The document discusses cell wall associated mechanisms of plant disease resistance and susceptibility. It describes how plants first recognize intruding pathogens based on nonself molecules in the apoplast. Plants then activate cell wall-associated defenses like inhibiting fungal cell wall degrading enzymes, secreting antimicrobial compounds, and strengthening the cell wall. It also examines how some virulent pathogens are able to suppress plant defenses and gain accommodation by reprogramming the host. Future research opportunities are identified in further elucidating genes involved in non-specific resistance at the cell wall using genetic approaches.
Plant Disease Resistant And Genetic EngineeringShweta Jhakhar
Study the adverse effects of different viruses and other fungal diseases on the plants and their growth. Discuss the methods e.g. plant disease resistant and genetic engineering to protect the plants.
plant pathogen interaction
different types of pathogens
gene for gene hypothesis
direct receptor model
Elicitor receptor model
suppersor repressor model
gaurd hypothesis
various pathogens attack and get established in plats causing several diseases. the attack of the pathogen on the host is by using mechanical force or by secreting varoius chemicals.. this powerpoint presentation is about the role of enzymes in plant pathogen attack
Includes definition, classification, history, formation, salient features, gene transfer( conjugation, transformation, transduction), antibiotic resistance, nutritional influence, quorum sensing, role in pathogenesis, and controversies.
Functional Genomics of Plant Pathogen interactions in Wheat Rust PathosystemSenthil Natesan
Cereal rust fungi are pathogens of major importance to agriculture, threatening cereal production worldwide. Targeted breeding for resistance, based on information from fungal surveys and population structure analyses of virulence, has been effective. Nevertheless, breakdown of resistance occurs frequently and continued efforts are needed to understand how these fungi overcome resistance and to determine the range of available resistance genes. The development of genomic resources for these fungi and their comparison has released a torrent of new ideas and approaches to use this information to assist pathologists and agriculture in general. The sequencing of gene transcripts and the analysis of proteins from haustoria has yielded candidate virulence factors among which could be defence-triggering avirulence genes. Genome-wide computational analyses, including genetic mapping and transcript analyses by RNA sequencing of many fungal isolates, will predict many more candidates (Bakkeren et al., 2012)
Dissecting the mechanisms of host-pathogen systems like wheat-rust, including pathogen counter-defenses will ensure a step ahead towards understanding current outcomes of interactions from a co-evolutionary point of view, and eventually move a step forward in building more durable strategies for management of diseases caused by fungi (Hadrami et al.,2012)
Microorganisms cause virtually all pathoses of the pulp and periapical tissues.
Once bacterial invasion of pulp tissues has taken place, both non-specific inflammation and specific immunologic response of the host have a profound effect on the progress of the disease.
Endodontic infection develops in root canals devoid of host defenses,
pulp necrosis (as a sequel to caries, trauma, periodontal disease,or iatrogenic operative procedures)
or pulp removal for treatment.
Biofilm-induced oral diseases.
ROUTES OF ROOT CANAL INFECTION
Caries
• Trauma-induced fractures
• Cracks
• Restorative procedures
• Scaling and root planing
• Attrition
• Abrasion
• Gaps in the cementoenamel junction
at the cervical root surface
• Dentinal tubules
• Direct pulp exposure
• Periodontal disease
• Anachoresis
Mechanisms of Microbial Pathogenicity and Virulence Factors
Pathogenicity : The ability of a microorganism to cause disease.
Virulence: Degree of pathogenicity of a microorganism.
Some microorganisms routinely cause disease in a given host and are called primary pathogens.
Other microorganisms cause disease only when host defenses are impaired and are called opportunistic pathogens by changing the balance of the host–bacteria relationship.
Bacterial strategies that contribute to pathogenicity include the ability to coaggregate and form biofilms.
In the pathogenesis of primary apical periodontitis
Bacteria in caries lesions form authentic biofilms adhered to dentin.
Diffusion of bacterial products through dentinal tubules induces pulpal inflammation
After pulp exposure, the exposed pulp tissue is in direct contact with bacteria and their products
and responds with severe inflammation. Some tissue invasion by bacteria may also occur.
Bacteria in the battlefront have to survive the attack from the host defenses and at the same time acquire nutrients to keep themselves alive.
In this bacteria–pulp clash, the latter invariably is “defeated” and becomes necrotic, so bacteria move forward and “occupy the territory”—that is, they colonize the necrotic tissue.
