Mungbean yellow mosaic virus (MYMV): a threat to green gram ( Vigna radiata ) production in Asia
Post on 14-May-2023
0 Views
Preview:
Transcript
This article was downloaded by: [A. Karthikeyan]On: 02 January 2015, At: 04:28Publisher: Taylor & FrancisInforma Ltd Registered in England and Wales Registered Number: 1072954 Registered office: MortimerHouse, 37-41 Mortimer Street, London W1T 3JH, UK
Click for updates
International Journal of Pest ManagementPublication details, including instructions for authors and subscription information:http://www.tandfonline.com/loi/ttpm20
Mungbean yellow mosaic virus (MYMV): a threat togreen gram (Vigna radiata) production in AsiaA. Karthikeyana, V.G. Shobhanaa, M. Sudhaa, M. Raveendrana, N. Senthila, M. Pandiyanb &P. Nagarajana
a Department of Plant Molecular Biology & Biotechnology, Centre for Plant MolecularBiology, Tamil Nadu Agricultural University, Coimbatore, Indiab National Pulse Research Centre, Tamil Nadu Agricultural University Vamban,Pudukkottai, IndiaPublished online: 26 Nov 2014.
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, InternationalJournal 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
PLEASE SCROLL DOWN FOR ARTICLE
Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) containedin the publications on our platform. However, Taylor & Francis, our agents, and our licensors make norepresentations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose ofthe Content. Any opinions and views expressed in this publication are the opinions and views of the authors,and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be reliedupon and should be independently verified with primary sources of information. Taylor and Francis shallnot be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and otherliabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to orarising out of the use of the Content.
This article may be used for research, teaching, and private study purposes. Any substantial or systematicreproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in anyform to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http://www.tandfonline.com/page/terms-and-conditions
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
aDepartment 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
(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 renownedin India for more than five decades. It is caused by a group of geminiviruses belonging to the genus, begomovirus of thefamily, Geminiviridae. They are transmitted through whitefly in a persistent manner. The economic losses due to this virusaccount up to 85% in green gram which is spreading faster towards newer areas. The escalating economic importance ofMYMV has resulted in the call for accurate detection and identification procedures that inspire rigorous research effortsfocussing 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 commerciallyoffered genotypes are only partially resistant. Therefore, the hunt for newer sources of disease resistance needs to beintensified. This review updates all the accessible information on MYMV and outlines the areas in which advance researchis 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 Indo-
Burmese 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 pro-
duction (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 work-
ing on mungbean for the past four decades. Prior to incep-
tion of AVRDC, national partners in mungbean producing
countries released more than 100 improved mungbean
cultivars for yield and resistance against pests and dis-
eases 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 mung-
bean 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 flour-
ishing production of mungbean in India, Sri Lanka, Paki-
stan, 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 vein-
lets 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 imple-
mented for MYMV disease and so far, no complete resis-
tance 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: karthik2373@gmail.comyAuthors A. Karthikeyan, V.G. Shobhana and M. Sudha contributed equally on this work.
� 2014 Taylor & Francis
International Journal of Pest Management, 2014
Vol. 60, No. 4, 314�324, http://dx.doi.org/10.1080/09670874.2014.982230
Dow
nloa
ded
by [
A. K
arth
ikey
an]
at 0
4:28
02
Janu
ary
2015
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 mid-
dle of 1950, it was noted that the experimental host range
of yellow mosaic disease (YMD) included numerous vari-
eties 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 coun-
tries 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 distri-
bution 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. Muruge-
san 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 pro-
duction. 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). There-
fore, 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
Figure 1. Distribution of mungbean yellow mosaic disease (MYMD) in Asia.
