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1
Associations between Glucosinolates, White Rust and Plant Defence
Activators in Brassica Plants: A Review.
DOI:10.1080/19315260.2013.832465
Astha Singh*, David Guest & Les Copeland
Publishing models and article dates explained
Accepted author version posted online: 18 Mar 2014, Published online: 18 Mar 2014
Astha Singh, David Guest and Les Copeland
Faculty of Agriculture and Environment, University of Sydney, 2006, Sydney, Australia
Address correspondence to: A. Singh at the above address. E-mail:
astha.singh@sydney.edu.au
Glucosinolates are key metabolites in Brassica plants and known for their anti-cancerous and
antimicrobial properties. Biotic stress in plants causes changes in metabolite biosynthesis.
Various biosynthetic pathways are also triggered in chemical treated plants. The influence of
hydrolysed glucosinolates and defence activator applications on the plant's ability to
withstand disease infection and the influence of disease on glucosinolate hydrolysis has been
examined. Potential effects of white rust disease caused by Albugo candida (Pers. Kuntze) on
glucosinolates and their interactions are reviewed here. Effects of external plant defence
activators Bion® and phosphonate on glucosinolate metabolism in Brassica plants infected
with Albugo candida has also been reviewed.
Plants synthesize thousands of secondary metabolites, many of which have plant defensive
properties. Some of these, toxins and chemical feeding deterrents, are effective against a wide
range of herbivores and pathogens (Kim and Jander, 2007; Wink, 1988). Glucosinolates are
secondary metabolites found in the Brassicaceae that can be hydrolysed by the enzyme
myrosinase to produce isothiocyanates following injury or infection (Eylen et al., 2009). The
role of glucosinolates in plants is participation in plant defences (Denance et al., 2013;
Kusnierczyk et al., 2008), and as attractant signals for some herbivorous insects (Sun et al.,
2009). Glucosinolates may contribute as functional foods because they have anticancerous
activity (Hong and Kim, 2008; Munday and Munday, 2004). More than 120 types of
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glucosinolates have been described in different Brassica plant parts (Fahey et al., 2001a) and
their concentrations have been studied in various crops (Antonious et al., 2009; Jones et al.,
2006). Brassicaceae has worldwide importance as it includes vegetables, oilseeds and herbs
(Chapman, 2007; Facciolo, 1998; Winkler and Turrel, 2009).
White rust, caused by the Oomycete Albugo candida (Pers.) Kuntze, is an important
disease of Brassica crops (Goyal et al., 1996; Kharbanda and Tewari, 1996; Kole et al.,
1996). White rust is common on broccoli (Brassica oleracea L.), rocket (Eruca sativa Mill.)
and Indian mustard (Brassica. juncea L. Czern); and other vegetable and oilseed crops (Kaur
et al., 2008; Petkowski et al., 2010; Scheck and Koike, 1999).
Research has been carried out on beneficial glucosinolates associated with human
health (Halkier and Gershenzon, 2006). Increased knowledge of improved nutrition has
prompted awareness of balanced diets and dietary supplements. There are dietary components
that provide balanced nutrition and components that provide health benefits beyond basic
dietary requirements. Examples of functional food components are the carotenoids, ß-
carotene, lutein and lycopene; dietary fibers - ß-glucan; and isothiocyanates, and derivatives
such as sulphoraphane which are found in Brassica crops (Faulkner et al., 1998; Rodrigues
and Rosa, 1999; Williams et al., 2008). Glucosinolates break down within the human
digestive system in form of plant myrosinase in the small intestine or bacterial myrosinase in
the colon (Kristensen et al., 2007). Isothiocyanates are subsequently absorbed at sites of
breakdown and metabolites are detectable in human urine approximately 2-3 hrs after
consumption of food containing these compounds (Johnson, 2002).
