Mungbean yellow mosaic virus \(MYMV\): a threat to green gram ...

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Mungbean yellow mosaic virus (MYMV): a threat to green gram (Vigna radiata) production in Asia Article in International Journal of Pest Management · November 2014 DOI: 10.1080/09670874.2014.982230

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Mungbean yellow mosaic virus (MYMV): a threat to green gram (Vigna radiata) production in Asia a

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A. Karthikeyan , V.G. Shobhana , M. Sudha , M. Raveendran , N. Senthil , M. Pandiyan & a

P. Nagarajan a

Department of Plant Molecular Biology & Biotechnology, Centre for Plant Molecular Biology, Tamil Nadu Agricultural University, Coimbatore, India b

National Pulse Research Centre, Tamil Nadu Agricultural University Vamban, Pudukkottai, India Published online: 26 Nov 2014.

Click for updates To cite this article: A. Karthikeyan, V.G. Shobhana, M. Sudha, M. Raveendran, N. Senthil, M. Pandiyan & P. Nagarajan (2014) Mungbean yellow mosaic virus (MYMV): a threat to green gram (Vigna radiata) production in Asia, International Journal of Pest Management, 60:4, 314-324, DOI: 10.1080/09670874.2014.982230 To link to this article: http://dx.doi.org/10.1080/09670874.2014.982230

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International Journal of Pest Management, 2014 Vol. 60, No. 4, 314324, http://dx.doi.org/10.1080/09670874.2014.982230

Mungbean yellow mosaic virus (MYMV): a threat to green gram (Vigna radiata) production in Asia A. Karthikeyana*y , V.G. Shobhanaay , M. Sudhaay , M. Raveendrana, N. Senthila, M. Pandiyanb and P. Nagarajana a Department of Plant Molecular Biology & Biotechnology, Centre for Plant Molecular Biology, Tamil Nadu Agricultural University, Coimbatore, India; bNational Pulse Research Centre, Tamil Nadu Agricultural University Vamban, Pudukkottai, India

Downloaded by [A. Karthikeyan] at 04:28 02 January 2015

(Received 28 February 2014; final version received 17 October 2014) Mungbean yellow mosaic virus (MYMV) disease is one of the most vicious diseases of green gram and has been renowned in India for more than five decades. It is caused by a group of geminiviruses belonging to the genus, begomovirus of the family, Geminiviridae. They are transmitted through whitefly in a persistent manner. The economic losses due to this virus account up to 85% in green gram which is spreading faster towards newer areas. The escalating economic importance of MYMV has resulted in the call for accurate detection and identification procedures that inspire rigorous research efforts focussing on the biology, diversity and epidemiology of the virus, so that viable management strategies could be designed. Breeding for resistance or tolerance appears to be the best approach to control this disease. However, the commercially offered genotypes are only partially resistant. Therefore, the hunt for newer sources of disease resistance needs to be intensified. This review updates all the accessible information on MYMV and outlines the areas in which advance research is indispensable. Keywords: Begomoviruses; mungbean yellow mosaic virus; Vigna radiata; whitefly

1. Introduction Vigna radiata (L.) Wilczek, commonly known as green gram or mungbean (originated in India or the IndoBurmese region), is a vital crop grown throughout Asia, Australia, West Indies, South and North America, tropical and subtropical Africa. It is well suited to a large number of cropping systems and constitutes an important source of cereal based diets, worldwide, covering more than six million hectares per annum. However, Asia, alone, accounts for 90% of world’s mungbean production. India is the world’s largest mungbean producer accounting for about 65% of world’s acreage and 54% of its global production (Singh 2011). Mungbean contains carbohydrate (51%), protein (24%26%), minerals (4%) and vitamins (3%). Besides, it has the remarkable quality of serving the symbiotic root rhizobia to fix atmospheric nitrogen and hence, augments soil fertility. Due to the importance of mungbean in Asian countries, the World Vegetable Center (formerly known as, Asian Vegetable Research and Development Center AVRDC) has been actively working on mungbean for the past four decades. Prior to inception of AVRDC, national partners in mungbean producing countries released more than 100 improved mungbean cultivars for yield and resistance against pests and diseases in South and South East Asia and most parts of the world (Somta et al. 2009). The standard worldwide yield of mungbean is very low (384 kg/ha) and its production has not considerably increased yet. The main reason for the low yield is the susceptibility of the crop to insects, weeds and diseases caused by fungus, virus or bacteria.

