In this article we will discuss about the pea rust disease caused by Uromyces Fabae.
Introduction to Pea:
Pea is one of the six major pulse crops cultivated globally and is second highest yielding legume, next to broad bean. It is consumed both as fresh vegetable as well as in a dried form constituting a significant amount of protein in the vegetarian diet.
Its seeds are highly nutritious and are grown for food as well as for rotational benefits in cereal grain production. The inclusion of peas in crop rotation is agronomically very significant.
Pea is a good predecessor to other crops as it enriches the soil with the nodule bacteria- rhizobia, which fixes atmospheric nitrogen. Moreover, peas have a higher capacity to utilize minerals, which are practically difficult to assimilate and are not available to the cereals.
The root system of peas penetrates to a depth of 1-1.5 m and as a result peas can extract mineral nutrients from the deeper soil layers unlike grain crops.
The nutritive value of dry pea seed is similar to other grain legumes and contains 18-30% protein, 35 -50% starch and 4-7% fiber. Pea protein is deficient in sulphur containing amino acid but contains relatively high levels of lysine making it a good dietary complement to cereals. Pea ranks second to dry bean among grain legumes for worldwide production and fourth in harvested area.
Dry pea is produced in more than 87 countries. India ranks fifth in production and third in harvested area (FAO, 2005). In India, pea occupies land area of 0.64 m ha with a production of 0.52 million tons and productivity of 890 kg /ha.
However, this productivity is quite low when compared to the highest productivity of 58.0 Q/ha in the Netherlands. Mc Phee (2003) described dry pea was domesticated 9000 years ago.
Pea originated in the near East and Mediterranean regions and has been grown since early neolithic times. Evidences indicate that pea has been cultivated with cereal crops such as wheat and barley after domestication.
Pea belongs to the genus Pisum, a member of family papilionaceae tribe viciae and is composed of species Pisum sativum L. (Ps) and Pisum fulvum (Sibth and Sn). Pisum sativum L. had been further divided to include several subspecies Ps. ssp sativum, Ps ssp. elatuis, Ps ssp humile, Ps ssp arvense and Ps. ssp hortense. In literature ssp elatius and ssp humile are the progenitors of Ps ssp sativum.
Major constraints in pea production include disease, pests, frost, drought and excessive heat. Major diseases affecting pea production are Fusarium root rot; Aphanomyces root rot, Fusarial wilt, pea enation mosaic virus, powdery mildew, downy mildew, Aschochyta blight and rust.
Many other minor diseases also affect the yield of this important crop. In India, problem of powdery mildew has been overcome by the use of powdery mildew resistance gene and it is mandatory to incorporate only powdery mildew resistant entries in All India Coordinated varietals Improvement trials.
Rust of pea caused by Uromyces fabae (Pers) de Bary is considered the most important under warm and humid conditions. It become a major problem under late sown conditions in India.
Distribution and Losses of Uromyces fabae:
Uromyces fabae has been reported from different part of Europe, Africa; Canada; Australia. In India it is reported from Eastern India, Central India, Southern parts of India and Himalayan region of Himachal Pradesh.
Uromyces fabae completely destroyed the crop in sub-mountainous region of North- India. Yield losses in pea due to rust was also reported by Upadhyay and Gupta (1998). Singh (1999) reported the losses in pea yield from Tarai regions. On an average of about 56.81% yield loss was reported in the year 1986-1988. They further classified the losses and reported 22.21% of loss occurs due to reduction in seed weight of the pea.
Losses also depends on different growth stages of plant. Early infections completely destroy the crop. Occurrence of disease at pod formation stage reduced the grain yield. Main attribute of yield loss is mainly due to the reduction in weight of 100 seed.
Symptoms of Pea Rust:
Pea rust is characterized by the appearance of two types of symptoms in India. Early symptoms develop on abaxial side of older leaves and form round to oval aecidia. Initially aecidia form creamy white to light yellow to bright orange colored pustules on the leaf and stem.
Under favorable environment these pustules further developed and spread to other parts of the plants. An aecidia is a cluster of several small cups like structure on the plant. Aeciospores released from the aecial cups are deposited as yellow powder.