International Journal of Pest Management 315
Dow
nloa
ded
by [
A. K
arth
ikey
an]
at 0
4:28
02
Janu
ary
2015
of MYMV were mapped using different mungbean popu-
lations (Shanmugasundaram 1996). These genes will be
the first targets of marker-assisted breeding with random
fragment length polymorphism (RFLP) markers. In north-
ern 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 occur-
rence of mungbean yellow mosaic disease, improvement
in production and productivity of mungbean is becoming
tricky and the disease is a major problem in Asian coun-
tries (Varma & Malathi 2003). Most of the reported resis-
tance 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 rec-
ognized 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 bipar-
tite (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 com-
plete 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 sub-
continent. Among the two, MYMV was studied extensively
and was reported from Thailand. The northern, central and
eastern regions of India are dominated by MYMIV infesta-
tions (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
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 compo-
nents 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 associ-
ated protein (Rep; a rolling-circle replication-initiator pro-
tein) 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 silenc-
ing (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 polypha-
gous pest Bemisia tabaci (Figure 3) in a persistent (circu-
lative) 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 2. (Color online) Genome organization of bipartitebegomovirus � DNA-A and DNA-B.
Figure 3. (Color online) Polyphagous vector � whitefly(Bemisa tabaci).
316 A. Karthikeyan et al.
Dow
nloa
ded
by [
A. K
arth
ikey
an]
at 0
4:28
02
Janu
ary
2015
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, respec-
tively. Thus, the female adults are three times more effi-
cient 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 influ-
ence the vector population. Whitefly is found to be high
during summer season compared to spring and rainy sea-
sons. 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 20�30 days old
leading to higher disease incidence (on the 45th day).
Spring and rainy seasons attribute to unfavourable condi-
tions 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 signifi-
cant 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 pH�7.8. There-
after no one reported any infestation caused by mechani-
cal 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 dis-
ease 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 differ-
ent level of stability or virulence, as reflected by the sever-
ity 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 occa-
sionally form aggregates having a paracrystalline or dou-
ble 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 epide-
miology 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 attrib-
uted 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 tol-
erant plants could remain as the sources of virus inocu-
lum, 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 legumi-
nous 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 varie-
ties, insect vector management, managing with alternative
International Journal of Pest Management 317
Dow
nloa
ded
by [
A. K
arth
ikey
an]
at 0
4:28
02
Janu
ary
2015
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 effec-
tive 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 cul-
tural, mechanical, botanical and chemical. Among the
various methods of whitefly management, chemical con-
trol is the primary method adopted. Systemic chemical
insecticides viz., acetamiprid, ethion, imidachlorpid, tria-
zophos, 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 expo-
sure on the underside of leaves (to the insecticides) where
nymphs are present. Ghosh (2008) showed that imidaclo-
prid 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 prac-
tice 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
Figure 4. (Color online) Symptoms exhibited by mungbean plants infected with mungbean yellow mosaic virus: (A) healthy plants inthe field, (B) plant showing symptoms in young leaves, (C) yellow mosaic symptom in matured plants with fewer pods, (D) infectedpods and (E) MYMD-infected field.
318 A. Karthikeyan et al.
Dow
nloa
ded
by [
A. K
arth
ikey
an]
at 0
4:28
02
Janu
ary
2015
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. 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 man-
aging MYMV. Upon infection, the susceptible (virus read-
ily 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 sen-
sitivity. Resistance to MYMV was visualized by symptom-
atology. 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 dif-
ferences 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; Pandur-
anga 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, informa-
tion 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 interspe-
cific crosses) has been reported in mungbean and is con-
ferred 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. sublo-
bata) 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 intra-
and 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
new isolates of MYMV, the understanding of its molecular
mechanism through conventional breeding approaches has
become very tricky and time consuming. Under such cir-
cumstances, a combination of plant breeding approaches
along with the traditional methods becomes obligatory for
the development of the resistant lines.