Among the three, the viruses are the most important group of plant pathogens affecting the production of the crop. They cause severe diseases and economic losses in mungbean by plummeting seed yield and quality (Kang et al. 2005). Mungbean yellow mosaic disease is transmitted by the vector, the whitefly (Bemisia tabaci). It is found to spread the begomoviruses, the major hazard to the flourishing production of mungbean in India, Sri Lanka, Pakistan, Bangladesh, Papu New Guinea, Philippines and Thailand (Honda et al. 1983; Chenulu & Verma 1988; Varma et al. 1992; Jones 2003; Haq et al. 2011a). Based on sequence identity analyses, the bipartite begomovirus isolates, namely, mungbean yellow mosaic virus (MYMV), mungbean yellow mosaic India virus (MYMIV) and horse gram yellow mosaic virus (HgYMV) are recognized as the causal agents of MYMD in different regions of the world (Qazi et al. 2007; Malathi & John 2008a; Ilyas et al. 2010). The most conspicuous symptom on the foliage starts as small yellow specks along the veinlets and spreads over the lamina; the pods become thin and curl upwards. Extensive records from the past showed that the disease occurs with different intensities in all of the mungbean producing areas in and around Asia. Depending on the severity of the disease infection, the yield penalty may reach up to 85%. Quite a lot of disease management strategies have been developed or implemented for MYMV disease and so far, no complete resistance to this disease has been incorporated into any of the commercially available mungbean cultivars. The disease still poses a major crisis to the economic production of

*Corresponding author. Email: [email protected] y Authors A. Karthikeyan, V.G. Shobhana and M. Sudha contributed equally on this work. Ó 2014 Taylor & Francis

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this crop in the Asian subcontinent. This review considers the understanding of the MYMV disease and highlights the urging scope to promote further research.

2. Historical perspectives and distribution Capoor and Varma (1948) of India were the first to report yellow mosaic disease of lima bean (Phaseolus lunatus) and later in Dolichos (Capoor & Varma 1950). In the middle of 1950, it was noted that the experimental host range of yellow mosaic disease (YMD) included numerous varieties of all groups of legumes. It was first identified as a problem in a mungbean field in India in 1955, at the experimental farm of the Indian Agricultural Research Institute, New Delhi. Nariani (1960) first described the yellow mosaic disease on mungbean and linked it with the virus. Nene (1968) named the virus as MYMV. After the initial discovery of MYMV disease in India, other countries also confirmed its presence in their own territories. It was confirmed in Pakistan (Ahmad 1975), Bangladesh (Jalaluddin & Shaikh 1981), Thailand (Thongmeearkom et al. 1981) and Sri Lanka (Shivanathan 1977). The distribution of MYMV in Asia has been illustrated in Figure 1. Between 1960 and 1980, most of the MYMD research was involved on managing the disease and so, more often, was based on the interaction of the vector population with insecticides, and resistance breeding. Studies were

performed (1970) to find out the chief vector of MYMV and white fly (Bemisia tabaci) was identified as the most prime vector at least in the Asian subcontinent. Murugesan and Chelliah (1977) reported a yellow mosaic on green gram which was higher during the months of March to May (summer season). The increased disease incidence might be attributed to the higher temperatures that were prevalent in summer season, which was favourable for the vector to develop and multiply. Thongmeearkom et al. (1981) were the first research group to see the MYMV particles in the leaf cells of Vigna radiata. MYMV was first purified by Honda et al. (1983). Various workers reported that the inheritance of resistance to the MYMV is controlled by a few set of genes (recessive gene (Singh & Patel 1977), a dominant gene (Sandhu et al. 1985), complementary recessive genes (Shukla & Pandya 1985) and two recessive genes (Verma & Singh 1988)). In 1990, MYMV had emerged as a great menace in mungbean production. The disease incidence was as high as 100% in the fields of farmers in the Asian subcontinent, often resulting in considerable yield losses (Varma et al. 1992). Therefore, in 1990s, AVRDC has accorded the high-priority mungbean improvement programmes and they started to work on the objective of incorporating the resistant genes for MYMV into the advanced breeding lines. The first complete sequence of an MYMD virus was isolated from mungbean reported by Morinaga et al. (1993). The genes

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Figure 1. Distribution of mungbean yellow mosaic disease (MYMD) in Asia.