These events advance through tissue compartments, coalesce, and move toward the apical part of the canal until virtually the entire root canal is necrotic and infected.
At this stage, involved bacteria can be regarded as the early root canal colonizers or pioneer species (play an important role in the initiation of the apical periodontitis disease process, modify the environment, making it conducive to the establishment of other bacterial groups)
Plant Disease Resistant And Genetic EngineeringShweta Jhakhar
Study the adverse effects of different viruses and other fungal diseases on the plants and their growth. Discuss the methods e.g. plant disease resistant and genetic engineering to protect the plants.
plant pathogen interaction
different types of pathogens
gene for gene hypothesis
direct receptor model
Elicitor receptor model
suppersor repressor model
gaurd hypothesis
various pathogens attack and get established in plats causing several diseases. the attack of the pathogen on the host is by using mechanical force or by secreting varoius chemicals.. this powerpoint presentation is about the role of enzymes in plant pathogen attack
Includes definition, classification, history, formation, salient features, gene transfer( conjugation, transformation, transduction), antibiotic resistance, nutritional influence, quorum sensing, role in pathogenesis, and controversies.
Functional Genomics of Plant Pathogen interactions in Wheat Rust PathosystemSenthil Natesan
Cereal rust fungi are pathogens of major importance to agriculture, threatening cereal production worldwide. Targeted breeding for resistance, based on information from fungal surveys and population structure analyses of virulence, has been effective. Nevertheless, breakdown of resistance occurs frequently and continued efforts are needed to understand how these fungi overcome resistance and to determine the range of available resistance genes. The development of genomic resources for these fungi and their comparison has released a torrent of new ideas and approaches to use this information to assist pathologists and agriculture in general. The sequencing of gene transcripts and the analysis of proteins from haustoria has yielded candidate virulence factors among which could be defence-triggering avirulence genes. Genome-wide computational analyses, including genetic mapping and transcript analyses by RNA sequencing of many fungal isolates, will predict many more candidates (Bakkeren et al., 2012)
Dissecting the mechanisms of host-pathogen systems like wheat-rust, including pathogen counter-defenses will ensure a step ahead towards understanding current outcomes of interactions from a co-evolutionary point of view, and eventually move a step forward in building more durable strategies for management of diseases caused by fungi (Hadrami et al.,2012)
Microorganisms cause virtually all pathoses of the pulp and periapical tissues.
Once bacterial invasion of pulp tissues has taken place, both non-specific inflammation and specific immunologic response of the host have a profound effect on the progress of the disease.
Endodontic infection develops in root canals devoid of host defenses,
pulp necrosis (as a sequel to caries, trauma, periodontal disease,or iatrogenic operative procedures)
or pulp removal for treatment.
Biofilm-induced oral diseases.
ROUTES OF ROOT CANAL INFECTION
Caries
• Trauma-induced fractures
• Cracks
• Restorative procedures
• Scaling and root planing
• Attrition
• Abrasion
• Gaps in the cementoenamel junction
at the cervical root surface
• Dentinal tubules
• Direct pulp exposure
• Periodontal disease
• Anachoresis
Mechanisms of Microbial Pathogenicity and Virulence Factors
Pathogenicity : The ability of a microorganism to cause disease.
Virulence: Degree of pathogenicity of a microorganism.
Some microorganisms routinely cause disease in a given host and are called primary pathogens.
Other microorganisms cause disease only when host defenses are impaired and are called opportunistic pathogens by changing the balance of the host–bacteria relationship.
Bacterial strategies that contribute to pathogenicity include the ability to coaggregate and form biofilms.
In the pathogenesis of primary apical periodontitis
Bacteria in caries lesions form authentic biofilms adhered to dentin.
Diffusion of bacterial products through dentinal tubules induces pulpal inflammation
After pulp exposure, the exposed pulp tissue is in direct contact with bacteria and their products
and responds with severe inflammation. Some tissue invasion by bacteria may also occur.
Bacteria in the battlefront have to survive the attack from the host defenses and at the same time acquire nutrients to keep themselves alive.
In this bacteria–pulp clash, the latter invariably is “defeated” and becomes necrotic, so bacteria move forward and “occupy the territory”—that is, they colonize the necrotic tissue.
These events advance through tissue compartments, coalesce, and move toward the apical part of the canal until virtually the entire root canal is necrotic and infected.
