the increased weed interference period, was accompanied by simultaneous reduction in plant dry weight, number of branches, pods per plant and 100-seed weight. This was supported by significant and positive correlations between these traits and chickpea seed yield. There was no significant correlation between the number of seeds per pod and seed yield. A linear regression model was used to describe the relationship between weed dry weight and seed yield loss.     

Pathogenicity and histopathology of Pratylenchus thornei populations on selected chickpea genotypes

Four populations of Pratylenchus thornei from different locations were tested for reproductive fitness in axenic carrot disc cultures and for pathogenicity to chickpea cultivars JG 62 and UC 27 and lines K 850 and ILC 1929. Parasitism and histopathology on selected chickpea genotypes (JG 62, UC 27 and lines ILC 482, ICC 11324 and ICC 12237) were also investigated. Reproductive fitness, assessed as the ratio of the final number of nematodes per carrot disc to the number of nematodes inoculated, was similar among the populations tested and the four populations reproduced to a similar extent in a given chickpea genotype. However, the extent of reproduction was significantly affected by the chickpea genotype, JG 62 and UC 27 being the best and poorest hosts, respectively. Pathogenicity to chickpea genotypes was assessed by the difference in fresh root and dry shoot weights between infected and uninfected plants 90 days after inoculation. Plant growth was significantly reduced by the four nematode populations in all chickpea genotypes, with the exception of cv. JG 62, which was tolerant of P. thornei . Severity of root necrosis caused by nematode infection was similar for all populations. Histopathological studies of chickpea genotypes infected by P. thornei showed that all were suitable hosts according to nematode reproduction and host reaction. P. thornei always migrated through epidermal and cortical cells by breaking down cell walls along the nematode pathway. In the most susceptible lines (ILC 482 and JG 62), damage to endodermal cells adjacent to nematode feeding sites was occasionally observed.     

In planta-polymerase-chain-reaction detection of the wilt-inducing pathotype ofFusarium oxysporumf.sp.cicerisin chickpea (Cicer arietinumL.)

A 1.6 kb fragment of random amplified polymorphic DNA (RAPD-PCR, polymerase chain reaction), which was specific for race 5, a wilt-inducing isolate ofFusarium oxysporumf.sp.ciceris(Foc), was cloned and sequenced. This fragment was not detected in RAPD-PCR reactions with DNA from yellowing-inducing pathotypes ofFoc, or from other fungi tested. Specific PCR primers were designed from the sequence data and used to detect the presence of the fungus in genomic DNA isolated from symptomless chickpea plants, 16 days after inoculation. A single, 1.5 kb PCR product was only observed in PCR reactions with DNA from plants infected with a wilt-inducing isolate. No products were observed in reactions with DNA from plants infected with yellowing-inducing pathotypes, or from DNA isolated from uninfected chickpea cultivar controls. Southern hybridization demonstrated homology between the second PCR product and the original specific wilt-associated RAPD fragment. PCR products were detected with DNA extracted from roots and stem tissue, but no fungal DNA was detected in leaf tissue of the same infected plants. In a blind trial, the specific primers correctly identified the fungal pathotype in four different, wilt-infected chickpea cultivars.     

Cucumber mosaic virus infection of chickpea stands: temporal and spatial patterns of spread and yield‐limiting potential

Patterns of spread and yield losses were examined when migrant aphid vectors transmitted Cucumber mosaic virus (CMV) within chickpea (Cicer arietinum) plots. When numbers of chickpea plant infection foci were varied to provide initial infection incidences of 0·3–2%, rate of virus spread and its final incidence increased in proportion to initial virus incidence and pathogen progress curves reflected a polycyclic pattern of spread. Chickpea seed yields decreased by 44–45% when CMV incidence reached 61–74% at final assessment in plots with simulated 1–2% initial incidence. In chickpea plots with or without introduced lupin plant infection foci, cumulative spatial data for diseased plants were assessed using spatial analysis by distance indices (sadie ). When CMV spread within a plot, infection was concentrated in large patch clusters and was consistent with comprehensive localized spread around primary infection foci. When introduced infection foci were absent, there was more diffuse spread with many isolated clusters. In individual plants that developed CMV symptoms at different growth stages, shoot and pod dry weight were reduced by 60–65% and 77–79% (early infection) and 44 and 66% (late infection), respectively. Seed yield losses were 78–80% (early) and 65–67% (late), and reduction in 50‐seed weight was 20–25% regardless of time of infection, so seed number was reduced more by early than late infection. Infection also reduced seed quality as, in addition to smaller seed size, seed coats were discoloured and malformed: the proportions of malformed seeds were 9–11% (early), 3–6% (late) and 0·5% (healthy).     