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of MYMV were mapped using different mungbean populations (Shanmugasundaram 1996). These genes will be the first targets of marker-assisted breeding with random fragment length polymorphism (RFLP) markers. In northern Thailand, a severe outbreak of MYMD in mungbean occurred in 1997. This caused major losses to production and initiated a shift in cropping practices. Due to occurrence of mungbean yellow mosaic disease, improvement in production and productivity of mungbean is becoming tricky and the disease is a major problem in Asian countries (Varma & Malathi 2003). Most of the reported resistance screening to date has been done only in India and Pakistan (Malathi et al. 2005).


2.1.

A begomovirus associated with mungbean yellow mosaic disease MYMV disease is caused by begomoviruses, popularly recognized as geminiviruses which are the leading and the most significant genus within the family, Geminiviridae. They are plant-infecting single-stranded DNA viruses and have archetypal geminate incomplete icosahedral particles. They are branded as monopartite (a single DNA) or a bipartite (with two DNA components: DNA-A and DNA-B) (Figure 2), based on their genome organization (Mansoor et al. 2003; Jeske 2009), infecting mostly dicotyledonous plants like mungbean, urdbean and soybean (Haq et al. 2011a). The two DNA components namely, DNA-A and DNA-B, are roughly 2.8 kb in size (Borah & Dasgupta 2012). Bipartite begomoviruses, namely MYMIV, MYMV and horsegram yellow mosaic virus (HgYMV), are accepted as causal agents of MYMD in different regions of the world (Qazi et al. 2007; Malathi & John 2008a; Ilyas et al. 2010). Of all these viruses, HgYMV is the least studied. Its complete sequence is available in the databases but no detailed studies are conducted on this virus. The other two pathogens namely, MYMV and MYMIV, occur across the Indian subcontinent. Among the two, MYMV was studied extensively and was reported from Thailand. The northern, central and eastern regions of India are dominated by MYMIV infestations (Usharani et al. 2004) but MYMV is more ubiquitous in the southern (Karthikeyan et al. 2004; Girish & Usha 2005) and western regions of the country. The viral genomes consist of two circular single-stranded DNA

Figure 2. (Color online) Genome organization of bipartite begomovirus DNA-A and DNA-B.

components (DNA-A and DNA-B) which are about 2800 nucleotides in length (Qazi et al. 2007). The isolates of the larger DNA of the two components (the DNA-A) of MYMIV and MYMV share only 82% identity between their DNA sequences and so justify their separation into distinct species. There are numerous DNA-B components associated with yellow mosaic viruses (John et al. 2008). The cognate DNA-Bs of groups (i), (iii) and (iv) represent MYMIV, MYMV and HgYMV. The second group of DNA-B components are associated with either MYMV or MYMIV. These are closely associated to each other. They are more related to MYMIV than to MYMV (92%). DNA-A is involved in various nuclear functions. It encodes for all the factors required for viral DNA replication (the replication associated protein (Rep; a rolling-circle replication-initiator protein) and DNA helicase (Choudhury et al. 2006) and the replication enhancer protein (REn), regulation of gene expression (the transcriptional activator protein (TrAP)) and encapsidation/insect transmission [the coat protein (CP))). The functions of the V2 and C4 proteins remain unclear. In other begomoviruses, these two proteins have been shown to have a possible role in movement and overcoming plant host defences mediated by post-transcriptional gene silencing (PTGS). In MYMIV, the AC5 protein, encoded by a gene (not well conserved between the begomoviruses) has been shown to have a potential function in the viral DNA replication (Raghavan et al. 2004). The DNA-B component encodes two genes. They are the nuclear shuttle protein (NSP) and the movement protein (MP) act together to move the virus from one cell to the other within the plant. In depth analysis of the gene expression, studies of MYMV have shown the splicing of transcripts in a begomovirus for the first time (Shivaprasad et al. 2005). 2.2.

Transmission and epidemiology of disease

MYMV disease is transmitted principally by the polyphagous pest Bemisia tabaci (Figure 3) in a persistent (circulative) manner and grafting but not by sap, seed or soil. The latent period of whitefly is less than four hours, so it is a tremendously efficient vector for virus transmission. A single viruliferous adult is capable of transmitting the dreadful virus and it can transmit the virus within an acquisition and inoculation access period of 24 hours. Acquisition and inoculation by whitefly adults can be affected in a minimum of 15 minutes. The insect may attain the virus after a single bite and its transmission

Figure 3. (Color online) Polyphagous vector whitefly (Bemisa tabaci).