2.8. Marker-assisted selection (MAS)
The development of DNA markers (RFLP, random ampli-
fied 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 (Chattopad-
hyay 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 suc-
cess too. New sources of resistance to MYMV, for exam-
ple, 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 geno-
types 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 culti-
vars, 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 essen-
tial 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,
International Journal of Pest Management 319
Dow
nloa
ded
by [
A. K
arth
ikey
an]
at 0
4:28
02
Janu
ary
2015
protease and MP genes inside the host plants. The pheno-
types resulting out of PDR-mediated protection exhibit
various conspicuous characters such as delayed develop-
ment of symptoms, reduced symptoms, and virion accu-
mulation 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 iso-
lated in tobacco plants showed an inhibition of viral repli-
cation 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 eas-
ily by the transgenic plant. The PDR can also be achieved
without the expression of such proteins through mecha-
nism 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 Anti-
Rep construct, the symptom severity as well as the per-
centage of infection was almost negligible. It was only
20% in mungbean plants. The mungbean co-inoculated
with antisense construct showed 44% reduction in infec-
tivity. The symptoms were attenuated and the plants
almost appeared healthy. CP deletion (N0 terminal dele-
tion of 75 and 150 amino acids) showed the mutation of
MYMIV. It affected the systemic spread and pathogenic-
ity 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 clon-
ing vector called Phannibal. The results indicate that co-
agroinoculation of the CP hairpin construct (Cphp) pre-
vented 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 favour-
able. Therefore, the disease can be controlled by the nega-
tive 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 (June�July 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 resis-
tance: breeding methods are used to understand the differ-
ent 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 infec-
tious virus strain are some major challenges. Meanwhile,
considering the vector management option, reduction of
vector populations in the field has been proven to be diffi-
cult and is, as yet, seldom used in yellow mosaic virus dis-
ease. 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 dis-
sect 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
320 A. Karthikeyan et al.
Dow
nloa
ded
by [
A. K
arth
ikey
an]
at 0
4:28
02
Janu
ary
2015
the population structure of the pathogen from a wider geo-
graphic area is required in order to develop a database on
virus isolates and consequently determine the best strat-
egy for the deployment of resistance and or to incorporate
the non-matching resistance genes to the existing patho-
gen. 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 com-
mon bean, or even with comparison with one of its rela-
tive, 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 map-
based 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 validat-
ing 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 bal-
anced 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 popula-
tion, 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 dis-
eases 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 mung-
bean. 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 trans-
gene, exploitation of agroinoculation to screen the germ-
plasms 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 suc-
cess. Even later, it was unsuccessful in developing a resis-
tant variety due to rapid explosion of new isolates of
MYMV and also due to the complex mechanism that con-
trols 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 conven-
tional methods will be certainly powerful and promising
for the development of resistance reaction against the
virus.
Reference
Ahmad M. 1975. Screening of mungbean (Vigna radiata) andurdbean (V. mungo) for germplasms resistance to yellowmosaic virus. J Agric Res. 13:349�354.
Akthar KP, Ghulam S, Abbas G, Muhammad JA, Nighat Sarwar,Tariq M. Shah. 2011. Screening of mungbean germplasmagainst mungbean yellow mosaic India virus and its vectorBemisia tabaci. Crop Prot. 30(9):1202�1209.
Ammavasai S, Phogat DS, Solanki IS. 2004. Inheritance of resis-tance to mungbean yellow mosaic virus (MYMV) in greengram (Vigna radiata L. Wilczek). Indian J Genet.64:145�146.
Anusuya. 2009. Marker assisted selection for yellow mosaicvirus (MYMV) in mungbean [Vigna radiata (L.) Wilczek]
International Journal of Pest Management 321
Dow
nloa
ded
by [
A. K
arth
ikey
an]
at 0
4:28
02
Janu
ary
2015
[unpublished MSc thesis]. Coimbatore: Tamil Nadu Agricul-tural University Library.
Ara MR, Masud MM, Akanda AM. 2012. Detection of plantviruses in some ornamental plants that act as alternate hosts.The Agriculturists. 10(2):46�54.
Bisht IS, Bhat KV, Lakhanpaul S, Latha M, Jayan, Biswas BK,Singh AK. 2005. Diversity and genetic resources of wildVigna species in India. Genet Resour Crop Evol. 52:53�68.
Borah, BK, Dasgupta I. 2012. Begomovirus research in India: acritical appraisal. Bioscience. 37(4):791�806.
Capoor SP, Varma PM. 1948. Yellow mosaic of Phaseolus luna-tus L. Curr Sci. 17:152�153.
Capoor SP, Varma PM. 1950. A new virus disease of Dolichoslablab. Curr Sci. 19:248�249.