DNA methylation changes in fusarium wilt resistant and sensitive chickpea genotypes (Cicer arietinum L.)

DNA methylation plays an important role in the regulation of gene expression in biotic and abiotic stresses. In the present study, a methylation-sensitive amplified polymorphism (MSAP) analysis was performed to profile DNA methylation changes in seven resistant and sensitive chickpea genotypes following inoculation with Fusarium oxysporum f. sp. ciceris. In all, 27468 DNA fragments, each representing a recognition site cleaved by either or both of two isoschizomers, were amplified using nine selective primer pairs. DNA methylation was evaluated in leaves, stems and roots in control and inoculated plants. Extensive cytosine methylation alterations were found in the pathogen-treated genotypes compared with the corresponding control, including hypermethylation and demethylation as well as the potential conversion of methylation types. For all genotypes, the percentage of demethylated sites were more than methylated sites in infected plants compared with the corresponding control. No significant differences were observed for banding patterns in infected and control leaf tissues, while the differences between percentage of unchanged, methylated and demethylated sites were significant in stem and root tissues. The total numbers of methylated polymorphic bands ranged from 137 to 154 bands in Sel95th1716 and Arman, accounting for 36.81%–44.64% of all bands, respectively. Ten fragments that were differentially amplified between infected and control plants were isolated and sequenced in three tissues separately. Most of sequenced fragments showed homology with disease related genes in GenBank. The results suggest that significant differences in cytosine methylation exist between resistant and sensitive chickpea genotypes, and that hypermethylation or hypomethylation of specific genes may be involved in the chickpea resistance to Fusarium wilt.     

The role of seedling infection in epiphytotics of ascochyta blight on chickpea

Didymella rabiei, the causal agent of ascochyta blight, survives on infected seeds and seedlings. Diseased seedlings originating from infected seeds occasionally serve as the source for primary infection in chickpea crops. Experiments carried out independently in Australia and in Israel provided quantitative information on the temporal and spatial distribution of ascochyta blight from initial infections and on the relationship between the amount of initial infection and the intensity of subsequent epiphytotics for cultivars differing in susceptibility to the pathogen. Disease spread over short distances (<10 m) from individual primary infections, was governed by rain and wind, and was up to five times greater down-wind than up-wind. Cultivar response to D. rabiei significantly affected the distance and area over which disease spread and the intensity of the disease on infected plants. At onset of the epiphytotic, the relationship between disease spread and time was exponential (P < 0.05; R ² > 0.95) and the area of the resulting foci was over 10 times greater in susceptible cultivars than in resistant cultivars. Regression equations showed the relationship between disease severity and the distance from the focus-plants was inverse-linear for all cultivars tested (P < 0.05). A simulation model based on the experimental data revealed that even if primary infection is infrequent (less than 1% of plants), the consequences are potentially devastating when susceptible cultivars are used. The epidemiological information and simulation model generated by this study provide an increased understanding of the development of an epiphytotic in which the primary foci of disease originate from infected chickpea seedlings.     