Variation in glucosinolate content was found in broccoli infected with A. candida and
Bion® and phosphonate application. Maximum accumulation of aliphatic glucosinolates was
found after 30 days post-infection (Singh, 2011). Oomycete diseases are controlled by
phosphonate (Greenhalgh et al., 1994; Guest et al., 1995) and potentially by Bion® (Cole,
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1999; Sarwar et al., 2005). Phosphonate is a systemically translocated chemical used to
protect plants against oomycete pathogens and induces rapid defence responses (Guest and
Grant, 1991). Bion® is a salicylic acid (SA) analogue that initiates resistance in plants against
various pathogens (Oostendorp et al., 2001, Thakur and Sohal, 2013) and has been used to
control diseases in many crops (Bokshi et al., 2003). Phosphite blocks mitogen-activated
protein kinase (MPK4) in Arabidopsis inoculated with Hyaloperonospora spp. MPK4 is a
negative inhibitor of SA-induced responses; blocking MPK4 increases SA signalling, and
priming. Phosphite negatively regulates SA initiating defence responses in Arabidopsis spp.
following Hyaloperenospora spp. infection (Massoud et al., 2012). Various levels of defence
activators cause accumulation of SA initiating defence responses against oomycete infection
(Massoud et al., 2012; Lovelock et al., 2013).
Glucosinolates and white rust
After the major outbreaks of white rust of Brassica in several
European countries and disease incidence in India in the 1980s (Chaurasia et al. 1982; Santos
and Dias, 2004), it was first reported in Australia to cause economic loss in broccoli and
cauliflower in 2001. The disease became endemic within 18 months (Minchinton, 2005;
2007). White rust has also been reported in Brassica in the 1990s in the U.S. (Scheck and
Koike, 1999). White rust (A. candida) is a biotrophic, obligate parasite and a filamentous
Oomycete (Alexander and Burdon, 1984). It causes white blisters or pustules on lower leaf
surfaces causing white rust in Brassicas. Sporangia of A. candida are formed on leaf surfaces
at later stages of infection (Soylu, 2004). Oospores survive in crop debris and act as a source
of primary inoculum; the pathogen primarily spreads through sexual spores (Vanterpool,
1959). Oospores are spherical, verrucose with warts (Choi et al., 2007), usually found in
fields after heavy infestation. They can survive for more than 20 years in crop debris (Choi et
al., 2007).
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There is an association between plant resistance to fungi and glucosinolate content
(Fan et al., 2008), the role of insect attack (Bodnaryk, 1992; Kim and Jander, 2007), and
water stress (Bouchereau et al., 1996). Plant age and species (Antonious et al., 2009) affects
glucosinolate content; however limited research has been carried out on effects of fungi
infection on glucosinolate level (Islam, 2009). White rust on Indian mustard seed has been
exhibited minimum disease severity when SA was applied and glucosinolate level
measurement suggested imparting disease resistance in mustard (Tirmali and Kolte, 2011).
Four aliphatic and 2 aromatic glucosinolate levels were evaluated in broccoli. A significant
increase, 3-fold as compared to control, occurred in glucoiberin and progoitrin, 30 days after
inoculation with A. candida in broccoli leaves. A similar pattern occurred in inoculated roots
of Indian mustard (Singh, 2011).
Bion and phosphonate in plant defence
Phosphonate is a xylem and phloem translocated ambimobile ion containing a proton
covalently bonded to a phosphorus atom (Groussol et al., 1986). It is systemically
translocated, and a selective fungicide used to control several diseases caused by Oomycetes
(Guest and Bompeix, 1990). It operates via a complex mode of action (Guest and Grant,
1991), and at low rates does not directly suppress the pathogen, but primes the host defence
(Grant et al., 1990; Daniel et al., 2005). Phosphonates cause interruptions at metabolic sites in
mycelia and inhibit sporulation, but are fungistatic rather than fungitoxic (Guest and Grant,
1991). Phosphonate also affects plants by modifying their hypersensitive response.