Chattopadhyay K, Ali M. Nasim, Sarkar HK, Mandai N, Bhatta-charyya S. 2005. Diversity analysis by RAPD and ISSRmarkers among the selected mungbean [Vigna radiata (L.)Wilczek] genotypes. Indian J Genet Plant Breed. 65(3):173�175.
Chellappan P, Masona MV, Vanitharani R, Taylor NJ, FauquetCM. 2004. Broad spectrum resistance to ssDNA virusesassociated with transgene-induced gene silencing in cassava.Plant Mol Biol. 56:601�611.
Chen HM, Ku HM, Schafleitner R, Bains TS, Kuo GS, Liu CA,Nair RM. 2012. The major quantitative trait locus for Mung-bean yellow mosaic Indian virus resistance is tightly linkedin repulsion phase to the major bruchid resistance locus in across between mungbean [Vigna radiata (L.) Wilczek] andits wild relative Vigna radiata ssp. sublobata. Euphytica.192(2):205�216.
Chenulu VV, Verma A. 1988. Virus and virus-like diseases ofpulse crops commonly grown in India. In: Baldev, B, Rama-junam, S, Jain, HK, editors. Pulse crops. New Delhi: Oxfordand IBH; p. 338�370.
Choudhury NC, Malik PS, Singh DK, Islam MN, Kaliappan K,Mukherjee SK. 2006. The oligomeric Rep protein of mung-bean yellow mosaic India virus (MYMIV) is a likely replica-tive helicase. Nucleic Acids Res. 34:6362�6377.
Datta S, Sarika Gangwar, Kumar Shiv, Gupta Sanjeev, Rai Rita,Kaashyap Mayank, Singh Pallavi, Nadarajan Nagaswamy.2012. Genetic diversity in selected Indian mungbean [Vignaradiata (L.) Wilczek] cultivars using RAPD markers. Am JPlant Sci. 3:1085�1091.
Dhole VJ, Kanda Reddy. 2013. Development of a SCAR markerlinked with a MYMV resistance gene in mungbean (Vignaradiata L. Wilczek). Plant Breed. 132(1):127�132.
Di R, Purcell V, Collins GB, Ghabrial SA. 1996. Production oftransgenic soybean lines expressing the bean pod mottle viruscoat protein precursor gene. Plant Cell Rep. 15:746�750.
Dubey NK, Shukla R, Kumar A, Singh P, Prakash B. 2011.Global scenario on the application of natural products inintegrated pest management programmes. In: Dubey NK,editor. Natural products in plant pest management, Vol. 1.Wallingford: CAB International; p. 1�20.
Ghosh A. 2008. Management of yellow mosaic virus by chemi-cal control of its vector, Whitefly (Bemisia tabaci) and itsimpact on performance of green gram (Phaseolus aureus)under rainfed lowland rice fallow. Arch Phytopathol PlantProt. 41(1):75�78.
Girish KR, Usha R. 2005. Molecular characterization of two soy-bean-infecting begomoviruses from India and evidence forrecombination among legume-infecting begomovirusesfrom South-East Asia. Virus Res. 108:167�176.
Grewal JS. 1988. Diseases of pulse crops � an overview. IndianPhytopathol. 41(1):1�14.
Haq QMI, Arif A, Malathi VG. 2010. Engineering resistanceagainst mungbean yellow mosaic India virus using antisenseRNA. Indian J Virol. 21:82�85.
Haq, QMI. Arif A, Malathi VG. 2011a. Infectivity analysis of ablackgram isolate of mungbean yellow mosaic virus and
genetic assortment with MYMIV in selective hosts. VirusGenes. 42(3):429�439.
Haq QMI, Jyothsna P, Arif A, Malathi. VG. 2011b. Coat proteindeletion mutation of mungbean yellow mosaic India virus(MYMIV). J Plant Biochem Biotechnol. 20(2):182�189.
Honda Y, Iwaki M, Saito Y. 1983. Mechanical transmission,purification and some properties of whitefly-borne mung-bean yellow mosaic virus in Thailand. Plant Dis.67:801�804.
Ilyas M, Qazi J, Mansoor S, Briddon RW. 2009. Molecular char-acterization and infectivity of a “Legumovirus” (genusBegomovirus: family Geminiviridae) infecting the legumi-nous weed Rhynchosia minima in Pakistan. Virus Res.145:279�284.