International Journal of Pest Management 317 efficiency increases with time on the source plant of virus as well as on the healthy mungbean plant (Malathi & John 2008a). The most efficient female and male adults in a population can retain infectivity for 10 and 3 days, respectively. Thus, the female adults are three times more efficient as vectors than males. Neither female nor male adults can retain infectivity throughout their life span. Nymphs of B. tabaci can acquire the virus from diseased leaves and the virus does not pass through eggs of B. tabaci. Nevertheless, the cropping seasons highly influence the vector population. Whitefly is found to be high during summer season compared to spring and rainy seasons. They thrive best under hot and humid conditions and the population also towers with higher temperatures. Moreover, the spread of MYMV on a local (within and between fields) and a regional basis reflects its dispersal. Its population is correlated with disease incidence. High populations appear on the crop that are 2030 days old leading to higher disease incidence (on the 45th day). Spring and rainy seasons attribute to unfavourable conditions for the multiplication of the whitefly. Therefore, the disease incidence is not high during those seasons. Nath (1994) studied the effect of the weather parameters on the population of whitefly and the incidence of yellow mosaic virus on green gram. He reported a simple positive significant correlation between the disease incidence and the population of the fly, temperature, the relative humidity, rainfall and the number of rainy days necessary for the infection. Honda et al. (1983) reported the mechanical transmission of the isolate of MYMV of Thailand and they obtained the highest transmission rates with 0.1 M potassium or sodium phosphate buffer of pH7.8. Thereafter no one reported any infestation caused by mechanical transmission. Attempts were made by Grewal (1988) to transmit the disease by sap inoculation by rubbing freshly extracted sap of mosaic affected leaves on the healthy young seedlings of mungbean. However, the disease could not be transmitted in this manner. 2.3.

Impact of MYMD infection on mungbean

Each group of the virus isolates (genetically distinct strains, reassortants and recombinants) may have a different level of stability or virulence, as reflected by the severity of the symptom in each line of mungbean. The whitefly delivers the virus through proboscis to the phloem cells of the host plant where it gets multiplied. In leaf cells, the virus particles often form loose aggregates that sometimes fill the nuclei of infected phloem cells. In mungbean, hypertrophied nucleoli, aggregates of virus particles and fibrillar bodies appear in the nuclei of phloem cells as early as two days before the appearance of the symptom. Virus particles are often scattered in distribution but occasionally form aggregates having a paracrystalline or double cylindrical arrangement in the vacuoles of infected sieve elements (Thongmeearkom et al. 1981). It causes yellow-coloured spots scattered on young leaves followed by yellow mosaic pattern. Later, the spots gradually increase in size resulting in complete yellowing of leaves

(Figure 4). The yellow leaves slowly dry and wither. Infected plants bear few flowers and pods with some immature and deformed seeds, thus affecting the yield both qualitatively and quantitatively. Pods of the infected plants are reduced in size and turn yellow in colour. In severe cases, other plant parts become completely yellow (Figure 4). Disease infection decreases the photosynthetic efficiency and as a consequence the yield of the crop is affected (Malathi & John 2008b). The economic impact of MYMV on yield depends upon the time of virus infection and is related to the plant development. Early infection by the virus gives the highest reduction in yield. If the infection occurs after three weeks from planting, then the yield loss surmounts to 100%. However, the losses will be meagre if infestation occurs after eight weeks from planting. Over a broad geographic range, the yield reductions between 10% and 85% have been reported (Grewal JS 1988; Varma et al. 1992; Khattak et al. 2000; Varma & Malathi 2003; Kang et al. 2005).

2.4. Source of inoculum for disease development MYMV disease causes heavy damage when infection occurs in early growth stages in mungbean (Varma & Malathi 2003). Therefore, elimination of the primary sources of inoculums will facilitate disease management. This is particularly so in view of the lack of commercial cultivars with MYMV resistance. Perennial weeds and summer whitefly are potential sources of MYMV during the early growth stages (Malathi & John 2008b; Ilyas et al. 2009; Akthar et al. 2011; Ara et al. 2012). Roles of whitefly and weed reservoirs (alternate hosts) in the epidemiology of MYMV are yet to be critically assessed. The potential for disease control through management of the whitefly will be enhanced by accurate identification of source(s). The increased disease incidence might be attributed to the higher temperatures prevalent during summer season, which was favourable for the whitefly to develop and multiply. The only concern might be that infected tolerant plants could remain as the sources of virus inoculum, as well as promoting the adaptation of the virus to overcome resistance. The agriculturally significant hosts of MYMV include mungbean and urdbean (V. mungo), mothbean (V. aconitifolia), pigeon pea (Cajanus cajan), soybean (Glycine max), cowpea (V. unguiculata) and common bean (Phaseolus vulgaris) (Varma et al. 1992; Usharani et al. 2004; Karthikeyan et al. 2004; Malathi et al. 2005; Qazi et al. 2007). Alternatively, other leguminous hosts may provide a means for the virus and could serve as virus reservoirs. In India, wild V. species, namely, V. hainiana and V. trilobata, have recently been established to be naturally infected with MYMIV (Naimuddin & Aditya 2011). 2.5.