Detection and molecular characterization of phytoplasma associated with chickpea phyllody disease in south India

Chickpea (Cicer arietinum L.) plants showing typical symptoms of infection by a phytoplasma that causes phyllody disease have been commonly observed in recent years in parts of south India. The symptoms included pale green leaves, bushy appearance due to excessive stunting of shoots, reduced internodal length and excessive axillary proliferation. The causal agent of the phyllody disease was identified based on symptoms, amplification of 16S rDNA of the phytoplasma by polymerase chain reaction (PCR) from infected samples, as well as by sequencing and phylogenetic analysis. First round PCR and nested-PCR protocols were standardized for improved efficiency and reliability of the diagnostic protocols. Using the primers P1/P7 and R16F2n/R16R2, 1,800?bp and 1,200?bp size products were amplified in first round PCR and nested-PCR protocols, respectively. The PCR product was cloned and sequenced and compared with the reference phytoplasma sequences from the database (NCBI). The Indian chickpea phyllody phytoplasma 16S rDNA sequences shared the highest nucleotide identity (>98%) with the 16S rII group phytoplasma candidates, also infecting chickpea from Australia and Pakistan. This is the first report of a phytoplasma of the 16SrII-group infecting chickpea from India. The genetic similarities and the potential threat of this new disease to chickpea cultivation in India are discussed.     

Pea seed-borne mosaic virus: occurrence in faba bean (Vicia faba) and lentil (Lens culinaris) in West Asia and North Africa,and further information on host range,transmission characteristics,and purification

In a survey for viruses of cultivated legumes in West Asia and North Africa, pea seed-borne mosaic virus (PSbMV) was found in faba bean, lentil and pea. Using ELISA, it was detected in 107 out of 1554 faba bean samples and 40 out of 496 lentil samples with virus-like symptoms collected in Algeria, Egypt, Ethiopia, Jordan, Lebanon., Libya, Morocco, Sudan, Tunisia and Turkey.A pea isolate (SP9-88) from Syria was further characterized. Out of 57 plant species tested, 35 were found susceptible, 19 of which are newly reported hosts of the virus. The virus was transmitted efficiently in the non-persistent manner by five aphid species, especiallyMyzus persicae. Purification from systemically infected faba bean plants yielded 10–15 mg of purified virus per kg of infected tissue. Sap-inoculation of the food and forage legume species chickpea, faba bean, lentil, pea,Vicia narbonensis, V. sativa, Lathyrus ochrus andL. sativus at flowering stage led to 66.0, 40.5, 44.6, 49.2, 31.7, 7.5, 35.7 and 12.0% yield loss, respectively, and to seed-transmission, rates of 0.7, 6.0, 10.8, 1.1, 0.3, 0.2 and 0.4%, respectively. No transmission was detected in chickpea seed embryo axes. However, the virus was detected in the seed coat of SPbMV-infected chickpea at an estimated rate of 1.81%.     

Diversity and occurrence of chickpea chlorotic dwarf virus on legumes from Iran

Chickpea chlorotic dwarf virus (CpCDV; genus Mastrevirus, family Geminiviridae) is one of the most important legume-infecting viruses with a wide host range and geographic distribution in Africa and Asia. In Iran, CpCDV is common in chickpea (Cicer arietinum), but there is limited information about diversity and infections in plants of other legume species. In the current study, a total of 1671 leaf samples from different pulse crops with symptoms were collected in nine provinces of Iran, and the CpCDV infection status was tested by PCR and/or rolling circle amplification (RCA), resulting in the detection of CpCDV in samples of chickpea, lentil (Lens culinaris) and faba bean (Vicia faba) from different regions. Sequence analysis of complete genomes of 18 isolates recovered by digestion of RCA products revealed infection with isolates of the strains CpCDV-A and CpCDV-F in chickpea, lentil and faba bean. Phylogenetic analysis showed that the Iranian isolates of CpCDV were closely related to previously sequenced isolates of CpCDV-A and CpCDV-F. To the authors' knowledge, this is the first report of CpCDV-F in Iran. Using agroinoculation with infectious clones for one isolate each of CpCDV-A and CpCDV-F, infectivity was confirmed in both faba bean and chickpea, with plants developing leaf curling and/or yellowing. Both infectious clones also successfully infected Nicotiana benthamiana resulting in mild yellowing and intensive leaf curling for CpCDV-A, and dark-green mosaic, dwarfing and mild leaf curling for CpCDV-F.     