Nemestothy and Guest (1990) reported an increased hypersensitive response, and increased
production of phytoalexins, phenolics and lignin due to phosphonate application. An increase
in cytoplasmic activity, development of cytoplasmic aggregates, release of superoxide,
localized cell death and enhanced accumulation of phenolic materials around infected cells,
and other indicators were observed post-phosphonate application. Pathogen development was
5
severely restricted, and hyphae that develop in phosphonate treated seedlings appeared
distorted, and sporangial production was inhibited (Daniel and Guest, 2005). Apart from
induction of the hypersensitive response phosphonate also increases the level of SA and
induces systemic acquired resistance (SAR) Eshraghi et al. (2011). Phosphonate was applied
to Brassica crops before infecting with A. candida to cause white rust symptoms and
glucosinolate levels were recorded at all stages of the disease. Changes in glucosinolate levels
were observed suggesting the role of phosphonate in their accumulation (Singh, 2011).
Phosphonate is a defence priming compound and white rust is a stress to the crop caused by
the pathogen, so production of glucosinolates might be affected. It also suggests that the
symptoms of the disease and the glucosinolate concentrations may be related.
Role of Bion® in inducing resistance
Bion®, which induces systemic acquired resistance, is used as a systemic fungicide to control
various fungal diseases and activate, or induce, resistance. It is a salicylic acid analogue
(Tokunaga et al., 1999; Wendehenne et al., 1998) and induces resistance through the SA
dependant pathway (Achuo et al., 2002; Vlot et al., 2009). It is active systemically in plants
and can take the place of SA in the natural SAR signalling pathway (Oostendorp et al., 2001).
The compound has minimal fungicidal and bactericidal activity, but induces host plant
resistance via SAR.
Bion® assists in management of white rust disease, diseases of leafy vegetables and
bacterial leaf spots in tomato (Solanum lycopersicum L (Achuo et al., 2002; Cavalcanti et al.,
2006). Bion® exhibited systemic effects against white rust of spinach (Spinacia oleracea L.)
caused by Albugo occidentalis by inducing natural SAR in spinach (Leskover and Kolenda,
2002). Bion® induces plant defence when applied to Indian mustard (Kaur and Kolte, 2001).
Bion® and its analogues suppress Fusarium diseases on a few crops (Elmer and McGovern,
2004). However, high concentrations of Bion® can be phytotoxic (Elmer, 2006).
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Bion® is one of the best studied resistance activators that have long lasting effects in
the plant (Oostendorp et al., 2001). Phosphonate and Bion® have been used to elucidate the
SA dependent regulation of glucosinolates. This relationship between white rust stressed
Brassica crops and defence-activator application with regulations of glucosinolate levels in
leaves of plants has been shown by Singh (2011). Aromatic glucosinolates are induced by SA
treatment on oilseed rape plants and an increase in secondary metabolite content in response
to SA was found (Kiddle et al., 1994). Reduced white rust severity (3.62%) was found in
Indian mustard after application of SA. It was reported by Singh (2011) that combined
application of Bion® and phosphonate significantly suppressed white rust symptoms in
broccoli leaves. This demonstrates the role of SA in plant defence signalling. Bion® and
phosphonate can induce SAR and prime defences in plants, so the possibility of a direct or
indirect link with glucosinolate levels exists.
Glucosinolate accumulation and its stability
Glucosinolates are accumulated after mechanical plant damage or damage by insects. These
secondary plant products (β-thioglucoside N-hydroxysulfates) are found in more than 500
spp. in 16 families of dicotyledonous higher plants (Fahey et al., 2001a). The complexity of
the glucosinolate myrosinase system implies a diverse and multifunctional role in Brassica
crops (Kelly et al., 1998). Glycosides and myrosinases are separated by vacuoler membranes
in undamaged cells. When the cell wall ruptures due to damage in the plant cell, myrosinases
come in contact with glucosinolates and form isothiocyanates. Some glucosinolates are
effective deterrents to herbivores (Arany et al., 2008) and some are involved in plant defences
(Klingen, 2002; Rask et al., 2000). Glucosinolates are known to be located and translocated
in xylem and phloem (Chen and Andreasson, 2001; Ishii, 1991; Li and Kristiansen, 2011) and
possess physicochemical properties that allow phloem mobility (Brudenell et al., 1999).
7
According to Thangstad et al. (1991) myrosinase is contained in myrosin cells confined to
parenchymatous tissues of Brassica plants mostly in epidermal cells of leaves.
