Lecture 6: Mechanisms of Resistance in Plants PDF

By Hala Eissa Nermin Gamal  ‫رؤية كلية التكنولوجيا الحيوية‬ ‫أن تكون كلية معتمدة اكاديميا و رائدة في‬ ‫مجاالت التكنولوجيا الحيوية علي المستوي‬ ‫المحلي واألقليمي والدولى ‪.‬‬  ‫رسالة كلية التكنولوجيا الحيوية‬ ‫تلتزم كلية التكنولوجيا الحيوية – جامعة مصر للعلوم والتكنولوج...

By Hala Eissa Nermin Gamal  ‫رؤية كلية التكنولوجيا الحيوية‬ ‫أن تكون كلية معتمدة اكاديميا و رائدة في‬ ‫مجاالت التكنولوجيا الحيوية علي المستوي‬ ‫المحلي واألقليمي والدولى ‪.‬‬  ‫رسالة كلية التكنولوجيا الحيوية‬ ‫تلتزم كلية التكنولوجيا الحيوية – جامعة مصر للعلوم والتكنولوجيا‬ ‫بتخريج اخصائي تكنولوجيا حيوية طبقا للمعايير االكاديمية المعتمدة‬ ‫يلبي احتياجات سوق العمل المحلي واالقليمي في القطاعات الطبيه‬ ‫والصيدالنية والزاعية والبيئية واجراء بحوث علمية مبتكرة وتقديم‬ ‫خدمات مجتمعية واستشارات علمية في اطار قيم ارتقائية ‪.‬‬  Intended Learning Outcomes a.11List the causal agents of plant diseases  Just as pathogens have evolved to colonise living plants, so plants have developed means to prevent or resist their presence. Because plants are unable to move to escape these challenges, they have developed many diverse and unique strategies, and as each mechanism is studied in greater detail, so new layers of complexity are uncovered.  Classical concepts of resistance Most plants are resistant to most microbes, and it is generally only specialist organisms that have evolved the capacity to overcome these defences, so that many pathogens have narrow host ranges.  Classical concepts of resistance Classically, there are two levels of resistance: Non-host resistance is where the entire plant species or genus is resistant and therefore not a host for the particular pathogen. For example, wheat is not infected by the potato late blight oomycete, P. infestans, so is a non host. Host resistance is where individuals within a species have developed genetically inherited ways of defending themselves against an organism that causes disease on other individuals within that plant species. For example, wheat is infected by yellow (stripe) rust, P. striiformis, but certain genotypes will be resistant to specific races of the fungus. Rust  Classical concepts of resistance Whilst useful as concepts, these classical definitions do little to help with understanding the underlying mechanisms, which will involve both the lack of capacity for the potential pathogen to colonise this plant species, combined with constitutive and inducible defences in the plant. Perhaps the vector for the pathogen does not feed on the particular species, or the organism does not have the necessary pathogenicity factors to penetrate the host and/or access nutrients from it. Perhaps the cuticle of the plant is too thick, or the innate immune response in the plant (analogous to similar non-self recognition systems present in all eukaryotes), is able to recognise and respond to non-specific elicitors from the pathogen.  Mechanisms of resistance in plants Mechanisms of resistance in plants can be subdivided into two categories, Passive Active (Constitutive) (Induced)  Mechanisms of resistance in plants Mechanisms of resistance in plants Passive mechanisms Active or inducible defence - Hypersensitive response Structural elements Phytoanticipins -Induction of specific gene expression  Mechanisms of resistance in plants Passive mechanisms involve both structural elements, such as the cuticle and root border cells, and pre-formed antimicrobial chemical compounds within the plant termed Phytoanticipins. These form the initial layers of protection against microbial attack. Active or inducible defence mechanisms, which include the hypersensitive response (local plant cell death) and induction of specific gene expression within the plant, including genes involved in cell wall strengthening and/or repairing structural defences, genes for biosynthesis of additional antimicrobial compounds, and localised induction of genes encoding hydrolytic enzymes and other defence-related proteins.  Mechanisms of resistance in plants In addition to the localised induction of defence responses, there are mechanisms that induce resistance in other parts of the plant through systemic signals, such as systemic acquired resistance (SAR) and induced systemic resistance (ISR). SAR is induced by pathogens and insects while ISR is mediated by beneficial microbes living in the rhizosphere, like bacteria and fungi.  Mechanisms of resistance in plants Furthermore, plants can signal to neighbouring plants through volatile compounds to enhance resistance in these plants.  Mechanisms of resistance in plants Preformed defences Structural barriers Root border cells Phytoanticipins Induced defences Local signals Programmed cell death (PCD) Induced structural barriers Phytoalexins Pathogenesis-related proteins Other defence-related proteins Post-transcriptional gene silencing (PTGS) Systemic resistance mechanisms ‘Communal’ resistance  The first passive barrier that defends plants against microbes is the wax layer present on the cuticle of leaves and fruits. This forms a water-repellent surface that prevents formation of water droplets necessary for bacterial ingress and fungal spore germination. Surface hairs on leaves possess a similar function. The thick cuticle, composed of cutin, cellulose and pectin, in combination Surface hairs with the tough walls on epidermal cells form an additional barrier against all pathogens apart from those fungi that have the necessary pathogenicity factors for direct penetration, and vectors that are potentially carrying pathogens.  