Alternative hosts and plant tissues for the survival,sporulation and spread of the Ascochyta blight pathogen of chickpea

Various crop and weed species were infected naturally by Didymella rabiei (anamorph: Ascochyta rabiei) in blight-affected chickpea fields in the Palouse region of eastern Washington and northern Idaho, USA. The fungus was isolated from asymptomatic plants of 16 species commonly found in commercial crops in this region. Isolates of the pathogen from crop and weed species were pathogenic to chickpea and indistinguishable in cultural and morphological characteristics from isolates of D. rabiei from chickpea. Both mating types of D. rabiei were isolated from eight naturally infected plant species. Chickpeas were infected by D. rabiei when plants emerged through infested debris of seven crop and weed species. The teleomorph developed on overwintered tissues of seven plant species infected naturally by D. rabiei in a blight screening nursery and on debris of wheat, white sweet clover and pea inoculated with ascospores of D. rabiei or conidia of two compatible isolates of the pathogen. Didymella rabiei naturally infected 31 accessions of 12 Cicer spp. and the teleomorph developed on the overwintered debris of all accessions, including those of three highly resistant perennial species. The fungus developed on the stem and leaf pieces of ten plant species common to southern Spain inoculated with conidia of two compatible isolates of D. rabiei, and formed pseudothecia with asci and viable ascospores on six of ten species and pycnidia with conidia on all plant species.     

Development of ascochyta blight (Ascochyta rabiei) in chickpea as affected by host resistance and plant age

Ascochyta blight caused by Ascochyta rabiei, is the most destructive disease in many chickpea growing countries. Disease development varies with the growth stage and host resistance. Hence, disease development was studied in cvs ICCX 810800 (resistant), ICCV 90201 (moderately resistant), C 235 (moderately susceptible), ICCV 96029 and Pb 7 (susceptible) under controlled environment (ICRISAT, Patencheru) and field conditions (Dhaulakuan, Himachal Pradesh) at seedling, post-seedling, vegetative, flowering and podding stages. Under controlled environment, the incubation period and terminal disease reaction (TDR) did not vary significantly at different growth stages against virulent isolate AB 4. Cultivars ICCX 810800, ICCV 90201 and C 235 showed a significantly longer incubation period than the susceptible cv. Pb 7. Cultivar ICCX 810800 showed slow disease progress and the least TDR. Field experiments were conducted during the 2003–2004 and 2004–2005 growing seasons. During 2003–2004, TDR was higher in plants inoculated at podding and the flowering stage and the lowest disease reaction was recorded in ICCX 810800. A severe epidemic during 2004–2005 was attributed to the favourable temperature, humidity and well distributed high rainfall. TDR did not differ significantly at any of the growth stages in susceptible cvs ICCV 96029 and Pb 7. With respect to seeding date and cultivar, the highest yield was recorded in the early-sown crop (1,276.7 kg ha⁻¹) and in ICCV 90201 (1,799.3 kg ha⁻¹), respectively. The yields were greatly reduced in all the cultivars during 2004–2005 and the highest yield was recorded in ICCX 810800 (524.7 kg ha⁻¹). Integrated disease management using resistant cultivars, optimum sowing period and foliar application of fungicides will improve chickpea production. The experiment under controlled environment and field conditions (during the epidemic year) showed a similar disease development.     