Small aecidial pustules are mostly confined to the leaf. However it can be seen on stem also. In tendril genotypes of pea it can also be seen on the stipules and tendril also. Uredial pustules developed on both the surface of leaf but mostly confined to the stem. They appear as powdery light brown pustules. The ruptured epidermis on infected portion of host exposes black to brown powdery mass.
Telial symptoms appear after aecial/uredial infection late in the same season or on the part of plant leading to senescence. Teliospores are formed in the aecial or uredial pustules. Some it is also formed independently Telia are mostly formed on the stem and tendril. Grain size is significantly reduced in badly infected genotype and colour of the grain becomes dull.
The casual organism of pea rust in most parts of India is Uromyces fabae (Pers.) de Bary. It is a biotrophic, macrocyclic, autocious rust. It belongs to the Division: Basidiomycotina, Class: Basidiomycetes, Subclass: Teliomycetidae, Order: Uredinales, Family: Pucciniaceae.
Host Range and Occurrence of the Pathogen:
Uppal (1933) and Prasada and Verma (1948) found several species of Vicia, Lathyrus, Pisum and Lentil susceptible to Uromyces fabae in India and abroad. In India species of Vicia, Lathyrus and Pisum are described as host plant for Uromyces fabae (Pers. de Bary).
They observed natural infection on Vicia sativa L. and V. hirsuta Gray, a common weed found in the fields of lentil in India also. Vicia faba L., V. biennes L., V. hirsuta L., and V. arborensis L. were described as highly susceptible to Uromyces fabae and Vicia sativa and Lathyrus aphaca were found to be disease free.
Conner and Bernier (1982) reported a total of 52 species oiVicia faba and 22 species of Lathyrus infected by Uromyces viciae-fabae.
They also found this pathogen on pea, lentil and faba bean. Butler (1912) reported the occurrence of rust pathogen Uromyces fabae on pea and other leguminous crops from India. Sydow and Butler (1912) reported this fungus from state of Maharastra.
Pea rust (Uromyces fabae) is of worldwide occurrence and attacks number of host species belonging to different genera of the family leguminoceae in the Indo-Gangetic Plains. Prasada and Verma (1948) also reported the occurrence of Uromyces fabae on lentil crop from Delhi. Roy (1949) in his list of fungi of Bengal recorded the prevalence of Uromyces fabae on the leaves and stems of Pisum sativum.
Mitter and Tandon (1930); Patel (1934); Pavgi and Upadhyay (1966) and Kapooria and Sinha (1966) reported the distribution of this pathogen in the regions of Uttar Pradesh, respectively. Bilgrami (1979) reported the occurrence of this pathogen on various host species of Pea, Lentil and Lathyrus. Baruah (1980) reported that rust infection on the pea plants is caused by both Uromyces fabae and U. pisi.
Of which U. pisi is of rare occurrence in India. Choudhary (1998). reported host non specificity in Uromyces fabae and found few legume genus infected, by the pathogen. Occurrence of Uromyces fabae have also been reported from Canada, Europe, Ethiopia and Australia in mild to severe forms on pea, lentil and faba bean.
Pathogenic variability has been reported in field collection of Uromyces fabae. The urediospores of Uromyces fabae was the only infective spore in temperate climate and is used in various resistance-screening programme in pea and sweet pea.
The existence of pea specific strains from NEPZ of India has also been reported. Aeciospores acts as as repeating spore in case of Uromyces fabae and play important role in the out-break of disease under warm humid conditions.
The aecidium is small, whitish and cup shaped structure and bear aeciospores. The aeciospores are round to angular or elliptical, yellow in colour and posses fine warts. They measures 14- 22 pm in diameter.
Aeciospores are sessile and formed in chain of 7 -8 spores. Aecidia are deep seated in the spongy mesophyll cells. Aeciospores released after rupturing peridium of aecial cups. Large amount of aeciospores are deposited on the plant surface look bright yellow.
The Urediospores are round to ovate, light brown, spiny with 3-4 germ pores, measure 20-30 x 18-26 pm. Uredia developed infrequently. Urediospores are stalked, round to elliptical. Urediospores come out in group after rupturing host epidermis.
