Plants Have To Constantly Fight Abiotic Biotic Stresses Biology Essay


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Plants live in the environment where they have to constantly fight against several abiotic and biotic stresses to successfully grow and reproduce. Abiotic stress includes stress caused by environmental factors like wind, temperature, water etc. Plants develop various structural modifications to overcome these stresses like thick cuticle, waxy covering, spines etc. Biotic stresses include stresses which are due to living organisms' i.e. by pathogens like virus, fungus, bacteria, nematode, or by insects. Plants are constantly being challenged by these aspiring pathogens but plants have evolved to defend themselves against them. This is the case with most of the plants which live in their natural habitat or what we called them as wild species. But the crop plants or the domesticated plants have a narrow genetic base due to excessive inbreeding which is required for introducing the desired characters in the plant of our interest. This has led to the decrease in genetic variability in the crop plants which ultimately affected their resistance capacity. They have now become a potential target for the number of pathogen to which their wild relatives were earlier resistant. This has led to the increase in the use of chemicals like fungicides, pesticides etc. to curb these pathogen attack on crop plant. In earlier days their use had led to a boom in agricultural production as pathogen affecting plants were not able to infect them, thus leading to the increase in yield. But soon it was realized that these affect our environment as they are hazardous non-biodegradable chemicals which lead to processes like bio magnification, eutrophication etc. So it has become a major environmental issue. Moreover using the same chemicals lead to the evolution of pathogens which are resistant to these chemicals. So an alternative was needed to curb these diseases in plants without using these chemicals as these diseases causes worldwide loss to our agricultural production which is a great loss to the mankind.

This has evoked the people's interest in mechanism by which these wild species do survive in the presence of these opportunistic micro-organisms. There must be some internal resistance process going on which help these plant to defend themselves. This has forced us to study about the pathogen attack and plant resistance mechanism.

In this article I will be concentrating on three main aspects: Firstly, I will be describing about molecular aspects of defense mechanism in plant against pathogen in general. Then secondly, I will emphasize on plant nematode interaction. Then lastly my focus will be on the techniques which can be employed to make the plants resistant against nematodes.


Pathogens are the micro-organisms which infect the plant and disturb their cell's metabolism by secreting toxins, cell wall degrading enzymes, growth regulators etc. and then feed upon these cells. There are three kinds of pathogen:

Bio trophic - these pathogens colonizes living cell, feed upon them and complete their life cycle inside these living cells only.

Hemibiotrophic - They initially colonizes living cell, feed upon them but complete their life cycle by killing the host cell.

Necrotrophic - they release the toxins inside the cell to kill them and then colonize them, feed upon them till they complete their life cycle.

So the pathogenicity is the ability of organism to interfere with one or more of the essential functions of the plant, thereby causing disease. There are three components necessary for a susceptible interaction between plant cell and pathogen:

Pathogen should be virulent and present in abundance

Condition of host should favour susceptibility

Environmental condition should favour disease

These three conditions can be represented by a triangle known as disease triangle that's each side represents one of the above conditions and the presence of each condition is necessary for a disease to occur. Absence of any one would not let the pathogen to infect the host. Therefore, in a susceptible reaction, pathogen is able to colonize the host and reproduce in it. This all occurs in favorable environmental conditions. Pathogen has to fight against various mechanism laid by plants like structural modifications, innate immunity and host specific immunity in order to get inside the plant. So this causes a tug of war between pathogen and plants.


Plants have various structural modifications which protects them from various pathogens like they have cuticle, cell wall etc which resist the entry of opportunistic pathogens. In order to get inside the plants, pathogens enter the plant through natural opening like stomata or through any wounds. Once they are inside the plant cell, they now need to cross the cell wall which they do it by releasing the cell wall dissolving enzymes, after which they have to face the cell membrane where the pathogen recognition receptors (PRRs) are present which recognizes pathogen associated molecular patterns (PAMPs). PAMPs are the specific molecules associated with pathogens. Recognition of PAMPs by PRRs triggers PTI (PAMP triggered immunity) as shown in figure 1. This will activates MAPK signal transduction which in turn activates transcription factors leading to the activation of basal defense response in plants against pathogens.

Fig: 1 (Ref: PAMP recognition and the plant-pathogen arms race.Robert A. Ingle, Maryke Carstens and Katherine J. Denby)

To escape this, pathogens have evolved a mechanism of directly releasing some effector proteins inside the cells which can then block the signaling pathways or may alter the PRRs. After countering this, pathogen get inside the plant cell where they are challenged by the effector triggered immunity (ETI). This mechanism has evolved by plants which includes R-genes which recognize effector proteins of pathogen and thus act against them. This all shows that there is a mechanistic link between basal and gene-for-gene hypothesis.