Options for disease management

In general, strategies for controlling MYMV disease include the following: planting resistant or tolerant varieties, insect vector management, managing with alternative


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Figure 4. (Color online) Symptoms exhibited by mungbean plants infected with mungbean yellow mosaic virus: (A) healthy plants in the field, (B) plant showing symptoms in young leaves, (C) yellow mosaic symptom in matured plants with fewer pods, (D) infected pods and (E) MYMD-infected field.

weed or crop hosts of viruses and changing crop cultural practices to those less favourable for disease development.

2.6.

Vector management

Plummeting the whitefly populations (vector) is an effective strategy to administer MYMV disease. At the same time, the management of whiteflies is very complex because whitefly does not go round in ones or twos but they go round in hordes of hundreds and even one attack can severely weaken a plant. They are not well controlled by any of the available management practices such as cultural, mechanical, botanical and chemical. Among the various methods of whitefly management, chemical control is the primary method adopted. Systemic chemical insecticides viz., acetamiprid, ethion, imidachlorpid, triazophos, provide better control of whiteflies; they also kill on contact, but are also taken inside the plant where they go onto protect against further attack for more than a few weeks (Wang et al. 2009). Younger stages are generally more sensitive to insecticides as compared to older stages and higher toxic levels of certain insecticides work well against the first and second instar nymph stages. Nymphs

of whitefly are more susceptible to insecticides; failure in control in crop fields may be due to the incomplete exposure on the underside of leaves (to the insecticides) where nymphs are present. Ghosh (2008) showed that imidacloprid reduced the whitefly populations to significant levels, if the insecticidal treatments are directed on the underside of the leaves, preventing the spread of MYMV and achieved more seed yield. Basal application of botanical insecticides controls the whitefly population in plants. Application of neem seed kernel extract (NSKE) and foliar spray of neem oil had a major impact by preventing the “nymphal” stage from developing into an adult; the nymphs tend to disappear from the treated plants (Dubey et al. 2011). Whitefly management should be achieved when their population is lower through cultural practices. Maintenance of good field sanitation by destroying and removing the crop residues and weeds is an effectual practice against whiteflies. Exclusion of leaves by hands in plants profoundly infested with the non-mobile nymphal and pupal stages may trim down populations to levels that natural enemies can contain. Water sprays (syringing) may also be useful in dislodging adults. Avoiding a lot of nitrogen fertilizer, including manures, is advised as

International Journal of Pest Management 319 succulent growth will amplify whitefly populations. Other methods to control whitefly populations resourcefully without environmental spoil can however be a useful component in the development of sustainable disease control.


2.7.

new isolates of MYMV, the understanding of its molecular mechanism through conventional breeding approaches has become very tricky and time consuming. Under such circumstances, a combination of plant breeding approaches along with the traditional methods becomes obligatory for the development of the resistant lines.