They are sub-globose ovate or elliptical with round or flattened apex which is considerably thicked and appears papilate the spore are smooth measures 25-30 x 18- 27 pm. The stalks are generally presistant on the detached spores and pale yellowish brown, thick and up to 90 pm.
The basidiospore of Uromyces fabae germinated within 3 days of rehydration and it was not influenced by the photoperiod. The germination per cent of basidiospores was high on the substrates except glass slide.
On water agar (2%) basidiospores produced long germtube 50-100 pm. The differentiation in the germtube starts after 3 days. Infection structure resoled better when germination was studied on 5% water agar.
The short germtube swell apical and formed small appressorium. Subsequently penetration peg formed and oblong vesicle expanded in agar. On the glass slide appressorium formation often occurs however vesicle formation rarely observed.
Basidiospore differentiation was most effectively induced on nitrocellulose membrane. Less than 5% basidiospore produced long germtube and majority of’ basidiospores reached to the appressorium stage. Two nuclei are always seen in basidiospore.
During early infection structure development both the nuclei migrated together from cytoplasm in to the vesicle. Subsequently penetration peg was plugged and vesicle grew apically, forming a primary hypha which was some time delimited by a septum. Up to primary hypha stage no more than two nuclei was observed.
Biotrophic plant pathogenic fungi differentiate specialized infection structures called haustorium within the living cells of their host plants. These haustoria have been linked to nutrient uptake ever since their discovery.
The flow of sugars from the host Vicia faba to the rust fungus Uromyces fabae seems to occur largely through the haustorial complex. One of the most abundantly expressed genes in rust haustoria, the expression of which is negligible in other fungal structures, codes for a hexose transporter.
Functional expression of the gene termed HXT1 in Saccharomyces cerevisiae and Xenopus laevis oocytes assigned a substrate specificity for D-glucose and D-fructose and indicated a proton symport mechanism. Abs against HXT1p exclusively labeled haustoria in immunofluorescence microscopy and the haustorial plasma membrane in electron microscopy.
These results suggest that the fungus concentrates this transporter in haustoria to take advantage of a specialized compartment of the haustorial complex. The extrahaustorial matrix, delimited by the plasma membranes of both host and parasite, constitutes a newly formed apoplastic compartment with qualities distinct from those of the bulk apoplast.
This organization might facilitate the competition of the parasite with natural sink organs of the host.
Mode of Survival of the Pathogen in Uromyces fabae:
The aeciospores and urediospores of Uromyces fabae did not survive at a temperature more than 30°C for one week therefore, they were not supposed to survive the high temperature of the intervening crop season. Teliospores survives during the intervening season and germinates to produce basidiospore that produced pycnia, and subsequently causes infection in pea.
The debris of pea plant carrying telelia inoculated to the pea plant and no spermagonia were found on the plants. However, aecial infection was observed on the few plants. This result needs to be verified at different places in order to confirm the role of teleospore in the initiation of primary infection.
Being a wide host range pathogen Conner and Bernier (1982) have suggested, the role of collateral host in the occurrence of disease on pea.
They reported Vicia and Lathyrus species as a collateral host to Uromyces fabae and pathogen survive on these hosts during the absence of the main crop. There is no information about the migration of pathogen form collateral hosts from India and other countries. Pea is grown through-out the year in the different part of the India but its role in the multiplication and further spread of the Uromyces fabae is not known.
In the recently concluded A.I.C.P.I.P experiment (2005) incidence of rust was noticed earlier in Pant Nagar than the Varanasi and Dholi. There is need of extensive survey of collateral hosts and offseason grown pea crop temperate, sub- tropical and tropical part of India to confirm the role of collateral hosts in perpetuation of the pathogen from year to year.
Germination of different Spores:
Germination of spores is independent of the host. Water agar (0.2%) was found to induce 46.67% germination in urediospore and 9.67% germination in aeciospores. Occasional germination was observed in teliospores that were stored for three years after the incubation at 18°C for 15 days.