Example there is a PRR protein in Arabidopsis called RIN-4 which is for basal defense. Pseudomonas syringae has developed AvrRpm1 and AvrRpt2 for evading basal defense response in Arabidopsis (Kim MG. et al., 2005; belkhadir Y et al., 2004) as shown in figure 2.

Fig: 2 (Ref: PAMP recognition and the plant-pathogen arms race. Robert A. Ingle, Maryke Carstens and Katherine J. Denby)

Plant has developed second line of defense called R gene against this P.syringae. AvrRpm1 phosphorylates RIN4 which in turn activates RPM1 and AvrRpt2 degrades RIN4, thus activates RPS2 as AvrRpt2 mediated cleavage by RIN4 release its association with RPS2 and thereby removes the negative regulation of RPS2 function by RIN4 (Kim HS. et al., 2005; Mackey D. et al., 2003; Mackey D. et al., 2002). Activation of RPM1 or RPS2 triggers R-protein which results in the induction of rapid defense responses.

So all these show multiple defense mechanism developed by plant to counteract pathogen attack. There occurs a constant battle between plant and pathogen. Pathogens try to evolve or develop some mechanism to evade recognition by plant. In them genetic diversity is high as they have short life cycle so the rate of mutation accumulation as well as recombination is high. In response to this plant is also regularly evolving to recognize vast array of the pathogenic elicitors. As mentioned above, plants have developed structural modifications to resist the entry of these pathogens. Then non host specific resistance also called as basal resistance comes into play. If pathogens escape this as well then host specific resistance acts upon them. This is referred to as R-gene mediated response.


Resistance genes are present in the plants which recognize the Avr determinant from pathogen. There are two hypothesis for recognition pattern of Avr determinant by R gene. One was given by Harold Henry Flor in 1955 called as gene for gene hypothesis. He worked on Flax (Linum usitatissimum) - Flax rust (Melamspora lini) pathosystem. According to this hypothesis, for an incompatible reaction, dominant product of Avr gene in pathogen should interact with dominant product of R gene in plants. If any of the two components is absent then there occurs a compatible reaction, i.e. pathogen is able to infect the host as shown in figure 3

Fig: 3

Here the R gene in plant (host) represents the resistance gene which is dominant one, whose presence confers resistance against the pathogen. Therefore presence of R gene either in homozygous (RR) or heterozygous (Rr) form will confer resistance to plants. On the other hand, avirulence gene present in the pathogen should also be dominant for the resistance to occur i.e. dominant Avr gene and dominant R gene interaction will bring about the incompatible or resistance reaction in plant and the pathogen is then not able to infect the plant.

The other hypothesis is Guard hypothesis given by Van der Biezen and Jones, according to which product of R gene is not directly involved in recognizing Avr determinant, rather it protects the protein product of other gene which is attacked upon by Avr determinant. This will bring about a conformational change in that protein which in turn will activate R gene and thus a signaling cascade is activated which results in resistance response.

Each R gene is specific against one or two particular pathogen as they recognize particular effector protein released by them. First thought to be R-gene isolated was Hm1 from maize which confers resistance against Cochliobolus carbonum (Johal GS, Brigge SP 1992). This gene codes for an enzyme that detoxifies the toxin produced by this pathogen. But recessive mutation which causes failure of production of this toxin, are however non-pathogenic rather than virulent, so this interaction does not strictly confirms to gene for gene hypothesis. Therefore strictly speaking the tomato Pto gene, which confers resistance to Psudomonas syringae carrying avrPto gene, was the first race specific gene to be isolated (Martin GB. et al., 1993).

Till date there are mainly five classes of plant disease resistance proteins (fig 4) which are identified which includes Xa21 and Cf-X proteins having transmembrane domains and extracellular LRRs, RPW8 gene product which carries a putative signal anchor at the N- terminus, Pto gene which encodes a cytoplasmic Ser/Thr kinase but may be membrane associated through its N- terminal myristolation site and there is a largest class of R proteins containing NBS and LRR domain.

Fig: 4 (Ref: Host-Microbe Interactions: Shaping the Evolution of the Plant Immune Response. Stephen T. Chisholm, Gitta Coaker, Brad Day and Brian J. Staskawicz)

NBS-LRR class is divided into two groups according to their N-terminal domain.