Ilyas M, Qazi J, Mansoor S, Briddon RW. 2010. Genetic diver-sity and phylogeography of begomoviruses infectinglegumes in Pakistan. J Gen Virol. 91:2091�2101.
Iqbal U, Iqbal MS et al. 2011. Screening of mungbean germ-plasm against mungbean yellow mosaic virus (MYMV)under field conditions. Pakistan J Phytopathol. 23(1):48�51.
Jalaluddin M, Shaikh MAQ. 1981. Evaluation of Mungbean(Vigana radiata L.) germplasm for resistance to mungbeanyellow mosaic virus. SABRAOJ. 13:61�68.
Jeske H. 2009. Geminiviruses. Curr Top Microbiol Immunol.331:185�226.
John P. Sivalingam PN, Haq QMI, Kumar N, Mishra A, Brid-don RW, Malathi VG. 2008. Cowpea golden mosaic dis-ease in Gujarat is caused by a mungbean yellow mosaicIndia virus isolate with a DNA B variant. Arch Virol.153:1359�1365.
Jones DR. 2003. Plant viruses transmitted by whiteflies. Eur JPlant Pathol. 109:195�219.
Kang BC, Yeam I, Jahn MM. 2005. Genetics of plant virus resis-tance. Annu Rev Phytopathol. 43:581�621.
Karthikeyan A, Sudha M, Pandiyan M, Senthil N, Shobhana VG,Nagarajan P. 2011. Screening of MYMV resistant mungbean(Vigna radiata (L) Wilczek) progenies through agroinocula-tion. Int J Plant Pathol. 2(3):115�125.
Karthikeyan A, Sudha M, Senthil N, Pandiyan M, RaveendranM, Nagarajan P. 2012. Screening and identification ofRAPD markers linked to MYMV resistance in mungbean(Vigna radiata (L) Wilczek). ArchPhytopathol Plant Prot.45:712�716.
Karthikeyan AS, Vanitharani R, Balaji V, Anuradha S, Thillai-chidambaram P, Shivaprasad PV, Parameswari C, Balaman,V, Saminathan M, Veluthambi K. 2004. Analysis of an iso-late of mungbean yellow mosaic virus (MYMV) with ahighly variable DNA B component. Arch Virol.149:1643�1652.
Khattak GSS, Haq MA, Ashraf M, Elahi T. 2000. Genetic ofmungbean yellow mosaic virus (MYMV) in mungbean(Vigna radiata L. Wilczek). J Genet Breed. 54:237�243.
Khattak GSS, Saeed I, Shah SA. 2008. Breeding high yieldingand disease resistant mungbean {Vigna radiata (L.) Wilc-zek} genotypes. Pakistan J Bot. 40:1411�1417.
Kumari A, Malathi VG. 2012. RNAi-Mediated strategy todevelop transgenic resistance in grain legumes targeting themungbean yellow mosaic India virus coat protein gene. In:Proceedings of the International Conference on Plant Bio-technology for Food Security: New Frontiers; 21�24 Feb2012; New Delhi, India.
Lambrides CJ, Diatloff AL, Liu CJ, Imrie BC. 1999. Proceedingsof the 11th Australasian Plant Breeding Conference; 19�23Apr 1999; Adelaide, Australia.
Liu B, Zhang S, Zhu X, Yang Q, Wu S, Mei M, Mauleon R,Leach J, Mew T, Leung H. 2004. Candidate defense genesas predictors of quantitative blast resistance in rice. MPMI.17(10):1146�1152.
Maiti S, Basak J, Kundagrami S, Kundu A, Pal A. 2011. Molecu-lar marker-assisted genotyping of mungbean yellow mosaic
322 A. Karthikeyan et al.
Dow
nloa
ded
by [
A. K
arth
ikey
an]
at 0
4:28
02
Janu
ary
2015
India virus resistant germplasms of mungbean and urdbean.Mol Biotechnol. 47:95�104.