Sympatric ascochyta complex of wild Cicer judaicum and domesticated chickpea

The aim of this study was to isolate, identify and characterize ascochyta blight pathogens from Cicer judaicum , a wild annual Cicer species which grows in Israel and other Mediterranean countries in sympatric distribution with legume crops, and determine their virulence and aggressiveness to other wild and domesticated legumes. Native C. judaicum plants exhibited symptoms resembling ascochyta diseases of grain legume crops. Two distinct pathogens were isolated and identified as Phoma pinodella and Didymella rabiei using morphological and molecular tools; their infectivity was verified using Koch's postulates. The virulence of these pathogens was examined on 13 legume species, of which P. pinodella was virulent to Pisum sativum , P. fulvum , C. judaicum , C. arietinum , C. reticulatum , C. pinnatifidum and C. bijugum . Didymella rabiei infected all these Cicer species, but not the other legume species tested. Aggressiveness of the pathogens was tested on wild and domesticated chickpea and pea. Didymella rabiei isolated from C. judaicum had significantly higher ( P  < 0·001) aggressiveness than P. pinodella from C. judaicum on both wild and domesticated chickpea. Disease severity on the former species ranged from 62·5% to 70% and on the latter from 41% to 56%. Phoma pinodella isolates from C. judaicum were more aggressive on C. arietinum and P. sativum than on C. judaicum and P. fulvum . Results of the current study suggest that C. judaicum may serve as an alternative host to ascochyta pathogens that endanger chickpea and possibly other crops and wild species growing in close proximity.     

Nematodes of food legumes in the Mediterranean Basin1

Several endoparasitic nematodes have been reported on leguminous plants in the Mediterranean area. The most widespread are the root-lesion nematodes Pratylenchus mediterraneus, P. penetrans and P. thornei. Symptoms induced by these nematodes usually are not very impressive, but 50% yield loss of chickpea may occur. Among root-knot nematodes, Meloidogyne artiellia is associated with severe yield losses of chickpea in Italy, Spain and especially Syria. Tolerance limits of 0.14 and 0.02 of this nematode per ml soil are reported for winter and spring-sown chickpea, respectively. Meloidogyne incognita and M. javanica can be noxious to French bean and cowpea in sandy soil. The cyst nematode Heterodera goettingiana reduces yields of pea, broad bean and vetch when its population densities exceed 0.5, 1, and 2.1 eggs per g of soil, respectively. Heterodera ciceri occurs in northern Syria and Turkey and is responsible for economic yield losses of chickpea and lentil in fields infested with more than 1 or 2.5 eggs per g of soil, respectively. Pea and grass pea also suffer from infestation of this nematode. The stem and bulb nematode Ditylenchus dipsaci causes severe decline of broad bean, pea and probably lentil during wet seasons. Other nematodes, although present in moderate numbers, appear to have little importance.     

Airborne ascospores ofDidymella rabiei as a major primary inoculum for Ascochyta blight epidemics in chickpea crops in southern Spain

The incidence and severity of Ascochyta blight in potted chickpea trap plants exposed for 1-wk periods near infested chickpea debris in Córdoba, Spain, or in chickpea trap crops at least 100 m from infested chickpea debris in several locations in southern Spain were correlated with pseudothecial maturity and ascospore production ofDidymella rabiei from nearby chickpea debris. The period of ascospore availability varied from January to May and depended on rain and maturity of pseudothecia. The airborne concentration of ascospores ofD. rabiei was also monitored in 1988. Ascospores were trapped mostly from the beginning of January to late February; this period coincided with that of maturity of pseudothecia on the chickpea debris. Most ascospores were trapped on rainy days during daylight and 70% were trapped between 12.00 and 18.00 h. Autumn-winter sowings of chickpea were exposed longer to ascospore inoculum than the more traditional spring sowings because the autumn-winter sowings were exposed to the entire period of ascospore production on infested chickpea debris lying on the soil surface.     

Effect of growth stages of chickpea on the genetic resistance of Ascochyta blight

Ascochyta blight (AB, Ascochyta rabiei (Pass.) Lab.) is one of the most important foliar disease of chickpea (Cicer arietinum L.), globally. Chickpea is attacked by AB at any growth stage in cool and humid weather depending on the inoculum availability. However, the disease epidemics are most prominent during the flowering and podding growth stages. The main objective of this study was to determine the effect of growth stages of chickpea on the genetic resistance of AB and use this information in a resistance breeding program. Two susceptible and two moderately resistant chickpea cultivars were spray inoculated at seedling (GS1), post-seedling (GS2), vegetative (GS3), flowering (GS4) and podding (GS5) growth stages with A. rabiei conidial suspension under controlled environment conditions. Irrespective of crop cultivars the incubation period (IP) was shorter in GS1, GS4 and GS5 and was significantly extended in GS2 and GS3. Symptom development was delayed significantly in moderately resistant cultivars. The AB severity 10 days after inoculation ranged between 7 and 9 on susceptible cultivars and 3 and 5 on moderately resistant cultivars. Further the correlation coefficient of disease severity between GS1, GS4 and GS5 was highly significant (r = 0.95) indicating that, evaluation for resistance to AB can be done at GS 1 (seedling stage), and or GS4 (flowering stage) to GS5 (podding stage) growth stages of chickpea. This supports the evaluation for AB resistance using 10-day-old-seedlings in controlled environment at ICRISAT and adult plant field screening at hot-spot locations in Dhaulakuan and Ludhiana in India.     