A nearly constant feature of the R-gene is the presence of leucine rich repeat motif which contains leucine or other hydrophobic amino acids at regular intervals within a sequence of about 24 amino acids. These LRR motifs are responsible for protein-protein and protein-receptor ligand interaction (Kobe and Deisenhofer., 1995; Jones and Jones., 1996). Thus it is thought to be involved in the binding of Avr protein and all other host proteins. β strand of LRR (with consensus sequence of XXLXLXX) determines the specificity of each R protein. Of the R genes characterized thus far, only Pto does not include this motif. It is a tomato gene that encodes a serine/threonine protein kinase and confers resistance to strains of Pseudomonas syringae carrying the avirulence gene avrPto (Martin et al., 1993). However Pto requires a presence of second gene Prf for recognition of Avr determinant from pathogen, which does contain a characteristic LRR region to confer resistance (Salmeron et al., 1996). NBS region of the R proteins contain several conserved motifs. This region is believed to have ATP or GTP binding site which can then activate some defense response (Saraste M., Sibbald P. R. and Wittinghofer. A., 1990). Loss of NBS and LRR function leads to constitutively active R protein which shows that R proteins are under negative regulation which may be due to intramolecular protein interaction.

Presence of CC or TIR region at the N terminal domain suggests a role of this domain in signaling but not ligand binding. Function of Coiled coil (CC) region has not been defined yet and Toll/Interleukin 1 recptor (TIR) domain function has been characterized in animal innate immunity. Plant Resistance proteins use their TIR domains for pathogen detection, and they may also function in the nucleus to direct the expression of genes involved in defense responses. Recent evidence suggests that the TIR/CC may be involved in intra-molecular interactions and in binding of AVR gene and R gene. (Lukasik and Takken Current Opinion in Plant Biology 12:427-436). CC-NB-LRR and TIR-NB-LRR genes may interact with different sets of downstream components

Some R genes are transmembranous and some are cytoplasmic. This confers resistance to elicitors which are produced by pathogens outside as well as directly inside the cell and thus making the defense system of plant more effective.


As described earlier pathogen attack will activate defense response in plants. In both the cases of susceptible and resistance reaction defense mechanism is mediated. In case of susceptible reaction, the extent of this mechanism is low that is why pathogen is able to infect the host plant whereas in case of resistant interaction where both the basal as well as R mediated mechanism is induced, the extent of defense response is much higher which will inhibit the pathogen to colonize the host. There occur many changes in the plants which will ultimately lead to the resistance response.

There are some signaling components required for resistance mediated by R proteins which are specific to the particular domain at N - Terminal. CC domain signal through NDR1 and TIR domain signal through EDS1 (Aarts, N. et al, 1998). RAR1 is required for resistance mediated by both TIR-NBS-LRR and CC-NBS-LRR (Muskett, P.R., et al., 2002; Torneto, P., et al 2002). Example SGT1 which is a RAR1 interacting protein. Its silencing cause compromised disease in Barley towards Powdery mildew (Azevedo, C., et al 2002) and in Arabidopsis to Perenospora parasitica (Austin, M.J., et al 2002; Tor, M., et al 2002).

There occurs the oxidative burst which is dependent on changes in fluxes of ions such as calcium, calmodulin family members and calmodulin like protein domain kinases (CDPKs). There occurs the formation of reactive oxygen species (ROS) species. Example Oâ‚‚° (superoxide). It forms outside the cell. This would be converted to Hâ‚‚Oâ‚‚ (Hydrogen peroxide) by membrane bound NADPH oxidase enzyme. Now this Hâ‚‚Oâ‚‚ contribute to structural reinforcement of plant cell wall by cross linking various hydroxyproline rich and proline rich glycoproteins to the polysaccharide matrix or by increasing rate of lignin polymer formation by peroxidase enzyme activity. This will reduce the extent of leakage from plant cell wall and also make it more resistance towards enzyme released by pathogens. Hâ‚‚Oâ‚‚ is also directly toxic to pathogen. This Hâ‚‚Oâ‚‚ can cross the plasma membrane where it will get converted to Hâ‚‚O with the help of enzyme like catalase, ascorbate peroxidase etc.

This Hâ‚‚Oâ‚‚ will also induce BA2-H (benzoic acid 2- hydroxylase) formation which is required for biosynthesis of salicylic acid.

Salicylic acid which is produced by BA2-H leads to protein phosphorylation which ultimately activate transcription factors which will bind to defense gene and make them express.

There is also an increase in NO production which will bind to heme which causes inhibition of catalase, ascorbate peroxidase etc. which will detoxify Hâ‚‚Oâ‚‚, thus leading to rapid cell death or we can call it as HR or hypersensitive response.

As discussed above ROS and NO stimulate SA production which in turn potentiate ROS and NO mediated responses, thus appears to act upstream and downstream of these two.