The germination of teliospores was less than the 1%. Aeciospore, urediospores and teliospores germinated by a single germ tube. Germination in the aeciospore was initiated after 8 hrs on 0.2% water agar at 25°C. The urediospores were also found to germinate on 0.2% water agar at 15°C after 4 hours of incubation.
Effect of relative humidities and temperatures on the aeciospore and urediospore germination:
The optimum condition for aeciospore germination was 25°C in combination with 100% relative humidity. The percent germination of the aeciospores decreased gradually with the decreasing temperature below 25°C.
None of the aeciospores germinated at relative humidity of 88.5% at a temperature below 25°C. Aeciospores germination was minimum (0.17%) at 5°C in combination with 100% relative humidity. Relative humidity of 98% in combination with 15°C favored maximum (3.5%) urediospore germination. Longer leaf wet duration increased the rust severity.
Relationship between Temperature and Disease Severity:
The mean temperature during the initiation of the disease ranged between 15-20°C. The incidence of the disease was delayed when occurrence optimum temperature'(25-30°C) was late in the season due to delayed onset of cool weather.
Urediospores of U. viciae-fabae (broad bean rust) germinated well in the range 5-26°C, with fastest germination at 20°C. Exposure to 30°C gave poor germination and damaged the spores. Infection of Vicia faba leaves depended on a moisture film.
At 20°C some infection occurred with only 4 h leaf wetness, but longer wet periods up to 24 h gave increased infection. At lower temperatures, the infection process was slower and final pustule numbers were also less. Spore germination was delayed by daylight and by all artificial light sources that contained far-red (700-800 nm) wavelengths.
The delay was increased at higher light intensities. When spores were subjected to alternating periods of light and darkness, it was found that 40 min of darkness was sufficient for the irreversible induction of germination at 20°C.
Penetration by Uredia:
The pre-penetration phase:
The uredospores of the rust fungus Uromyces fabae form an adhesion pad and release a cutinase and two specific esterases after contacting the host cuticle. Apparently, adhesion of the pads is improved by these enzymes. The spores have reduced ability to attach to the leaf surface when these enzymes are inactivated.
Host surface perception:
Appressorium formation by urediospbre germ tubes of the bean rust Uromyces appendiculatus is induced by physical differences in the topography of the leaf surface, such as stomatal lips of guard cells, or by defined ridges of 0.5 m height formed on an artificial surface. In addition, it has been shown that many rust fungi exhibit species-specific responses on membranes with defined topographies.
Cell wall degradation (by enzymatic action):
Nevertheless, penetration by obligately biotrophic parasites, such as rust fungi and powdery mildews or some hemibiotrophs, requires only minor damage of the cell wall. Degradation of the cell wall is limited to the site of penetration as shown by Xu and Mendgen (1997). Secretion of cellulytic enzymes of these pathogens is either developmentally regulated or triggered by environmental signals.
For example, cellulase activity of Uromyces fabae germlings has been shown to be strictly regulated by differentiation. It increases during appressorium formation and reaches a maximum during development of infection hyphae and haustorial mother cells.
Also, the production of the pectic enzymes pectin methylesterase and polyglacturonate lyase and extracellular proteases of this rust fungus depends on the differentiation of infection structures.
Apparently, the concerted action of cell wall degrading enzymes enables the hyphal growth through the leaf tissue but prevents extensive cell wall maceration and cell death which would interfere with the biotrophic lifestyle of the fungus also.
The fungus penetrates through leaf stomata and forms a fusiform substomatal vesicle Haustorial mother cells elongate and attempt to penetrate the leaf mesophyll cells.
If penetration succeeds, a nutrient absorbing haustorium develop in the mesophyll cell and enables fungal growth of subsequent hyphae. The rust infection can be hampered at very early stages of fungal development from spore deposition to stomata recognition, resulting in reduced infection. Nevertheless most germinating spores proceed and develop normal haustorial mother cells.
However, haustorium formation may be prevented by papilla formation within mesophyll cells. Papillae have callose matrix and contain various inorganic and inorganic constituents including antimicrobial proteins and auto fluorescence phenolic compounds.