Ameliorative effects of Mesorhizobium sp. MRC4 on chickpea yield and yield components under different doses of herbicide stress

The present study was conducted to assess the plant growth promoting activities of Mesorhizobium sp. in the presence of technical grade herbicides and its ameliorating effects on herbicide toxicity to chickpea grown in herbicide treated soils. The quizalafop-p-ethyl and clodinafop-tolerant Mesorhizobium isolate MRC4 recovered from the nodules of chickpea plants significantly produced IAA, siderophores, hydrogen cyanide and ammonia in medium amended with or without technical grade quizalafop-p-ethyl and clodinafop. Quizalafop-p-ethyl at 40, 80 and 120 μg kg⁻¹ soil and clodinafop at 400, 800 and 1200 μg kg⁻¹ soil in general, decreased the growth attributes of chickpea plants inoculated with Mesorhizobium MRC4 and un-inoculated chickpeas. The three concentrations of quizalafop-p-ethyl were comparatively more toxic and substantially decreased biomass, nodulation and leghaemoglobin content, nutrient uptake, seed yield and grain protein over the un-inoculated chickpea. Interestingly, Mesorhizobium isolate MRC4 with any concentration of the two herbicides significantly increased the measured parameters when compared to the plants grown in soils treated solely (without inoculant) with similar concentration of each herbicide. Conclusively, Mesorhizobium isolate MRC4 could be exploited as bio-inoculant for facilitating chickpea growth under herbicide stress.     

Sclerotinia rot losses in processing tomatoes grown under centre pivot irrigation in central Brazil

Sclerotinia rot caused by Sclerotinia sclerotiorum is one of the most important diseases of processing tomatoes in Central Brazil. Yield losses in tomato cultivars (cv.) IPA-5 were assessed in mature plants from 1995 to 1997, and related to different disease intensities, in a naturally infested area irrigated by centre pivot. Over the 3 years, there were no differences (Tukey at 5%) in fruit numbers between plants without symptoms (NS) and with intermediate symptoms (IS), which yielded higher numbers than plants with severe symptoms (SS). The greatest reduction in fruit number was 56.8% in 1997. Significant differences were observed in fruit weight and size among NS, IS and SS plants in 1995 and 1997. In 1996, NS and IS plants were similar, but different from SS, which yielded significantly less. Weight and size reductions in SS plants reached 84.3% and 62.0%, respectively, in 1997. In 1996 and 1997, yield losses related to time of symptom appearance and physiological age were also assessed. Significant correlations were found ( P  < 0.01), with nearly total losses observed when plants were infected from early to mid bloom, as opposed to plants infected near harvest, which had lower disease incidence and produced economically acceptable yields. Quadratic and exponential models best fitted the relationship between yield and time of symptom appearance, and yield vs physiological age could be explained by logistic and Gompertz functions.     