NO, SA, ROS play a central role in the activation of the defense response. All three messengers act synergistically in triggering HR and other defense responses which include production of glutathione s- transferase (GST), peroxidases, cell wall proteins, proteinase inhibitors, hydrolytic enzymes (example chitinase and β- 1,3 -glucanases), pathogenesis related (PR) proteins and phytoalexins biosynthetic enzymes, such as phenylalanine ammonia lyase (PAL) and chalcone synthase (CHS, Hammond - Kosack and Jones, 1996)

Ethylene and jasmonic acid are also produced. Both are required for activation of proteinase inhibitor (PI) genes and certain PR (pathogenesis related) and chitinase gene.

There is a cross talk between these secondary signals like ethylene, jasmonic acid, salicylic acid etc as shown in fig 5. These all will lead to activation of transcription factors which bind to defense related genes and thus activate them. Example in case of Avrpto and pto and prf gene as shown below:

Fig :5

R - Gene dependent pathogen recognition appears to trigger a feedback loop amplifying the initial signal and leading to effective activation of downstream defense responses. Gene expression pattern associated with compatible and incompatible resistance proved to be quite similar. A large number of defense related genes are upregulated to a comparable extent in both defense situations. R-Dependent responses are however more rapid and to a higher amplitude which is explained in figure 6.

Fig: 6


It has also been seen the secondary signals produced during plant's response to a pathogen attack also activate defense responses in uninfected plant parts so that entire plant will be ready or resistant to the pathogen attack. This is called Systemic Acquired Resistance (SAR). It is long lasting and confers broad resistance to variety of different pathogens (Ryal et al 1996; Delaney, 1997). Onset of SAR is accompanied by increase in endogenous level of salicylic acid. But it is not the mobile signal for SAR. Instead there is a putative apoplastic lipid transfer protein encode by DIR1 (defective in induced resistance 1) gene which is required for pathogen induced SAR. This shows that lipid derived signals are important component of long distance signal in SAR. When an uninfected tissue of plant receives long distance SAR signal, it leads to accumulation of SA in the tissue, resulting in the up regulation of a large set of defensive genes, including those that encode PR proteins. All these process i.e. transduction of SA signal to activate PR gene expression and SAR requires the function of NPR1. NPR1 is translocated in the nucleus upon induction by SAR. It acts as a modulator of PR gene expression by binding to the DNA through members of TGA subclass of the basic leucine zipper (bZIP) family of transcription factors. Therefore in all it is seen that SAR is important for plants as it will up regulate the defense responses in uninfected parts of the plants, thus making them resistant against pathogen attack.

After discussing molecular aspects of resistance mechanism in plants against pathogens, I will now talk about plant nematode interaction and defense mechanism in hosts against nematodes.


Nematodes are from phylum Nematoda. They are tiny roundworms found in great numbers on this earth. They can be free living as well as parasitic (Maggnenti., 1981) which sustains on specific range of host. Plant parasitic nematodes can be ectoparasites or endoparasites which feed on plant's cell cytoplasm. The sedentary endoparasites of the family Heteroderidae causes the most economic loss. Family Heteroderidae is divided into two groups: Cyst nematodes and Root knot nematodes. Cyst nematodes include genera Globodera and Heterodera. They have a narrow host range. Root knot nematodes include genera Meloidogyne. They have a wide host range. Nematodes in these three genera have complex interaction with their host plants that generally last for more than a month and result in major morphological and developmental changes in both organisms. Infective stage of nematode is motile, second stage juvenile which penetrates the roots and migrates to a site near the vascular tissue. Nematode triggers elaborate developmental and morphological changes in host cells. They have two types of feeding strategies which can be migratory or sedentary. Most of the phytophagous nematodes are migratory ectoparasites or endoparasites browsers that frequently kill the cell on which they feed before moving on to another cell. Endoparasites are sedentary nematodes that have developed complex and intimate relationship with their hosts by developing special feeding site within their host plants. Once feeding is initiated the nematode becomes sedentary and undergoes three molts to develop into the adult. The bulbous, non-motile adult females begin to lay eggs at about 3-6 weeks, depending upon species and environmental conditions. Gender is determined epigenetically, with males increasing in frequency under conditions of crowding or poor nutrition (Triantaphyllou., 1973).

Feeding sites of both nematodes appear similar both being very large, metabolically active, multinucleate cell. But in cyst nematode syncytia formation occurs by dissolution of cell wall and their fusion. In root knot nematode cell expansion and nuclear division create the giant cell. It is believed that secretion from esophageal gland may cause formation of syncytia and giant cell formation. Despite the considerable differences in structure and formation, both types of feeding site act as nutrient sinks and transfer cells to fulfill the same purpose of providing nutrition to the nematode to allow development to a mature, egg-laying female.