Malathi VG, John P. 2008a. Geminiviruses infecting legumes.In: Govind P, Rao P, Kumar P Lava, Holguin-Pena RJ, edi-tors. Characterization, diagnosis & management of plantviruses. Houston, TX: Stadium Press LLC; p. 97�123.
Malathi VG, John P. 2008b. Mungbean yellow mosaic viruses.In: Mahy BWJ, Van Regenmortel MHV, editors. Desk ency-clopedia of plant and fungal virology in encyclopedia ofvirology, Vol. 8. Amsterdam: Elsevier; p. 364�371.
Malathi VG, Surendranath B, Naghma A, Roy A. 2005. Adapta-tion to new hosts shown by the cloned components of mung-bean yellow mosaic India virus causing cowpea goldenmosaic in northern India. Can J Plant Pathol. 27:439�447.
Mansoor S, Briddon RW, Zafar Y, Stanley J. 2003. Geminivirusdisease complexes: an emerging threat. Trends Plant Sci.8:128�134.
Manosalva PM, Davidson RM, Liu B, Zhu X, Hulbert SH,Leung H, Leach JE. 2009. A germin-like protein gene familyfunctions as a complex quantitative trait locus conferringbroad-spectrum disease resistance in rice. Plant Physiol.149:286�296.
Marappa N, Savithramma DL, Nagaraju, Prameela, HA, Krish-namurthy RA. 2003. Evaluation of mungbean genotypesagainst powdery mildew, yellow mosaic virus and bacterialblight diseases at Bangalore. In: Annual Meeting and Sym-posium on Recent Developments in the Diagnosis and Man-agement of Plant Diseases for Meeting Global Challenges;18�20 Dec 2003; Dharwad: University of Agricultural Sci-ences; p. 31.
Monika KP, Singh, Sareen PK. 2001. Cytogenetics studies inmungbean-rice bean Hybrids. J Cytol Genet. 2:13�16.
Morinaga TM, Ikegami, Miura K. 1993. The nucleotidesequence and genome structure of mungbean yellow mosaicgeminivirus. Microbiol Immunol. 37:471�476.
Murugesan S, Chelliah S. 1977. Influence of sowing time on theincidence of the vector Bemisia tabaci (Genn.) and theyellow mosaic disease of greengram. Madras Agric J.64(2):128�130.
Naimuddin Mohd. Akram, Aditya P. 2011. First report of naturalinfection of mungbean yellow mosaic India virus in twowild species of Vigna. New Dis Rep. 23:21�22.
Nair RM, Schafleitner R, Kenyon L, Srinivasanw R Easdown,Ebertand AW, Hanson P. 2013. Genetic improvement ofmungbean, SABRAO. J Breed Genet. 44(2):177�190.
Nariani TK. 1960. Yellow mosaic of mung (Phaseolus aureus).Indian Phytopathol. 13:24�29.
Nath PD. 1994. Effect of sowing time on the incidence of yellowmosaic virus disease and whitefly population on greengram.Ann Agric Res. 15(2):174�17.
Naz AA, Kunert A, Lind V, Pillen K, L�eon J. 2008. AB-QTLanalysis in winter wheat: II. Genetic analysis of seedling andfield resistance against leaf rust in a wheat advanced back-cross population. Theor Appl Genet. 116:1095�1104.
Nene YL. 1968. A survey of the viral disease of pulses crops inUttar Pradesh, India. In: First Annual Report, FG-In-358.Pantnagar: UP Agricultural University.
Pandiyan M, Ramamoorthi N, Ganesh SK, Jebaraj S, NagarajanP, Balasubramanian P. 2008. Broadening the genetic baseand introgression of MYMV resistance and yield improve-ment through unexplored genes from wild relatives in mung-bean. Plant Mutation Rep. 2:33�43.
Panduranga GS, Vijayalakshmi K, Reddy K, Loka, RajashekaraH. 2011. Evaluation of mungbean germplasm for resistanceagainst whitefly (Bemisia Tabaci Genn.) and mungbean yel-low mosaic virus (MYMV) disease. Indian J Entomol. 73(4):338�342.
Peerajade DA, Ravikumar RL, Rao MSL. 2004. Screeningof local mungbean collections for powdery mildew and
yellow mosaic virus resistance. Indian J Pulses Res.17(2):190�191.