Breeding for resistance

Breeding for resistance to MYMV disease has been known to virologists and plant breeders since 1970. It is largely advocated as the key scheme for the control of MYMV in mungbean. The bringing into play of host resistance is most effectual, easy on the pocket and ecological for managing MYMV. Upon infection, the susceptible (virus readily infects and/or replicates and/or invades) or resistant (virus infection and/or replication and/or invasion is restricted) plant reactions show a range of tolerance or sensitivity. Resistance to MYMV was visualized by symptomatology. Symptomless lines were assumed to be resistant. In a few circumstances, some germplasms of mungbean showed no symptoms even after infection. Hence, these lines could not be used as resistant lines. Screening of germplasm will hopefully reveal the resistance genes. In the absence of a true source of resistance, these lines could be used as tolerant lines. The levels of tolerance among lines vary among the available germplasm and several differences in response have been identified among various germplasm sources. Resistance in mungbean germplasm against MYMV has been recognized earlier by different workers by using a common acceptable scale based on the severity of the disease (Marappa et al. 2003; Peerajade et al. 2004; Khattak et al. 2008; Iqbal et al. 2011; Panduranga et al. 2011). However, it is crucial that the germplasm evaluation considers the diversity among the various strains of the virus too. For breeding resistant cultivars, information on the inheritance and sources of resistance genes is very important. Several resistance sources have been reported for MYMV disease. The inheritance of resistance to MYMV (in the intraspecific as well as in the interspecific crosses) has been reported in mungbean and is conferred by a single recessive gene (Reddy & Singh 1995; Saleem et al. 1998; Reddy 2009), a dominant gene (Sandhu et al. 1985), two recessive genes (Verma & Singh 1988; Ammavasai et al. 2004) and complementary recessive genes (Shukla & Pandya 1985). Commonly, intraspecific hybridization is used for the improvement of resistance to MYMV in mungbean. Resistance to MYMV has also been recognized in the wild species (V. umbellata and V. sublobata) of mungbean and may consent the introduction of such resistance by means of interspecific hybridization (Monika et al. 2001; Bisht et al. 2005; Pandiyan et al. 2008; Sudha et al. 2013a). Through the practices of intraand inter-specific hybridization, several promising lines which are not only tolerance/resistance to MYMV but are also high yielding have been developed and released for commercial cultivation (Reddy & Singh 1995; Saleem et al. 1998). However, this has been attributed to the increased disease infestation and whitefly populations and unstable levels of resistance. Due to the rapid explosion of

2.8.

Marker-assisted selection (MAS)

The development of DNA markers (RFLP, random amplified polymorphic DNA (RAPD) markers, inter simple sequence repeat (ISSR), simple sequence repeat (SSR), single-nucleotide polymorphism (SNP)) has irreversibly changed the disciplines of plant genetics and breeding. While there are several applications of DNA markers in breeding, the most promising for cultivar development is called marker-assisted selection (MAS). Studying the diversity among the germplasms, finding the linked marker for resistant gene and construction of QTL maps through molecular markers, has increased the efficiency in the breeding programmes conferring resistance for MYMV (Sudha et al. 2013a). By determining the allele of a DNA marker, plants that possess particular genes or quantitative trait loci (QTLs) may be identified based on their genotype rather than their phenotype. Different markers are used to study genetic diversity (Chattopadhyay et al. 2005; Roopa et al. 2008; Zhao et al. 2010; Datta et al. 2012; Raturi et al. 2012; Zhong et al. 2012) and tag the MYMV resistance genes in mungbean (Selvi et al. 2006; Chen et al. 2012; Karthikeyan et al. 2012; Dhole & Kanda 2013; Sudha et al. 2013a). MAS, to a great extent, has improved the efficiency of resistance breeding in MYMV and has shown some significant success too. New sources of resistance to MYMV, for example, the use of donors from interspecific sources, have been identified and newer molecular markers linked to resistance genes are becoming more accessible these days (Maiti et al. 2011; Chen et al. 2012). These resistant genotypes will be tested to conclude whether they are able to offer good shield against the major strains of both MYMV and MYMIV in hot spot regions. 2.9. Pathogen-derived resistance Diverse transgenic mechanisms have been developed for engineering virus resistance in crops. In the midst of all of them, pathogen-derived resistance (PDR) is considered as one of the best options offered for crop protection. In the absence of resistance in the commercial mungbean cultivars, researchers have resorted to transgenic resistance utilizing PDR. The concept of PDR, first proposed by Sanford and Johnston 1985, has been successfully utilized over the past 17 years to confer resistance against viruses in many crop plants (Di et al. 1996; Chellappan et al. 2004; Zhang et al. 2013). The expression of viral genes in the host plant and the subsequent disruption of the essential pathogenic processes to confer resistance are referred to as PDR. PDR has been attained, by expressing various forms of functional or dysfunctional viral CP, replicase,