Fig:7 Life cycle of root knot nematode inside the plant.

Sedentary endoparasitism has been developed by nematodes because it has number of evolutionary advantages like it would provide protection to nematodes from predator as well as insulate them from fluctuating environment. Secondly they have to spend less energy in maintaining a feeding site than migrating from one site to another.


Plant parasitic nematodes possess two specialized structures, stylet and esophageal secretory glands which are thought to be essential for many aspects of parasitism (Hussey 1989; Hussey and Mims 1990). The stylet is hollow and protusible structure at the anterior end of the nematode that is used to pierce plant cell walls. In species of root knot nematode and cyst nematode, the subventral gland cells are active early during the parasitic process, whereas the dorsal gland enlarges and becomes more active as parasitism progresses. Secretions from the esophageal glands are released through the stylet. These secretions are thought to have direct effect on recipient host cells. These include cell wall modification and potential interactions with signal transduction receptors in the extracellular space, as well as direct introduction of proteins into host cells that might influence cellular metabolism, the cell cycle, selective protein degradation, a localized defense response and regulatory activity within the host cell nucleus which will ultimately lead to the formation of giant cell and syncytium. Figure 8 demonstrates the piercing of cell wall of host by stylet of nematode which then release its secretion into the host cell which will then bring about the further modifications.

Fig:8 ( Ref: Nematode Pathogenesis and Resistance in Plants. Valerie Moroz Williamson and Richard S. Hussey)

Cyst and root knot nematode establish a prolonged biotrophic feeding association with the feeding cells, feeding periodically from the syncytial cell or from each of the giant cells. If the nematodes enter a susceptible plant then they can establish themselves and multiply there whereas in case of resistant plant they fail to do so and egress from the roots 3-5 days later.


In case of susceptible host, root cells of host are transformed into special feeding cells which require extensive changes in the gene expression in infected root cell. The pathogens have evolved an ability to recruit these plant genes to manipulate host functions to their own benefit. These will bring changes to certain fundamental aspects of plant development, such as defense and hormone response, cell wall, cell cycle and cytoskeleton organization. Root knot nematodes induce long term changes in organization of the cytoskeleton of the giant cells (de Almeida Engler et al., 2004). All members of class A and class B expansin superfamily regulated upon Meloidogyne infestation have been shown to be activated in Arabidopsis thaliana (Jammes et al., 2005). LeEXPAS, encoding a tomato expansin, is strongly expressed upon root knot nematode infestation and the silencing of this gene affects root knot development and the ability of the nematode to complete its life cycle (Gal et al., 2006). A transcriptome analysis of 635 transporter genes identified 50 genes up or down regulated in whole root knot nematode infected roots (Hammes et al., 2005). Global analysis has shown that the successful establishment of root knot nematode infestation is associated with the suppression of plant defense responses (Jammes et al., 2005).

Thus in Arabidopsis thaliana, 70% of the nematode regulated genes involved in defense pathways were repressed locally. The suppression of plant defense includes effects on resistance genes and resistance associated genes, jasmonic acid/ ethylene dependent pathway associated genes and potential antimicrobial genes. Root knot nematodes invade the root tissues by providing cell wall degrading enzymes similar to some pathogenic bacteria and fungi. The similarity in some of root knot nematodes and bacterial genes producing these enzymes may be due to horizontal gene transfer from bacteria (Scholl and Bird., 2005; Ledger et al., 2006).

Symptoms of these diseased plants infected by these groups of nematodes include stunted growth, wilting and susceptibility to other pathogen. This has decreased the yield to a considerable extent. So there is a need for some resistance mechanism in plants which would not allow these nematodes to grow inside them.


Plants are identified as resistant to nematodes when they support reduced levels of reproduction and are generally characterized by host cell death at or near the feeding site of the worm. Resistance to cyst nematode in solanaceous and cereal crops often involve a delayed response occurring several days after initiation of the syncytium whereas in case of root knot nematode it is often mediated by a more rapid hyper sensitive response. This occurs soon after invasion and is characterized by the generation of ROS in plant root cells associated with the J2s and in those selected to become giant cells (Mellilo et al., 2006).

First nematode resistance gene cloned was Hs1pro-1 from wild relative of sugarbeet (Cai D, et al., 1997). When this gene was introduced in sugarbeet it provides resistance against Heterodera sahachtii. The amino acid sequence of Hs1pro-1 deduced indicates the presence of amino terminal signal sequence and a possible membrane spanning region. But structure and function of this gene is not similar to the other known R-proteins. Others like Mi-1, Hero A, Gpa 2 and Gro1-4 falls in NBS-LRR category of R-genes. Some of the cloned and mapped genes are listed in the table given below.