Significant variation in glucosinolate content occurs during plant development
(Rodman and Louda, 1984). It is known that high amounts of glucosinolates were found in
leaves and roots at vegetative stages (Sang et al., 1984) and in flowers (at 50% flowering) at
reproductive stage of wild radish (Malik et al., 2010). However limited information is
available on glucosinolate variation within the Brassica plant and the relationship between
their pattern and concentration in aerial parts and roots (Rosa, 1997).
Glucosinolate accumulation is unstable; during rapid growth of the plant,
glucosinolate accumulation increases (Clossaisbesnard and Larher, 1991). Accumulation
increases significantly as a result of elevated CO2 in Indian mustard leaves (Mathur et al.,
2013). Glucosinolate concentrations were higher in young as compared to fully expanded
leaves suggesting their role in protection of young foliage (Porter et al., 1991).
Understanding biosynthetic pathways of glucosinolate formation is complicated. In
in-situ localization, glucosinolates are lost to the material used to fix them if conventional
fixation and dehydration procedures are followed. Analysis using ELISA and raising
antibodies against complexes of glucosinolates was done (Kelly et al., 1998). The vacuole
has been suggested as an alternative location of glucobrassicin and sinigrin (Grob and Matile,
1979).
Glucosinolate biosynthesis
There are 3 phases in glucosinolate biosynthesis-conversion of the amino acid to its aldoxime
and side-chain elongation, formation of the core glucosinolate structure and side-chain
decoration (Halkeir and Gershenzon, 2006; Sonderby et al., 2010). In the first phase,
conversion of methionine, branched chain amino acids or aromatic amino acids occurs. In the
biosynthesis from methionine, several amino acids can be converted, i.e., homo-methionine,
8
tri-homo-methionine and others. From branched chain amino acids like valine, isoleucine and
leucine, conversion of 2-oxo-3 methyl butanoic acid, 2-oxo-3 methyl pentanoic acid and 2-
oxo-4 methyl pentanoic acid happens and corresponding glucosinolates are biosynthesized.
Biosynthesis from aromatic amino acids phenyl alanine, tyrosine and tryotophan involves
conversion of L-phenylalanine, homo-phenylalanine, L-tryptophan and L-tyrosine to
corresponding glucosinolates (Frisch and Moller, 2012).
The key regulatory enzyme in the biosynthesis of aromatic glucosinolates, PAL
diverts phenylalanine from primary to secondary metabolism. PAL converts phenylalanine to
cinnamic acid, the basic building block for phenylpropanoids, alkaloids and side-chains of
aromatic glucosinolates (Evans et al., 1987). PAL activity increases following a range of
stresses, including disease (Shukla et al., 2010), leading to formation of phytoalexins, lignin
and SA, a key regulator of SAR (Sticher et al., 1997). Changes in level of aromatic
glucosinolates may result from changes in PAL activity, or a switch in the balance of
pathways using cinnamic acid (Fig. 1) (MacDonald and D’Cunha, 2007). Phenylalanine is
converted to cinnamic acid via PAL enzyme and is followed by various pathways like
phenylpropanoid metabolism, ligning formation, SA metabolism and aromatic glucosinolate
biosynthesis.
9
Fig. 1. Pathway of glucosinolate biosynthesis from amino acid, tryptophan. Activity of
phenylalanine ammonia lyase (PAL) and formation of cinnamic acid (Reprinted by
permission from Macmillan Publishers Ltd: [Nature] (Dixon, 2001), copyright (2001).
Factors affecting glucosinolate biosynthesis
Salicylic acid is a key signal regulating plant defences and its application has been used in
minimizing symptoms of several fungal disease (Thakur and Sohal, 2013; Li et al., 2000).