Papillae are deposited on the inner surface of the mesophyll cell walls where fungus attempt to penetrate and act as a physical or chemical barrier when penetration resistance fail’s and haustoria develop within the host cells.
Post Penetration Development:
Aeciospores germinate to give rise germ tube and later on approsorium this process found to take about 48 to 72 hours in host tissue later there is formation of infection peg which grows intercellularly inside the host tissue after entering through stomatal opening then substomatal vesicle is formed which give rise to haustorial mother cell which give rise to First haustorium formed inside host cell.
Post-penetration process consist of spread of mycelium in the inter celluar spaces and later on thy replace some of the host spongy mesophyll cells.
A perdial layaer of single cell was formed around the mycelial aggregation. These structure expend further and attained a size (pM). Through-out the development of aecium mycelium was dikaryotic.
Dikaryotic mycelium later on which forms sporogenous cells of the aecium or aeciosporophores its form at the base of the aecial primordium each cell contains two nuclei that divide conjugately during the formation of an aeciospore initial. Two of the daughter nuclei remain in the sporogenous cell and the other two moves towards aeciospores initials.
After the initial is delimited from the mother cell by septum, the nuclei in the initial divide again and a transverse septum separates the initial into a binucleate aeciospores and small wedge shaped, binucleate sterile, intercalary or disjunctor cell. The entire process repeated several times resulting in the formation of a chain of aeciospores a disjunctor cell.
Arrangement of aeciospores is younger towards the base while older towards the apex-initial arised in the aecial cavity. Peripheral cells of the aecial base undergo successive division to produce a wall that surrounds the spore chains. This wall is the peridium. In a young aecium that has not broken the host epidermis the peridium surrounds the spore chains on all sides, forming a complete dome over them.
As the aecium mature the spore chains push through the roof of the peridium forms a lip around the aecial cup. As an aecium develops, the disjunctor cells disintegrate and spores separate from each other. When aecia develop in a leaf they generally are located in the lower portion and break through the lower epidermis.
In case of extra sensitive variety of pea generally large number of aecial initials start and form the aecidiophoere but the development of aeciospores are hampered and resulted in the non brusting aecidia. In these pea genoypes it has also been observed that number of aecidiosporophores are significantly less than the other genotypes. But the number of aeciospores in chain was almost 3-6 per aeciosporophore.
The reduction of number of aecisporephore comes mostly from the reduction of aecisporophoes. In Uromyces fabae number of aecidiospores varied from 10 – 40. The aecidiosporophores grow up right in the cavity towards the epidermis. The perdial layer replace the mesophyll cell reached below epidermis. After some time pressure exerted by the mature aeciospores rupture the epidermis.
Basidiospores were binucleate. Vesicle contains two nuclei and septum’seprate two nuclei in infection structure. Nuclear staining of aeciospore and urediospore clearly revealed the binucleate structure. Both the nuclei they were together during the septum formation in the germ tube.
Effect of Host Factor on the Out-Break of Disease:
Effect of temperatures and plant growth stages on spore production:
The aeciospores were produced abundantly at both the temperature regimes i.e. 10-15°C and 20-25°C at all the growth stages of crop. At higher temperature regime (20-25°C), during pod formation the number of aecidia/pustules/leaf was highest.
Higher temperature promoted more numbers of aecial pustules than the lower temperature. Teliospores were produced, when plants entered into the senescence stage (110-130 days after sowing).
Resistance Components in Host:
There are several resistance components that individually or in tandem with other components reinforce the resistance. Most of these components are influenced by the environmental factors i.e. temperature and relative humidity. Therefore a multi-year and multi locations testing of these components are most essential in order to capitalize these traits in the crop improvement.
Most of the cases these traits are scattered among the germplasm lines of pea, lentil and vicia. Individual effects of these components are very less therefore difficult to demonstrate under field conditions. However, using molecular techniques these can be detected.
The protection efficiency of these traits can be verified by comparing the disease severity, AUDPC, test weight under protected and unprotected conditions. Yield gain under fungicidal protection will be always higher in the susceptible genotype than slow rusting.