Cloned and Mapped Nem-R genes







Sugar beet

Sugar beet cyst nematode: Heterodera schachtii

Cai, D. et al., 1997



Root-knot nematode: Meloidogyne incognita, M. javanica, M. arenaria;

Potato aphid: Macrosiphum euphorbiae

White fly: Bremisia tabaci

Milligan, S.B. et al., 1998; Vos, P. et al., 1998

Hero A


Potato cyst nematode: Globodera rostochinensis pathotypes Ro1, Ro3 and Ro5; Globodera pallida pathotypes Pa2 and Pa3, and Luffnes

Ernst, K. et al., 2002; Sobczak, M. et al., 2005



Potato cyst nematode: specific populations of G. pallida

Van der vossen, E.A. et al., 2000



Potato cyst nematode: G. rostochinensis, pathotype Ro1

Paal, J. et al., 2004

Rhg1 and Rhg4


Soyabean cyst nematode: Heterodera glycines type 0

Hauge, B.M. et al., 2001; Lightfoot, D. and Meksem, K. 2002




Potato cyst nematode: G. rostochinensis, pathotypes Ro1 and Ro4

Bakker, E. et al., 2004



Root-knot nematode: Meloidogyne incognita, M. javanica, M. arenaria

Yaghoobi, J. et al., 2005



Root-knot nematodes: M. incognita

Ammiraju, J.S. et al., 2003



Cereal cyst nematode: Heterodera avenae, European and Australian pathotypes

De majnik, J. et al., 2003



Cereal cyst nematode: H. avenae, Australian pathotype

De majnik, J. et al., 2003



Root knot nematodes: all species tested

Claverie, M. et al., 2004



Cyst nematode: Heterodera sacchari

Lorieux, M. et al., 2003



Root knot nematodes: Meloidogyne incognita, M. arenaria, M. javanica and some M. hapla isolates.

Djian-Caporalino, C. et al., 2001



Root knot nematode: Meloidogyne chitwoodi, M. fallax and some M. hapla isolates

Rouppe van der Voort, J.N.A.M. et al., 1999

Table:1 Nematode resistance in plants: the battle underground. Valerie M. Williamson and Amar Kumar


This gene has been cloned from tomato and confers resistance against several root-knot nematode species (Williamson VM., 1998). Mi encodes a protein of 1257 amino acids which is characterized by the presence of NBS and LRR motifs. It lacks signal sequence which suggests that recognition of nematode by host, if mediated by Mi, occurs in the cytoplasm. Mi has a sequence motif which indicates its participation in complex interactions with other proteins. It has LRR, NBS and LZ sequence motifs.




Mi gene was isolated by positional cloning and its identity confirmed by complementation of functions (Kaloshtan I, et al., 1998; Milligan S, et al., 1998). This gene was introduced into cultivated tomato, Lycopersicon esculentum, from the wild species L. peruvianum by embryo rescue of the interspecific cross (Smith, 1944). Transgenic plants with Mi were found to be resistant to the aphid, Macrosiphum euphorbiae along with root knot nematode, indicating that this gene confers resistance to the aphid as well as to root knot nematodes. Mi works in accordance with guard hypothesis i.e. it protects a protein REM1 which when attacked by pathogen or insect, activates Mi gene mediated resistance. Avr determinant from pathogen modifies RME1 and this modification is detected by Mi-1, which brings a conformational change in Mi-1 and activates resistance signaling pathways. Mi is also associated with sgt1 and Hsp90 which have a role in signaling pathway. They together with Mi will activate signaling cascade involving salicylic acid and MAPK resulting in activation of PR genes which will then lead to the cell death as demonstrated in figure 9.

Fig: 9 (Ref: The Mi-1-Mediated Pest Resistance Requires Hsp90 and Sgt1. (Kishor K. Bhattarai, Qi Li, Yule Liu, Savithramma P. Dinesh-Kumar, and Isgouhi Kaloshian)