Pooggin M, Shivaprasad PV, Veluthambi K, Hohn T. 2003.RNAi targeting of a DNA virus in plants. Nat Biotechnol.21:131�132.
Qazi J, Ilyas M, Mansoor S, Briddon RW. 2007. Legume yellowmosaic virus genetically isolated begomoviruses. Mol PlantPathol. 8:343�348.
Raghavan V, Malik PS, Choudhury NR, Mukherjee SK. 2004.The DNA-A component of a plant geminivirus (Indianmung bean yellow mosaic virus) replicates in budding cells.J Virol. 78:2405�2413.
Raturi A, Singh SK, Sharma V, Pathak R. 2012. Molecular char-acterization of Vigna radiata (L.) Wilczek genotypes basedon nuclear ribosomal DNA and RAPD polymorphism. MolBiol Rep. 39(3):2455�2465.
Reddy KS. 2009. A new mutant for yellow mosaic virus resis-tance in mungbean (Vigna radiata L. Wilczek) varietySML-668 by recurrent Gamma-ray irradiation. In: Shu QY,editor. Induced plant mutation in the genomics Era,361�362. Rome: Food and Agriculture Organization of theUnited Nations.
Reddy KR, Singh DP. 1995. Inheritance of resistance to mung-bean yellow mosaic virus. Madras Agric J. 88:199�201.
Roopa LG, Srivastava J, Shirish A Ranade. 2008. Molecularassessment of genetic diversity in mung bean germplasm.J Genet. 87(1):65�74.
Saleem, M., Haris WAA, Malik A. 1998. Inheritance of yellowmosaic virus in mungbean (Vigna radiata L. Wilczek). Paki-stan J Phytopathol. 10:30�32.
Sandhu TS, Brar JS, Sandhu SS, Verma MM. 1985. Inheritanceof resistance to mungbean yellow mosaic virus in green-gram. J Res Punjab Agric Univ. 22:607�611.
Sanford JC, Johnston SA. 1985. The concept of parasite-derivedresistance: Deriving resistance genes from the parasite’sown genome. J Theor Biol. 113:395�405.
Schmalenbach I, Korber N, Pillen K. 2008. Selecting a set ofwild barley introgression lines and verification of QTLeffects for resistance to powdery mildew and leaf rust. TheorAppl Genet. 117:1093�1106.
Selvi R, Muthiah AR, Manivannan N, Manickam A. 2006.Tagging of RAPD marker for MYMV resistance inmungbean (Vigna radiata (L.) Wilczek). Asian J Plant Sci.5(2):277�280.
Shanmugasundaram. 1996. Mungbean varietal improvements.Tainan: Asian Vegetable Research and Development Center;p. 53�54.
Shivanathan. 1977. Tropical Agriculture Research Series No. 10;Japan: Tropical Agriculture Research Center; p. 65�68.
Shivaprasad PV, Akbergenov R, Trinks D, Rajeswaran R, Velu-thambi K, Hohn T, Pooggin MM. 2005. Promoters, tran-scripts, and regulatory proteins of mungbean yellow mosaicgeminivirus. J Virol. 79:8149�8163.
Shivaprasad P, Thillaichidambaram P, Balaji V, Veluthambi K.2006. Expression of full length and truncated Repgenes from mungbean yellow mosaic virus-Vigna inhibits viralreplication in transgenic tobacco. Virus Genes. 33:365�375.
Shukla GP, Pandya BP. 1985. Resistance to yellow mosaic ingreengram. SABRAO J. 17:165�171.
Singh BB. 2011. Project coordinators report. All India Coordi-nated Research Project on MULLaRP. Annual Group Meet;11�13 May 2011; Kanpur: Indian Council of AgriculturalResearch, Indian Institute of Pulses Research.
Singh D, Patel PN. 1977. Studies on resistance in crops to bacte-rial diseases in India, Part VIII. Investigations on inheritanceof reactions to bacterial leaf spot and yellow mosaic diseasesand linkage, if any, with other characters in mungbean.Indian Phytopathol. 30:202�206.