Effect of Incubation and Latent Period on Rust Severity:
Incubation period of aeciospre ranged from 7.17-17.84 days on different pea genotypes. The correlation, between incubation period and AUDPC were negative -0.68. Highest incubation period was shown by Pant P 13 and lowest incubation period was represented by HUVP 1.
varied from 8.23 to 17.83 days among the pea genotypes. Latent period affects the disease severity and its spread. Genotype having higher latent period delayed the out-break of disease. The correlation (r) between latent period and AUDPC were negative -0.58.
There are many genotypes having higher latent period. Latent period has great significance in delaying the onset of disease and its further spread. Most of resistance pea genotypes screened at rust hot spots like Bangalore, Pune and Varanasi are generally possess higher latent period.
Significant difference were reported among the lentil cultivars for the latent period for urediospores in the susceptible cultivars it was noticed 8 days while same amount of pustule was noticed after 15 days in the resistant cultivars.
There was significant difference in the latent period in the Vicia germplasm lines. Most of the slow rusting lines had longer latent period than the susceptible one. Latent period was negatively correlated with the disease severity, AUDPC and rate of spread. The LP was negatively correlated with the CS, AUDPC, DS, and r.
Significant difference are reported for the aecial colony size that varied from 1.9 to 4.9 mm2. Small colony size are often associated with the slow rusting genotypes. However, in some cases effect of small colony size is nullified by the high frequency of colony/unit area.
The difference in the pustules size were reported in lentil that varied from 0.096 0.56 mm2.
Colony measured after inoculation were larger on seedlings than the adult plant. In the susceptible control, the colony size was almost double in size than on the adult plant. The hypersensitive lines showed the smallest colonies at both plant maturity stages. Few non hypersensitive lines also showed smaller colonies than the susceptible check.
Under field condition some of the pea line showed less number of colony on the leaf when spores were blowing on all the lines. But the infection frequency increased when free water prolonged for longer period on plant surface with a temperature 25-30°G.
Lentil genotypes displayed enough variation for the infection frequency. Most of the lines with the low infection frequency retard the disease development and identified as slow rusting types.
A significant difference was recorded among the vicia genotypes for infection frequency when inoculated with the equal amount of urediospre under indentical conditions of disease development. Most of the slow rusting lines showed low infection as compare to the susceptible one. This trend was also noticed under field situation.
Inheritance of resistance:
Several faba bean sources showed two different types of incomplete resistance to U. viciae – fabae. One type of resistance is expressed as a reduction of disease severity without any microscopically visible necrosis. In other hypersensitive resistance has been described as incomplete resistance associated with late – acting necrosis of the host tissue resulting in a reduction of the infection type.
Both type of incomplete resistance differ only in the presence or absence of microscopically visible necrosis. The genetic basis of hypersensitive resistance was suggested monogenic. Emeran (2001) suggested race specific nature of hypersensitive resistance. The evidences of physiological specialization in U. viciae fabae implies that the use of single resistance gene in cultivars would likely not result in long term rust control
The progress in the development of resistant varieties has been slow due to lack of well characterized resistant sources in pea. Incomplete resistance make the problem tricky to the pea breeders. The available resistant sources are of slow rusting type and it retards rate, resulting in intermediate to low disease levels against prevalent pathogen.
However, no study has been undertaken to characterize slow rusting components in pea, which is urgently needed in order to select appropriate slow rusting lines against this pathogen. Against a variable pathogen population only slow rusting lines are known to display durable resistance.
Slow rusting is a form of quantitative resistance and quantitative resistance is greatly affected by growth stages of plants and environmental conditions, which masks the actual performance of resistance.
Therefore, it is required to ascertain the actual performance of the various genotypes and separate the environmental influence on resistance and its components to establish its usefulness in a breeding programme. These resistance components can thereby, assist selection procedures in a pea improvement programme.
Inheritance studies on rust resistance in pea are limited and still not well established. There were reports of existence of both monogenic as well as polygenic forms of resistance towards rust in pea. Lack of hypersensitive reaction in pea against Uromyces fabae suggests the absence of race specific monogenic forms of resistance.