Glucosinolate accumulation in leaves of oilseed rape plants was affected by SA applied as a
soil drench (Kiddle et al., 1994). Byun et al. (2009) reported that cold stress activates genes
related to SA synthesis and glucosinolate synthesis in A. thaliana, indicating their
interdependent relationship as an early response to cold stress. Glucosinolate accumulation is
affected by a range of environmental stimuli. PAL provides a readily monitored surrogate
indicator of glucosinolate biosynthesis following pathogen attack. Along with glucosinolate
concentrations, monitoring PAL can be an effective indication of glucosinolate metabolism
post-pathogen attack (Singh, 2011). Wielanek et al. (2009) reported that salicylic and
ethylene signalling regulate jasmonate mediated gene expression and glucosinolate content
following herbivore attack in A. thaliana. Jasmonate also plays an important role in plant
defences (Kubicka and Zadernowski, 2007).
Breakdown
Disruption of plant tissues (by mechanical damage) brings the degradative enzyme into
contact with glucosinolate and sets off reactions that release bioactive chemicals. Following
tissue disruption, enzyme and substrate come into contact, causing hydrolysis of
thioglucosidic bond, yielding glucose and an unstable aglycone, the thiohydroxamate-O-
sulfonate. The latter undergoes spontaneous rearrangement into different possible products:
isothiocyanates, nitriles and elemental sulfur, thiocyanates, epithionitriles, oxazolidine-2-
thiones, or aromatic compounds. The chemical structure of the resulting product depends on
10
side chain structure and on reaction conditions (Holst and Williamson, 2008). Myrosinases,
also known as thioglucosidases, are enzymes that hydrolyse glucosinolates into their
derivatives. The glucosinolate myrosinase system is also believed to be a part of plant
defence against animals and pathogens (Pontoppidan, 2001; Wielanek and Urbanek, 2006).
The myrosinase enzyme is a transitional stage of formation of isothiocyanates so it might
help in studies related to elucidating greater understanding of hydrolysis of glucosinolates.
Interaction between plant defence and phytochemicals
Plants have an array of defence mechanisms that lead to formation of a wide range of
phytochemicals and products soon after pathogen infection occurs and the plant responds to
the incompatible interaction (Dixon, 2001; Pozo et al., 2009; Yao et al., 2007). An example
of these defence responses was shown by Ali et al. (2000) as a synergistic interaction
between phosphonate and Bion® on Pinus, Banksia and Isopogon spp. against Phytophthora
cinnamomi. It was shown that combinations of phosphonate and Bion® and their application
separately reduced infection but in combination with low phosphonate doses was the most
effective (Ali et al., 2000).
Another defence response involves phenylpropanoid metabolism in which
phenylalanine conversion to cinnamic acid and ammonia is catalysed by the enzyme PAL.
The phenylpropanoid metabolism leads to various signalling pathways (Gomez-Vesquez et
al., 2004) one of which has as the end product SA, the signalling molecule (Hammerschmidt
and Smith-Becker, 1999).
Glucoberteroin and a few other glucosinolates elicitation was reported when
Thellungiella salsuginea (Pallas) was infected with A. candida, however significant
glucosinolate accumulation was found after UV elicitation suggested that abiotic stress
impacted the plant more than biotic stress (Pedras and Zheng, 2010) as in the case of elevated
CO2 effect on B. juncea var. Tarak infected with A. candida (Mathur et al., 2013). However,
11
broccoli (B. oleracea L.) roots were found to accumulate high amounts of glucosinolates as a
result of club root infection (Islam, 2009).
Arabidopsis thaliana has a defence mechanism that involves synthesis of tryptophan
derived indole glucosinolates followed by enhancing non-host resistance of the plant against
a biotrophic fungus (Sanchez-Vallet et al., 2010). A role exists for tryptophan derived
secondary metabolites in disease resistance of A. thaliana to Phytophthora brassicae (De
Bary) that induces genes encoding enzymes involved in aromatic glucosinolates biosynthesis
in response to this pathogen. Disease resistance of Arabidopsis to P. brassicae is established
by aromatic glucosinolate activity (Schlaeppi et al., 2010). This suggests a role of
phytochemicals in resistance and that there is a potential advantage to manipulation in level
of beneficial phytochemicals, in this case glucosinolates. Metabolism of glucosinolates
involves precursor amino acid phenylalanine and its deamination is catalyzed by PAL to form
trans-cinnamic acid (Wielanek and Urbanek, 2006).