At this stage, involved bacteria can be regarded as the early root canal colonizers or pioneer species (play an important role in the initiation of the apical periodontitis disease process, modify the environment, making it conducive to the establishment of other bacterial groups)
Enzybiotics New era of antimicrobials.pptMedhavi27
In the current era of emergence of resistance against traditionally used antibiotics researchers are trying to devise treatment strategies to combat resistant infections. Phage derived lysins are such effective and alternative antimicrobials which kill bacteria with very low chances of developing resistance.
The mouth, like all external surfaces of the body and the gut,
has a substantial microflora living in symbiosis with a healthy
host.
• The microflora of the mouth contains hundreds of species of
aerobic and anaerobic bacteria.
• Cultural studies indicate that more than 500 distinct microbial
species can be found in dental plaque.
5
• Although bacteria are necessary for periodontal disease to
take place, a susceptible host is also needed.
• The immune-inflammatory response that develops in the
gingival and periodontal tissues in response to the chronic
presence of plaque bacteria results in destruction of
structural components of the periodontium leading,
ultimately, to clinical signs of periodontitis.
6
• The host response is essentially protective, but both
hyporesponsiveness and hyper-responsiveness of certain
pathways can result in enhanced tissue destruction (Bruce
Pihlstrom 2005 ).
• Closer investigations of the destructive pathway of periodontal
disease began to focus on the relation-ship between bacteria
and the host response in the initiation and progression of
periodontal disease.
7
• This shift in etiological theory produced a paradigm that
called attention to the fact that although microorganisms are
the cause of periodontitis, the clinical expression of the disease
depends on how the host responds to the extent and virulence
of the microbial burden.
• It was found that degradation of host tissue results from this
bacterial-host interaction.
In plants some structures are already present to defend the attack while in others, the structures to defend the host develops after the infection. In this way, structural defense can be characterized as
Richard's aventures in two entangled wonderlandsRichard Gill
Since the loophole-free Bell experiments of 2020 and the Nobel prizes in physics of 2022, critics of Bell's work have retreated to the fortress of super-determinism. Now, super-determinism is a derogatory word - it just means "determinism". Palmer, Hance and Hossenfelder argue that quantum mechanics and determinism are not incompatible, using a sophisticated mathematical construction based on a subtle thinning of allowed states and measurements in quantum mechanics, such that what is left appears to make Bell's argument fail, without altering the empirical predictions of quantum mechanics. I think however that it is a smoke screen, and the slogan "lost in math" comes to my mind. I will discuss some other recent disproofs of Bell's theorem using the language of causality based on causal graphs. Causal thinking is also central to law and justice. I will mention surprising connections to my work on serial killer nurse cases, in particular the Dutch case of Lucia de Berk and the current UK case of Lucy Letby.
What is greenhouse gasses and how many gasses are there to affect the Earth.moosaasad1975
What are greenhouse gasses how they affect the earth and its environment what is the future of the environment and earth how the weather and the climate effects.
Slide 1: Title Slide
Extrachromosomal Inheritance
Slide 2: Introduction to Extrachromosomal Inheritance
Definition: Extrachromosomal inheritance refers to the transmission of genetic material that is not found within the nucleus.
Key Components: Involves genes located in mitochondria, chloroplasts, and plasmids.
Slide 3: Mitochondrial Inheritance
Mitochondria: Organelles responsible for energy production.
Mitochondrial DNA (mtDNA): Circular DNA molecule found in mitochondria.
Inheritance Pattern: Maternally inherited, meaning it is passed from mothers to all their offspring.
Diseases: Examples include Leber’s hereditary optic neuropathy (LHON) and mitochondrial myopathy.
Slide 4: Chloroplast Inheritance
Chloroplasts: Organelles responsible for photosynthesis in plants.
Chloroplast DNA (cpDNA): Circular DNA molecule found in chloroplasts.
Inheritance Pattern: Often maternally inherited in most plants, but can vary in some species.
Examples: Variegation in plants, where leaf color patterns are determined by chloroplast DNA.
Slide 5: Plasmid Inheritance
Plasmids: Small, circular DNA molecules found in bacteria and some eukaryotes.
Features: Can carry antibiotic resistance genes and can be transferred between cells through processes like conjugation.
Significance: Important in biotechnology for gene cloning and genetic engineering.
Slide 6: Mechanisms of Extrachromosomal Inheritance
Non-Mendelian Patterns: Do not follow Mendel’s laws of inheritance.