This leaves natural openings such as stomata as the main weakness in structural defences, and whilst some fungi are able to force their way through closed stomata, others, such as the cereal rust fungi, have to wait for stomata to open. This can form an additional line of defence in plants and some resistant wheat varieties delay stomatal opening until late in the day so that any rust germ-tubes that are on the leaf surface following germination of urediospores the previous night desiccate.  Root tips that are rapidly elongating as they move towards nutrients and water in the soil are a major potential weakness in the structural defences of plants. This rapid growth of newly synthesised tissue through an environment with a high capacity to cause abrasive damage that is rich in potentially pathogenic microbes makes them extremely vulnerable to attack. In these cells, inducible defences such as programmed cell death of a few plant cells (as occurs in other parts of the plant including behind the root tips) would not be an effective defence since this would terminate root growth. Instead, root tips have developed a mechanism through which they surround themselves with large numbers of detached somatic cells termed root ‘border’ cells, that effectively guard the root tip from pathogen attack.  Production of these border cells is tightly regulated and may range from 12 per day in some plant species such as tobacco, to 10000 per day for others such as cotton. Once detached from the root, the metabolic activity of these cells increases and gene expression undergoes a global switch to produce anthocyanins and antimicrobial antibiotics. This, in combination with the production of a mucilage layer repels bacteria. The border cells also appear to produce chemical signals that attract fungal zoospores, essentially acting as decoys, so that the border cells become infected rather than the root tips, and there is evidence that they may perform a similar decoy role against nematode infestations.  Chemical barriers in plants have generally been classified as phytoanticipins or phytoalexins depending on whether they are preformed inhibitors of pathogens or synthesised de novo following pathogen attack. However, this distinction is somewhat arbitrary, since there are examples of compounds that may be preformed inhibitors in one plant species but induced in another. In other cases, it has not been possible to confirm that the compounds are at appropriate concentrations or locations in plants to be antimicrobial until induced.  Defence responses in plants can be induced by a number of factors and the exact nature of the response varies depending on what these are. There is evidence that some defences are induced by the physical presence of fungal spores on the leaf surface, whilst others require the pathogen to penetrate the surface before induction. Induction may be in response to non-specific elicitors, or may follow the classical gene-for-gene resistance model originally described by Oort and Flor in the 1940s, which is the mechanism underlying host resistance  This is essentially a highly evolved form of inducible resistance, in which the product of a specific resistance gene in the plant is involved in recognition of a specific elicitor from the pathogen. These induced resistance responses have many similarities to the responses that occur when plants are wounded, but they are not identical.  One of the first responses activated in many incompatible interactions prior to the induction of gene expression and protein synthesis is the production of reactive oxygen species (ROS) (also known as active oxygen species (AOS) or reactive oxygen intermediates (ROI)), production of nitric oxide (NO) and phosphorylation cascades. These are recognised as important signalling mechanisms in many organisms  a compatible interaction (successful infection leading to disease), or an incompatible interaction (successful plant defence).  One of the most visible responses of plants to pathogen attack is the hypersensitive response (HR), which is the localised death of plant cells. This is a temporally and spatially co-ordinated mechanism to limit the amount of host tissue lost to the pathogen, and one that restricts the ingress of biotrophic pathogens that require living cells as their source of nutrients. Programmed cell death (PCD) is a general term used to describe the induced cell suicide that occurs in organisms, and amongst the events that occur in the dying cell as part of PCD are membrane blebbing, chromatin condensation and DNA cleavage. These phenomena have been shown to occur as part of the hypersensitive response in plants  Plants have a number of inducible structural defences. The first of these is cytoskeleton-based to fend off attack from potential pathogens prior to penetration, involving sensing of the developing pathogen on the surface. At the site of contact, there is accumulation of cytoplasm and sometimes movement of the nucleus in plant cells, along with precise rearrangements of the plant microtubules in the cytoskeleton.  Formation of appositions referred to as papillae, consisting of callose (a β-1,3-glucan polymer) and phenolics, on the inner surface of cell walls, along with deposition of hydroxyproline-rich glycoproteins such as extensin, phenolic compounds such as lignin and suberin, and minerals such as silicon and calcium also occurs, and these become cross-linked to form insoluble defensive structures and an additional barrier against pathogen invasion and ingress. Blockage of plasmodesmata by callose is also believed to be a key defence against viruses inhibiting their movement. These same structural defences are induced by wounding of plants and in abscission although the signalling mechanisms in these cases are different.  