Phenylalanine Ammonia Lyase activity
Phenylalanine is a precursor of some aromatic glucosinolates during early biosynthesis
(Kryzymanski, 1995) and the enzyme PAL is a key enzyme in phenolic metabolism in plants
(Mathur et al., 2013). The PAL activity is relevant as an indicator of aromatic glucosinolate
synthesis, however, there are other pathways where PAL is involved; the SA pathway and
phenylpropanoid metabolism.
PAL activity is affected by wounding of the plant as seen in PAL accumulation that
was measured 24 hr after wounding maize (Zea mays L) mesocotyls (Pascholati et al., 1986).
PAL activity can be affected by chilling injury; injury was found directly proportional to PAL
activity (Bojorquez Galvez et al., 2010). PAL activity increases soon after the plant is
challenged by a pathogen. As in the case of cassava (Manihot esculenta Crantz) following
elicitation by yeast, PAL was induced after 15 hr (Gomez-Vesquez et al., 2004).
12
The defence-activator Bion® affects PAL activity 6, 9 and 12 days after application in
tomato as a defence against Xanthomonas vesicatoria (Cavalcanti et al., 2007). Young et al.
(2005) reported that phenolic levels in stressed conventionally, or organically grown,
vegetable crops were high. This was due to increased PAL activity, following which more
phenolics were synthesized. PAL activity increased in inoculated genotypes of wheat
(Triticum aestivum L.) in first few hours following inoculation with Erysiphe (Green et al.,
1975). This implies that infection stimulates PAL activity, also shown by Singh (2011) in
white rust of broccoli. Studies of PAL-deficient mutants that are compromised in resistance
have similar results (El-Kereamy, 2011). These studies indicate that mutants with PAL
deficiency affect the phenylpropanoid pathway and the plants' ability to resist pathogens
(Ferrari, 2003; Taheri and Tarighi, 2010). PAL activity can be monitored to derive more
information about formation of phenolics like SA and some glucosinolates. Two possible
circumstances follow, one in which there is already accumulation of glucosinolate in the crop
and second, where it follows stress in the form of pathogen attack in the plant. In the first
case, glucosinolates are synthesised from amino acid precursors as the normal course. These
glucosinolates are in compartments within vacuoles, after injury or chewing these
compartments break and myrosinase acts to form isothiocyanates. If there is stress in the
plant phenylalanine is accumulated as a result of infection more glucosinolates accumulates.
It has also been reported that increase in PAL activity occurred after inoculation of B. juncea
with A. candida and suggested that infection triggers accumulation of PAL in Brassica crops
(Singh et al., 1999). This can possibly be directed towards research for developing Brassica
vegetables beneficial to human health.
Toxic, or sour tasting, glucosinolates were previously removed from Brassica
vegetable crops by breeding and other genetic techniques (Kushad et al., 1999) and recent
research involves exclusion of detrimental glucosinolates and inclusion of beneficial
13
glucosinolates through gene silencing (Liu et al., 2012). There is limited information on the
interaction between glucosinolates and plant fungal diseases and their effect on
glucosinolates level. As a disease response, change in concentrations of glucosinolates occurs
in the case of white rust (Tirmali and Kolte, 2011) and club root disease of Brassica (Islam,
2009). Potential relationship between infection, resistance and glucosinolate formation
Brader et al. (2006) exists. Significant information has been provided on biosynthetic
pathway of glucosinolate formation through PAL and other related enzymes. The PAL
activity and other key enzymes can be used to deduce the relationship between infection and
glucosinolates in specific detail (Singh, 2011). The role of glucosinolate metabolism in
determining plant fungi compatibility and interactions thereof remains an important area to be
further explored (Fan and Doemer, 2013).
Research based on information in the review will support the correlation between
defence response in Brassica crops and changes in glucosinolate levels against pathogens.
Further work will provide additional information about glucosinolate biosynthesis and
various pathways of glucosinolate accumulation following infection, and defence activator
application and will deduce the role of other important enzymes in biosynthesis.
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