Hero A

The Hero gene of tomato is a broad spectrum resistance gene that confers a high level of resistance to all pathotypes of the potato cyst nematodes Globodera rostochiensis and partial resistance to G. pallida. The gene was identified by map-based cloning, sequencing and complementation analysis of two susceptible tomato lines with an array of 13 overlapping cosmids spanning a total distance of 135 kb. Hero encodes a protein with a nucleotide-binding site (NBS) and a leucine-rich-repeat (LRR) domain and is a member of a gene family of 14 highly homologous genes, which are clustered within a continuous 118-kb region. It is located on chromosome 4 in resistant tomato cultivar LA1792. Hero gene encodes a protein of 1283 amino acids with a predicted molecular weight of 148 KDa. Hero gene is more likely to encode a cytoplasmic protein as there is no apparent N-terminal sequence present in them. The predicted protein of Hero gene contains a putative NBS with a P-loop, a kinase 2 and a kinase 3a motif. The C-terminal region consists of 12 imperfect leucine rich repeats. The N-terminal region is similarly rich in leucine residues and in between them leucine zipper (LZ) motif is present. It also contains acidic coiled coil region within its LRR which is coded by compound hexanucleotide microsatellite. The Hero gene is thus far the only NBS-LRR resistance coding for such an acidic loop in the LRR domain.

Fig: 10 (Ref: Putative functional motifs in the predicted Hero protein. The protein consists of 1283 amino acids. Numbers refer to the position of amino acid residues in the protein. CC: Coiled-coil motif, H: hydrophobic region, NBS: nucleotide-binding site, a: acidic domain, LRR: leucine-rich repeat.

(The broad-spectrum potato cyst nematode resistance gene (Hero) from tomato is the only member of a large gene family of NBS-LRR genes with an unusual amino acid repeat in the LRR region

Karin Ernst, Amar Kumar, Doris Kriseleit, Dorothee-U. Kloos, Mark S. Phillips and Martin W. Ganal)

In resistance plants containing Hero A gene, nematodes usually are able to invade and develop but their reproduction is severely compromised. In them delayed hypersensitive response is observed. It appears after syncytium induction and leads to slow deterioration or abnormal development of the feeding site. In incompatible reaction, phenyl ammonia lyase (PAL) and Myb related genes are upregulated. Along with this expression of pyruvate dehydrogenase (PDC) and alcohol dehydrogenase (ADH) also increases. There is also an induction in salicylic acid (SA) dependent PR genes during incompatible reaction. On the other hand all these are down regulated during compatible reaction when the nematode is able to successfully colonize the plant.

Fig: 11


This gene is also a member of NBS-LRR class of R genes which contains a possible LZ motif at its amino terminal.




This gene confers resistance against some isolates of the potato cyst nematodes Globodera pallida. This was again cloned by positional cloning strategy. NBS-LRR motifs are common in nematode R genes. NBS-LRR genes have been identified as co-mapping with Gro-1, a gene mediating resistance against potato cyst nematode Globodera rostochinensis (Leister D, et al., 1996).

In bread wheat three copies of a gene encoding a protein with NBS-LRR motifs have not so far been genetically separated from Cre3, a cereal cyst nematode (CCN) resistance gene, making these good candidates for the resistance gene. Mi-1 and Hero A genes isolated from tomato confers broad spectrum resistance against several root knot nematodes and against several pathotypes of two potato cyst nematode species resp. Potato gene Gpa2 and Gro1-4 confers resistance to narrow range of pathotypes of a single potato cyst nematode species.


Most R genes are ubiquitously and constitutively expressed in the plants but the level of expression is typically low. Their general mechanism of action has been already been described earlier. The timing, localization and action of different R genes associated with different plants may be different. They in general cause localized necrosis, suggesting a hypersensitive response within a few days of infection which is mostly near the anterior end of the nematode. They encode the effector proteins that detect effector molecules from pathogens directly or indirectly and initiate an effective defense response. In resistant plants, nematodes do enter the plants but they are not able to form a feeding structure in that plant and thus have to migrate out or die. The presence of specific elicitors produced by nematodes causes conformational change in Nem-R gene that result in the signaling of a defense response. Other molecules like Salicylic acid, jasmonic acid, ethylene etc are also required in defense signaling pathways as mentioned earlier. A bacterial gene nahG (Salicylate hydroxylase gene) encodes for catechol which degrades salicylic acid. Its expression in tomato results in loss of resistance response harbouring Mi-1 (Branch, C. et al., 2004).

Rme 1 is unlinked to Mi-1 but is necessary for resistance against nematodes, aphid, whitefly in tomato (Martinez de Ilarduya, O et al., 2004). It acts early in the signaling pathway and is also not required by other resistance genes supporting guard hypothesis as in this case nematode target Rme 1 gene product which in turn is guarded by product of Mi-1. Veech and McClure (1997) observed an association between the expression of incompatibility in cotton to M.incognata and post infection increase in phytoalexins, such as methoxy- substituted terpenoid aldehydes. Much lower levels of the compounds were detected in compatible interactions. A plant may also benefit from an earlier attack by a less aggressive nematode species that activates its physiological defenses which in turn enhance its capacity to suppress damage from sequential infections. Therefore post infection induction of resistance or susceptibility in plants due to previous nematode attacks may have significant etiological and ecological role with regard to plant tolerance and population dynamics. Ibrahim and Lewis (1981) reported that prior inoculation of M. incognita on M. arenaria susceptibility soyabean decreased root galls and egg mass production by M. arenaria.