Clear information about inheritance of rust resistance in pea would help to design a suitable strategy to enhance existing resistance in pea and could be helpful in any pea improvement programme. It would also allow for the development of suitable long-term disease management strategies.
Resistance breeding would be greatly facilitated if information on the biology of this pathogen and its interaction with environment were available.
Plant growth stages also affect the infection and influence the total yield loss. Only, specific yield attributing characters are affected under such conditions. Since disease appears during late vegetative stages it is only the seed weight that is most affected in pea.
Therefore, it becomes necessary to establish a relationship between the disease and reduction in seed weight incurred by it. This will also enable the workers to predict the losses in the yield by knowing the stage for disease incidence and its severity.
Selection of resistance component under field:
Selection for rust resistance in breeding programme implies a disease screening process that is difficult or unreliable in some cases. Like wise the obligate nature of U. viciae fabae makes it difficult to maintain the pathogen in culture and apply to screen segregating population under controlled growth condition. Complication is likely to increase when both the uredial and aecidial spores create disease.
Since, infection process of both the spore state is different. Infection by uredia is mostly confined to the epidermal cells and few layers of mesophyll cell. Whereas in the case of aecidial state the infection are deep in the mesophyll and spongy tissues in order to form the aecial cups.
Therefore, the level of resistance of same genotype may vary with the different spore and need to be worked out. Natural occurrence of disease under field relied on appropriate environmental conditions that further complicates resistant breeding programme.
However the maximum resistant components along with the yield traits are likely to be selected when the distribution of rust in the screening field would be normal with 90% rust severity on susceptible check and <20% on the resistance check.
Selection gain of these lines can be verified in term of less disease severity, low AUDPC, higher seed test weight than the susceptible checks. The gain in increased yield and test weight would be less in resistant genotypes when grown under fungicide protected and unprotected condition.
Molecular markers for resistance:
Two RAPD markers viz.SC10-82360 (primer, GCCGTGAAGT) and SCRI-711000 (primer, GTGGCGTAGT), flanking the rust resistance gene (Ruf) with the distance of 10.8 cM (0.097 rf and LOD of 5.05) and 24.5 cM (0.194 rf and LOD of 2.72) were identified.
These RAPD markers are not close enough of Ruf to allow a dependable marker – assisted selection for rust resistance. However, if the two markers flanking Ruf are used together, the effectiveness of MAS would be improved considerabley.
Bulk segregant analysis was used to identify RAPD markers linked to a gene determining hypersensitive resistance. The monogenic nature of resistance was determined by analyzing the F2 population from a cross between resistant and susceptible line. Linkage of RAPD markers were confirmed by screening 55 F2 plants segregating for resistance.
Three RAPD markers (OPD13736 and.OPI20900) were mapped in coupling phase to the resistance gene for race l (Uvf-l). No recombination between OPI20900 and Uvf -1 were detected. Two additional markers (OPP201172 and OPR07930) were linked to the gene in repulsion phase at a distance of 9.9 and 11.5 cM respectively.
Although, fungicides provide an effective means to rust management. However, it is not cost effective and associated with several environmental and health related hazards. Therefore, cultivation of disease resistant varieties of the crop provides a cheap, effective and safe means of disease control. Resistant varieties as a component in integrated management are also recommended for this disease.
Optimum population and timely sowing of crop help in escaping of rust. Incidence of rust in the North India mostly appeared from second week of January on wards. October sown crop generally affected at later stage after grain filling. Late sown crop mostly coincide with most vulnerable stage.
Incidence of rust in different part of the country especially in the northern and southern hill should be investigated. Host range of rust population in the pea growing area should be worked out. Region wise involvement of uredial and acecial in out-break of rust will provide better insite into rust biology. Metrological factors that influence the onset of rust should be studied in detail.
Various features of the host which influence the disease is yet to be studied. Studies related to the inheritance of the rust resistance components are essential in order to pyramid the different components of resistance in agronomically suitable background.
Latent periods which influence the disease has been characterized in few donors and recombinant inbreed lines raised in susceptible back ground need to be mapped by molecular tools Along with the bio chemical changes that delayed the on the set of disease needs to be investigated thourghly.