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protease and MP genes inside the host plants. The phenotypes resulting out of PDR-mediated protection exhibit various conspicuous characters such as delayed development of symptoms, reduced symptoms, and virion accumulation to apparent immunity. The variety of PDR phenotypes suggests multiple mechanisms underlying the resistance that is attained. For example, the expression of full-length and truncated REP genes from MYMV isolated in tobacco plants showed an inhibition of viral replication in transgenic tobacco (Shivaprasad et al. 2006). The resistance generated by the use of REP sequences is very tight; a high dosage of input virus can be resisted easily by the transgenic plant. The PDR can also be achieved without the expression of such proteins through mechanism of gene silencing and antisense RNA. In blackgram, DNA-A bidirectional promoter from MYMV has been used in a transient assay to activate PTGS against yellow mosaic virus but the transgenic plant did not show any resistance reaction (Pooggin et al. 2003). Haq et al. (2010) reported that the plants inoculated with infectious MYMIV clones showed 64% infection in mungbean. Those clones contain the complementary-sense gene (ACI) encoding replication initiation protein (Rep) which helps in the development of resistance against MYMIV. At the same time in the plants co-inoculated with the AntiRep construct, the symptom severity as well as the percentage of infection was almost negligible. It was only 20% in mungbean plants. The mungbean co-inoculated with antisense construct showed 44% reduction in infectivity. The symptoms were attenuated and the plants almost appeared healthy. CP deletion (N0 terminal deletion of 75 and 150 amino acids) showed the mutation of MYMIV. It affected the systemic spread and pathogenicity in mungbean (Haq et al. 2011b). The hairpin constructs of CP has 35s promoter (1.3 kb) with the sense sequence of MYMIV (130 bp), followed by an intron (741 bp), after which the antisense (130 bp) target sequence with the OCS terminator (765 bp) are placed and cloned in a cloning vector called Phannibal. The results indicate that coagroinoculation of the CP hairpin construct (Cphp) prevented the viral pathogenesis (Kumari & Malathi 2012). Screening the germplasms using different MYMV isolates through agroinoculation technique is the effective method for assessing the genetic diversity for MYMV resistance in mungbean (Karthikeyan et al. 2011). Recently, Sudha et al. (2013b) screened the mungbean germplasms using two different MYMV isolates. The results show that among the seventy eight mungbean genotypes screened, four genotypes exhibited resistance to the isolates of MYMV. 2.10.

Current status and challenges in managing MYMV The available evidence gathered since the 1960s suggests that the diversity of crop plants and the geographical area affected by the incidence of MYMV disease in mungbean have increased gradually. This can be attributed to an increase in the intensity of farming which requires

sustaining with the increasing population of southern Asia, so particularly in India. MYMV disease is the result of a three-way interaction between the host, the pathogen and the environment (Singh et al. 2004). An epidemic develops only if all the three of these factors are favourable. Therefore, the disease can be controlled by the negative manipulation of one or more of these factors so that conditions become unsuitable for replication, survival or infection by the pathogen. The control of the losses due to MYMV disease requires the amalgamation of methods aiming at preventing or delaying the infection of crop. All the resistance found in mungbean, to date, appears to be only the tolerance against the infection (infection with mild symptoms) rather than complete immunity. Recently, AVRDC released lines NM 92 and NM 94 which are known for their resistance to MYMV. NM 94 shows resistance to the disease during the summer season, but is susceptible during the kharif (JuneJuly sowing) season. Resistance has been attributed to various factors, including increase in disease and whitefly populations, and unstable levels of resistance (Nair et al. 2013). It shows that available strategies have not been enough and they are not able to control the disease and develop resistance: breeding methods are used to understand the different responses of the cultivars under the attack of the pathogen in the field. Knowing the molecular mechanism of virus and developing the resistant lines for every infectious virus strain are some major challenges. Meanwhile, considering the vector management option, reduction of vector populations in the field has been proven to be difficult and is, as yet, seldom used in yellow mosaic virus disease. Besides, control of vectors does not put a selection pressure on the virus to evolve to higher plant virus titre and at the same time increases the density of healthy plants. Thus, vector control has a small risk of failure due to selection for more damaging strains of the virus. In recent times, the use of molecular biotechnological approaches such as MAS and genetic engineering for developing the resistance against MYMV disease has shown greater triumph. However, supplementary research is required on these areas to succeed in MYMD studies. 3. Future research direction The prime goal of classifying the MYMV strains is to carry out a fundamental and applied research so as to dissect its genetic diversity. A universally accepted, uniform set of differentiation for the strains of this virus has not yet been developed anywhere in the world. Due to the non-homogeneous classifications of virus strains, the establishment of breeding programmes for resistance to disease is not well-built, but, instead, has only led to the rise of confusions among the breeders of mungbean. The identification of resistance sources, exchange of resistance information and utilization of the germplasm resources are still indistinct. A uniform differential system is needed for identifying strains so that scientists can exchange information and resistance germ materials based on that standard classification. Additionally, the determination of