International Journal of Pest Management 323
Dow
nloa
ded
by [
A. K
arth
ikey
an]
at 0
4:28
02
Janu
ary
2015
Singh G, Sharma YR, Shanmugasundaram S, Shih SL, GreenSK. 2004. Status of mungbean yellow mosaic virus resis-tance breeding. Proceedings of the Final Workshop andPlanning Meeting on Mungbean. Punjab Agricultural uni-versity; p. 204�213.
Somta P, Sommanas W, Srinives P. 2009. Molecular diversityassessment of AVRDC-The World Vegetable Center elite-parental mungbeans. Breed Sci. 59:149�157.
Sudha. 2009. An investigation on mungbean yellow mosaic virus(MYMV) resistance in mungbean [Vigna radiata (l.) wilc-zek] and ricebean [Vigna umbellata (thunb.) Ohwi and Oha-shi] interspecific crosses [unpublished PhD thesis].Coimbatore: Tamil Nadu Agricultural University.
Sudha M, Anusuya P, Ganesh NM, Karthikeyan A, Nagarajan P,Raveendran M, Senthil N, Pandiyan M, Angappan K, Bala-subramanian P. 2013a. Molecular studies on mungbean[Vigna radiata (L.) Wilczek] and ricebean [Vigna umbellata(Thunb.)] Interspecific hybridization for Mungbean yellowmosaic virus resistance and development of species specificSCAR marker for ricebean. Arch Phytopathol Plant Prot. 46(5):503�517.
Sudha M, Karthikeyan A, Nagarajan P, Raveendran M, SenthilN, Pandiyan M, Angappan K, Ramalingam J, Bharathi M,Rabindran R, Veluthambi K, Balasubramanian P. 2013b.Screening of mungbean (Vigna radiata) germplasm forresistance to mungbean yellow mosaic virus using agroino-culation. Can J Plant Pathol. 46(8):717�723.
Tanksley SD, Nelson JC. 1996. Advanced backcross QTL analy-sis: a method for the simultaneous discovery and transfer ofvaluable QTLs from unadapted germplasm into elite breed-ing lines. Theor Appl Genet. 92:191�203.
Thongmeearkom P, Honda Y, Saito Y, Syamananda R. 1981.Nuclear ultra structural changes and aggregates of virus likeparticles in mungbean cells affected by mungbean yellowmosaic disease. Phytopathology. 71:41�44.
Usharani KS, Surendranath B, Haq QMR, Malathi VG. 2004.Yellow mosaic virus infecting soybean in Northern India isdistinct from the species infecting soybean in southern andwestern India. Curr Sci. 86:845�850.
Varma A, Dhar AK, Mandal B. 1992. MYMV transmission andcontrol in India. In: Green SK, Kim D, editors. Mungbeanyellow mosaic disease. Taipei: Asian Vegetable Researchand Development Centre; p. 8�27.
Varma A, Malathi VG. 2003. Emerging geminivirus problems: aserious threat to crop production. Ann Appl Biol.142:145�164.
Verma RPS, Singh DP. 1988. Inheritance of resistance to mung-bean yellow mosaic virus in greengram. Ann Agric Res.9:98�100.
Wang ZY, Yao MD, Wu YD. 2009. Cross-resistance, inheritanceand biochemical mechanisms of imidacloprid resistance inB-biotype Bemisia tabaci. Pest Manag Sci. 65:1189�1194.
Zhang C, Whitham SA, Hill JH. 2013. Virus-induced genesilencing in soybean and common bean. Methods Mol Biol.975:149�156.
Zhao D, Cheng XZ, Wang LX, Wang SH, Ma YL. 2010. Integra-tion of mungbean (Vigna radiata) genetic linkage map. ActaAgron Sinica. 36(6):932�939.
Zhong Min, Cheng Xu-Zhen, Wang Li-Xia, Wang Su-Hua,Wang Xiao-Bao. 2012. Transferability of mungbean geno-mic-SSR markers in other Vigna species. Acta Agron Sinica.38(2):223�230.
324 A. Karthikeyan et al.
Dow
nloa
ded
by [
A. K
arth
ikey
an]
at 0
4:28
02
Janu
ary
2015
top related