Characterization of chickpea differentials for pathogenicity assay of ascochyta blight and identification of chickpea accessions resistant to Didymella rabiei

Forty-eight chickpea germplasm lines, including 22 differentials used in previous studies, were characterized for disease phenotypes following inoculation with six isolates of Didymella (anamorph Ascochyta ) rabiei , representing a wide spectrum of pathogenic variation. Representative isolates were also directly compared with six previously identified races on eight chickpea genotypes. Many of the chickpea differentials reacted similarly to inoculation with each isolate of D. rabiei , and several previously identified races caused similar levels of disease on the differentials. This indicates that the number of differentials can be reduced significantly without sacrificing accuracy in describing pathogenic variation of D. rabiei on chickpea. Pathogenic variation among samples of US isolates allowed classification of the isolates into two pathotypes. The distribution of disease phenotypes of the 48 germplasm lines was bimodal after inoculation with pathotype I isolates, whereas the distribution of disease phenotypes was continuous after inoculation with pathotype II isolates. Such distinct distribution patterns suggest that chickpea plants employ different resistance mechanisms to each pathotype and that the two pathotypes may have different genetic mechanisms controlling pathogenicity. The advantages of using the two-pathotype system in assaying pathogenicity of the pathogen and in studying resistance mechanisms of the host are discussed. Three chickpea accessions, PI 559361, PI 559363 and W6 22589, showed a high level of resistance to both pathotypes, and can be employed as resistance sources in chickpea breeding programmes for resistance to ascochyta blight.     

Molecular identification of 16SrII-D subgroup phytoplasmas associated with chickpea and faba bean in Sudan

In January 2011, symptomatic chickpea and faba bean plants were observed in fields located in the Gezira state (Sudan). Faba bean plants showed yellowing and stunting, whereas chickpea plants presented yellowing, reddening and little leaves. The disease etiology was investigated using nested polymerase chain reaction (PCR) with phytoplasma-specific primers which amplify a fragment of the 16S rRNA gene. Sequencing and restriction fragment length polymorphism (RFLP) analyses revealed that the tested phytoplasmas belonged to the group 16SrII. Phylogenetic analyses of the 16S rRNA gene of the obtained sequences indicated that the chickpea and faba bean phytoplasmas from Sudan were more closely related to the phytoplasmas subgroup 16SrII-D. To our knowledge, this is the first report of phytoplasmas from the group 16SrII-D infecting chickpea in Sudan, and faba bean worldwide.     

Pathogenicity of indole-3-acetic acid producing fungus <Emphasis Type="Italic">Fusarium delphinoides</Emphasis> strain GPK towards chickpea and pigeon pea

An indole-3-acetic acid (IAA) producing fungal strain was isolated from chickpea grown rhizospheric soil samples. Based on morphological and Internal Transcribed Spacer (ITS) region sequence analysis the new isolate was identified as Fusarium delphinoides. The Fusarium delphinoides strain produces and secretes IAA in-vitro as identified by HPLC and Mass spectrometry. The IAA production is dependent on tryptophan (Trp) as a nitrogen source in the medium. The IAA production is influenced by growth conditions such as pH of the medium, concentration of Trp and the nature of the carbon source. Additional nitrogen sources repress Trp dependent IAA production. Glucose and Trp served as the best carbon and nitrogen sources respectively. Pathogenicity of Fusarium delphinoides towards the plants was tested by electrolyte, nutrient leakage analysis and also by scoring the disease symptoms. Two cultivars of chickpea (ICCV-10 and L-550) and two cultivars of pigeon pea (Maruti and PT-221) were assessed for the pathogenicity by inoculating with spores of Fusarium delphinoides. The inoculation induced symptoms of Fusarium wilt as in the case of Fusarium oxysporum f. sp. ciceris (FOC), a known pathogen causing Fusarium wilt in chickpea. Electrolyte and nutrient leakage from the infected plants were used to assess the resistance, tolerance (moderately resistance) and susceptibility of the plants to the infection. Based on the results, both the pigeon pea cultivars (Maruti and PT-221) were rated as resistant, and ICCV-10 was rated as a tolerant cultivar of chickpea. However, chickpea cultivar L −550 was found to be a susceptible host for infection by Fusarium delphinoides. These results suggest that Fusarium delphinoides, which belongs to the Fusarium dimerum species group, is an IAA producing plant pathogen and causes wilt in chickpea. Further, along with pathogenicity tests, electrolyte and nutrient leakage analysis can be used to assess the pathogenicity of pathogenic fungi.