International Journal of Pest Management 321 the population structure of the pathogen from a wider geographic area is required in order to develop a database on virus isolates and consequently determine the best strategy for the deployment of resistance and or to incorporate the non-matching resistance genes to the existing pathogen. Genome research is not well developed in mungbean. Although some progress in genome research has been made in mungbean, it is still far behind the other major legume crops such as soybean, cowpea, urdbean and common bean, or even with comparison with one of its relative, but the less economically important, azuki bean. A variety of genomic resources like markers, e.g. RFLPs, RAPDs, AFLPs, SSRs and ISSRs, have been developed to speed up the MAS by discerning the genetic diversity and finding the linked markers for the MYMV resistant gene in mungbean so far; but no map contains enough number of markers to resolve all the 11 linkage groups. Tagging and mapping of genes and QTLs resistant to MYMV use markers of other related legume such as azuki bean, common bean, cowpea and soybean. However, in all such marker programmes, either the markers are not closely linked to the trait (>5 cM), or proper linkage or validation studies were not performed. Therefore, an urgent need to initiate development and validation of tightly linked molecular markers for genes resistant to MYMV has arisen. This could be rapidly transferred to the susceptible mungbean genotypes through MAS. The expressed sequence tags (ESTs) and genomic database of the legumes of related genera or species will be supportive in the development of high throughput markers such as SSRs and SNPs. These resources have the potential to develop a large number of markers especially SSRs and SNPs that would enable to identify the genomic regions (QTL) that underlie resistance to MYMV and on these QTL regions the examination of the reference genome will give the pipeline for identifying the candidate genes responsible for MYMD resistance. Continuous efforts are made in the production of BAC libraries in green gram that would smooth the progress of the research in mapbased cloning of the genes and QTLs resistant to MYMV. Furthermore, development of near-isogenic lines (NILs) is suggested from a self-cross of residual hetero zygote lines (RHLs) derived from recombinant inbred lines (RILs) which is a useful and simple protocol for validating the QTLs. This also facilitated in the isolation of genes identified as QTLs. This is because resistance against the mungbean yellow mosaic disease is difficult to evaluate under reproductive conditions in plants. Furthermore, MYMV disease resistance in mungbean has mainly concentrated on race-specific resistance. This kind of resistance is conferred by genes with major effects and recognized by their characteristic low-infection types. A battery of resistance genes (R genes) are derived from exotic germplasms which are used in this regard. In the exploitation of wild relatives of mungbean, with a balanced population design such as F2 or RILs, the problem is that a large number of negative traits from the donor parent will dominate the overall phenotype of the population, hampering the detection of positive QTLs due to the

poor agronomic performance of the individuals (Anusuya 2009; Sudha 2009). Advanced backcross quantitative trait locus (AB-QTL) is a competent method to utilize wild species by the simultaneous discovery and transfer of valuable QTLs with good agronomic performance from unadapted germplasm into elite breeding lines (Tanksley & Nelson 1996). The efficacy of the AB-QTL approach has been tested in numerous crop species in various diseases and has been proved to be a realistic method in crop breeding (Liu et al. 2004; Naz et al. 2008; Schmalenbach et al. 2008; Manosalva et al. 2009). The application of the AB-QTL strategy in mungbean will identify the source and beneficial alleles, and thus provides a means for quick progress in developing improved virus resistant mungbean lines. However, the development of the transgenic lines resistant to MYMV and their incorporation/merging into the commercial cultivars is a successful approach for the development of the resistant varieties of MYMV in mungbean. The genetically engineering mungbean plants that are resistant to viral pathogens have shown considerable feat, which have paved way for improving the resistance for MYMV in mungbean. The use of viral CP as a transgene, exploitation of agroinoculation to screen the germplasms using artificial isolates of MYMV and engineering the disease resistance using RNAi are successful strategies for producing disease-resistant plants but even more research is vital in these areas. At last, we imply that the development of resistance to MYMV is compulsory for the flourishing production of mungbean. The early attempts to control MYMD by conventional methods have progressed only in field studies with a very little success. Even later, it was unsuccessful in developing a resistant variety due to rapid explosion of new isolates of MYMV and also due to the complex mechanism that controls the resistance reaction of MYMV. Advances in plant molecular genetics now provide accurate gene detection (R gene) for resistant lines and has a great promise to assist plant breeders in understanding the molecular mechanisms of the plant viruses. Recently, it shows some success in the research groups involved in MYMV and hence doing extensive research on these areas with wide application of these technologies by the side of conventional methods will be certainly powerful and promising for the development of resistance reaction against the virus.

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