There are also different strategies by which we can control the nematode infestation in plants.


As from the above discussion it is clear that plant parasitic nematodes have cause much loss to the mankind as they are major pests of both temperate and tropical agricultural crops. Although they are rarely fatal for the plant whom they infect but there are substantial consequences of the interaction. They divert the flow of nutrients towards their feeding cell that result in malnutrition of the plant. This causes stunted growth, chlorosis and poor yields which affect us economically. There are certain resistant plants which occur in the nature which have evolved a mechanism to resist these plants like having R gene as described earlier. But for the plants which have not developed such kind of strategy especially crop plants, some strategies are required to protect them against the nematodes. Crop plants have narrow genetic constitution due to the bottleneck effect as we have selected the required traits in them through breeding program. This has resulted in loss of many genes in them which might have helped them in developing some mechanism to fight against nematodes. We cant even use nematicides against these pathogens because as said earlier they are hazardous to the environment and mankind and moreover conventional breeding program employed to introduce resistance gene from one plant to other has certain drawbacks like it is time consuming program and everytime a resistance gene which has been incorporated in a plant through this technique may not work as it might require other factors to become functional. Therefore we need to think about more efficient strategies which we can incorporate to make these plants resistant against nematodes.

These can also be controlled by using plant varieties which harbor resistance genes against them. Once identified these genes can be introduced in other plant of same species thus making them resistant. But transfer of these genes interspecifically has not been successful like transfer of tomato Hero A gene into potato did not result in resistance to potato cyst nematode (Sobczak, m et al., 2005). This may be because some other factors required for recognition of pathogen or in signaling pathway may not be present in another species. This has prompted us to identify those factors in order to make this technology useful.

Feeding site of nematode can be disrupted by inactivating it by gene silencing which can be done either by ribozyme or antisense constructs to target specific transcripts or one can design dominant negative mutations of gene to target protein. A nematode attempting to feed on cells varying nematode inducible promoter fused to a gene encoding one of these molecules would initiate gene expression resulting in the degradation of the feeding site.

There is another way of controlling nematodes i.e. by soaking infective juveniles in double stranded RNA corresponding to a gene which has to be silenced (Urwin, PE. et al., 2002; Rosso, M.N. et al., 2005; Chen, Q. et al., 2005).

Assaying gene expression on nematodes is very difficult because nematodes are buried deep inside the roots and moreover this gene silencing technology which has been mentioned above is short lived unlike the nematode cycle.

Cell walls are the entity which plays crucial role in defense so they can be the target of genetic engineering. We can introduce Avr gene in plant under the promoter activated by pathogen. Release of this product is at the cell wall. So when pathogen comes it will activate the gene and the elicitor of this Avr gene elicits the R-gene and hypersensitive reaction occurs. So artificially we are creating the condition where we can recognize pathogen earlier and thus less loss can occur.

In case of pathogen attack, pathogen releases some IAA which will activates production of more IAA by the host. This IAA in turn will activate expansions which will cause loosening of cell wall by breakdown of hydrogen bond between cell wall, thus making the job easier for pathogen to penetrate. If somehow we inactivate pathogen IAA then this whole phenomenon will not occur and this can thus help in curbing the entry of pathogen into the host cell.

Plants can be transformed with monoclonal antibodies called plantibodies which are single chain antibodies to specific stylet secretions or other components of the nematode in an attempt to block the establishment of a fedding site (Baum et al., 1996; Rosso et al., 1996).

A neutralizing gene that is constitutively expressed in the plants except the feeding structures can be incorporated (Sijmons et al., 1994)

Plants can be engineered with certain genes that have detrimental effect on namatodes like those encoding for proteinase inhibitor, collagenase (as the nematode cuticle is composed of collagen) or toxins.

Plants can be transformed with constructs designed to interrupt feeding cell development.


There has been extensive work on plant nematode interaction in the past decade which has given us the opportunity to understand their interaction in a much wider way. But still there is a lot more which has to be done to control these parasites in a manner so that they cannot damage plants. Gene silencing technology has lot more to promise and work is still going on in this area. To understand their interaction fully each and every component of the their interaction has to discovered then only we can move forward and see to it that we can transfer these Nem-R genes interspecifically to bring about the resistance in the susceptible host.

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