Antimicrobial compounds include a diverse array of low-molecular-weight secondary metabolites (i.e. compounds that are not essential for basic metabolic processes in plants), and these generally act against a broad range of pathogens. They include terpenoid derivatives (e.g. sesquiterpenes); saponins; aliphatic acid derivatives; phenolics and phenylpropanoids (e.g. isoflavonoids); nitrogencontaining organic compounds (e.g. alkaloids); and sulphur-containing compounds including inorganic elemental sulphur. Most of these compounds are derived from the isoprenoid, phenylpropanoid, alkaloid or fatty acid/polyketide pathways, and some of the genes encoding enzymes involved in these pathways, such as phenylalanine ammonia-lyases (PAL) and chalcone synthases (CHS) have been shown to be induced in defence responses in association with the hyper-sensitive response.  In addition to programmed cell death, strengthening of structural defences and production of antimicrobial phytoalexins, various novel proteins are induced during pathogen attack, known collectively as the pathogenesis-related (PR) proteins. These proteins are expressed at low levels in healthy plants, but certain isozymes are induced during pathogen attack both locally and systemically, and there is evidence that specific sequences in the promoter regions of these genes are important for the induction. The proteins induced have been grouped into 14 PR classes.  Plants have a specific cytoplasmic defence mechanism (PTGS) that targets dsRNA for destruction, and since most plant viruses replicate in the cytoplasm via dsRNA intermediates, these are candidates for degradation by such a defence mechanism.  In addition to systemic signalling within plants and the induction of defences, recent evidence has shown that plants can communicate with their neighbouring plants and induce the activation of defence genes in these. Volatile signals such as methyl jasmonate and methyl salicylate are produced from insect- and pathogen- infested plants, and in laboratory experiments at least, have been shown to induce defence gene expression. For example, methyl jasmonates released from big sagebrush (Artemisia tridentate) following insect feeding were able to induce production of proteinase inhibitors in adjacent tomato plants, and reduce the numbers of insects feeding. Similarly, volatiles from lima bean leaves released following spider mite damage induced glucanase, chitinase, lipoxygenase and PAL gene expression in adjacent plants.  Methyl salicylate released from TMV-infected tobacco plants containing the N resistance gene induced PR-1 expression in adjacent plants and increased resistance to disease. However, the role of such signalling and gene induction in natural plant populations and crops is unclear and studies are currently in progress to determine the significance of volatile signals in disease resistance. One feature that has been noted is that the volatiles produced when herbivorous insects feed on plants can act as attractants for predatory insects that feed on these herbivorous species, and this is being developed into a means of controlling insect infestations on plants.  As well as activation of defence genes by pathogen invasion, it has been found that the formation of a hypersensitive response, either as part of pathogen invasion or through the action of necrosis-inducing pathogens, results in systemic resistance responses. Systemic acquired resistance (SAR) is one form of inducible resistance that is activated throughout the whole plant and this resistance has some similarities with animal immune responses, in that it is long-lasting and can be boosted by repeat infections, but unlike animal immunity it can be effective against organisms other than the one used to stimulate the initial response, conferring broad-spectrum resistance.  The spectrum of pathogens against which systemic resistance is effective remains constant for each plant species, irrespective of the nature of the inducing pathogen. However, this spectrum varies between species. SAR can therefore be considered to provide a characteristic ‘fingerprint of protection’, which has been useful in discriminating SAR from other resistance mechanisms. However, SAR is not effective against all pathogens. For example, tobacco cannot be protected against challenge by B. cinerea and P. syringae pv. tomato, and cucurbits cannot be protected from powdery mildew. The nature of the resistance induced has led to the concept that SAR acts to prime host cells for a more rapid future deployment of defences  The phenomenon of induced systemic resistance (ISR) is similar to SAR, in giving protection to normally virulent pathogens. However, rather than induction by phytopathogens, ISR is activated by plant growth-promoting rhizobacteria. It also appears to provide protection against pathogens such as B. cinerea and Alternaria brassicicola, for which SAR is ineffective and vice versa, but the nature of the genes induced is unclear. Nevertheless, evidence exists for overlap and also antagonism between the mechanisms regulating resistance in SAR and ISR, In addition, some necrotrophic pathogens induce a further form of systemic resistance, also via jasmonic acid and ethylene but independent of SAR and ISR.  Systemic and airborne resistance mechanisms in plants. SAR (systemic acquired resistance), ISR (induced systemic resistance) and volatile signals that are transmitted to neighbouring plants to induce resistance. Mechanisms of resistance in plants