Cytoplasmic Segregation: During cell division, organelles like mitochondria and chloroplasts are randomly distributed to daughter cells.
Heteroplasmy: Presence of more than one type of organellar genome within a cell, leading to variation in expression.
Slide 7: Examples of Extrachromosomal Inheritance
Four O’clock Plant (Mirabilis jalapa): Shows variegated leaves due to different cpDNA in leaf cells.
Petite Mutants in Yeast: Result from mutations in mitochondrial DNA affecting respiration.
Slide 8: Importance of Extrachromosomal Inheritance
Evolution: Provides insight into the evolution of eukaryotic cells.
Medicine: Understanding mitochondrial inheritance helps in diagnosing and treating mitochondrial diseases.
Agriculture: Chloroplast inheritance can be used in plant breeding and genetic modification.
Slide 9: Recent Research and Advances
Gene Editing: Techniques like CRISPR-Cas9 are being used to edit mitochondrial and chloroplast DNA.
Therapies: Development of mitochondrial replacement therapy (MRT) for preventing mitochondrial diseases.
Slide 10: Conclusion
Summary: Extrachromosomal inheritance involves the transmission of genetic material outside the nucleus and plays a crucial role in genetics, medicine, and biotechnology.
Future Directions: Continued research and technological advancements hold promise for new treatments and applications.
Slide 11: Questions and Discussion
Invite Audience: Open the floor for any questions or further discussion on the topic.
A brief information about the SCOP protein database used in bioinformatics.
The Structural Classification of Proteins (SCOP) database is a comprehensive and authoritative resource for the structural and evolutionary relationships of proteins. It provides a detailed and curated classification of protein structures, grouping them into families, superfamilies, and folds based on their structural and sequence similarities.
This pdf is about the Schizophrenia.
For more details visit on YouTube; @SELF-EXPLANATORY;
https://www.youtube.com/channel/UCAiarMZDNhe1A3Rnpr_WkzA/videos
Thanks...!
In silico drugs analogue design: novobiocin analogues.pptx
Cell Wall Associated Mechanisms of Disease Resistance & Susceptibility
1. Cell Wall Associated Mechanisms of
Disease Resistance & Susceptibility
Master’s Seminar (APP-600)
Speaker : Pradeep Negi
ID No : 50939
2. Contents
1. Introduction
2. Cell Wall In Plant Recognition And Signalling
a. Recognition Of The Intruder
b. Elicitor-binding Host Proteins
c. Signal Transduction For Cell Wall Defences
3. Cell Wall In Plant Defence
a. Poisoning The Apoplast
b. Plant Cell Wall Strengthening
c. Trafficking Of Defence Compounds
4. The Plant’s Contribution To Fungal Accommodation
5. Summary
6. Future Issues
2
3. 3
• Plant defence system : cell wall,
waxes, hairs, antimicrobial
enzymes, and secondary
metabolites.
Introduction
4. • Pathogens penetrate plant apoplast.
• They possess a range of enzymatic and/or physical tools.
• Nonself recognition operates.
• Recognition induces apoplastic defence.
• HR + cell death.
4
6. • Pathogens circumvent recognition or suppress host defence.
• Special feeding structures or intracellular accommodation.
• CW is significant in basal resistance.
• How plants defend themselves and how pathogens cope with
such defence ?
6
14. Examples :
a) AvrPto, AvrPtoB, AvrE, and HopPtoM, effectors of P. syringae,
suppress callose deposition (Ammouneh et al., 2006).
b) Fusarium trichothecene toxins suppress wall-associated
defence in wheat (Maier, 2005).
• Fungi avoid chitin recognition by chitin-deacetylation
(Deising, 2002).
14
15. Elicitor-Binding Host Proteins
• Still poorly understood.
• WAK are RLK and play role in recognition.
• Associated with pectin and glycine-rich cell wall proteins
(Kohorn, 2001).
• Act as cell wall guardian.
• Arabidopsis RFO1 gene, against Fusarium oxysporum, has been
cloned, it codes for a WAK (Ausubel, 2005).
15
16. Signal Transduction for Cell Wall Defences
• It is initiated by cell surface receptors.
• ROS induced signalling includes MAP kinases, Ca2+ influx,
activation of transcription factors (Miedema et al., 2003).
• Transcription factors leads to defence gene expression (Somssich,
2002).
• Ca2+ influx influence cell wall rigidity (Kogel, 2004).
16
17. 17
Schematic overview of some events occurring in apoplast during
plant pathogen interactions
- Delaunois et al. (2014)
18. • In defence gene expression, phytoalexin production, HR + cell
death (Scheel, 1997).
• Protein antioxidants control levels of ROS (Foyer, 2002).
• Nitric Oxide regulates HR, defense gene expression and
penetration resistance (Lamb, 2001).
18
Reactive Oxygen Species are a key player…
19. 19
CLSM image of localized Nitric
Oxide generation in susceptible
barley epidermal cells at appresorial
germ tube contact site.
21. Poisoning the Apoplast
a) Inhibition of cell wall degrading enzymes.
b) Structural remodelling of the cell wall at sites of attempted
penetration.
c) Killing of potential intruders by antimicrobial means.
21
22. A. Inhibitors of Cell Wall Degrading Enzymes
• Inhibitors such as the Xylanase Inhibtors and Polygalacturonase Inhibitor
Proteins (PGIPs).
• PGIPs produces OGAs that are sensed as DAMPs (Federici et al., 2006).
• PGIPs : protecting function and communication function as well (Cervone,
2006).
22
23. B. Structural Remodelling
23
Actin filament reorganization around a
CWA at 20 h after
inoculation of barley with Bgh.
Non-successful penetration attempt of
B. graminis on barley.
- Huckelhoven (2007)
24. • Agents : Phytoalexins and Phytoanticipins.
• Antimicrobial proteins act synergistically.
• Phytoalexins : penetration resistance + induced CW mechanical
strengthening.
E.g. Barley mlo mutants are resistant to penetration by B. graminis, as
they produce p-coumaroyl-hydroxyagmatine. (Parr, 1998)
24
C. Killing Potential Intruders By Antimicrobial Means
25. • Cell wall–bound phenolics restrict fungal penetration.
• Toxic compounds as glucosides.
• Aglycons poison the pathogen.
• E.g. Sorghum bicolor produces fungitoxic 3-
desoxyanthocyanodin flavonoids against Colletotrichum
species (Nicholson, 1990).
25
26. Plant Cell Wall Strengthening
• Cell wall appositions.
• Local deposition of chemically modified cell wall material for
penetration resistance.
• Lignification.
• Lignified cell wall is less accessible to CWDE.
• Cell wall-bound phenolics accumulation.
26
27. 27
Cell wall dynamics in
case of necrotrophic
fungal attack
- Bellincampi et al. (2014)
28. 28
Cell wall dynamics in
case of biotrophic
fungal attack
- Bellincampi et al. (2014)
29. • H 𝟐O2 in cell wall–associated defence
• Peroxidase-dependent lignification + protein cross-
linking in the cell wall.
• Attack induces it, which reside in CWAs.
29
Continued...
30. • H 𝟐O2 presence in CWAs is a biochemical marker.
E.g. interaction of barley with B. graminis.
• Its removal enhances fungal penetration.
• It helps in cross-linking of proline-rich proteins in
the cell wall & makes resistant to CWDE.
30
31. • Speed of CW material deposition and its compaction are
significant.
E.g. Wild-type Arabidopsis attacked by B. graminis or
Colletrotrichum truncatum builds CWAs more quickly compared to
syntaxin mutant pen1 (Zimmerli et al., 2004).
• Callose as a defence compound.
• Reduced cellulose content by mutation of cellulose synthase
CESA3, makes Arabidopsis more resistant to different PM
pathogens (Cano-Delgado et al., 2003).
31
32. Trafficking of Defence Compounds
• Requires dynamic changes in membranes and cytoskeleton.
• Depends on local elicitor perception or mechanical pressure.
• The cytoskeleton and the endomembrane system are
dramatically rearranged.
E.g. In barley, cells attacked by B. graminis, the cytoskeleton
rapidly reorganizes during fungal attack.
32
33. • Golgi-derived vesicles are required for secretion of defence
related compounds into the apoplast.
• Together, transporter-mediated and Golgi-mediated secretion
allocate materials for extracellular defence.
33
35. The Plant’s Contribution to Fungal Accommodation
• Virulent pathogens bypass or suppress plant defence.
• They suppress host responses to infection and reprogram the host.
• Like when haustoria-forming or arbuscule-forming mycorrhizal
fungi enter plant cells, symbiosis-related arrays starts to support
pathogenesis.
• Fungal hypha doesn't simply force the host cell to rebuild, but rather
the host recognizes the friendly intruder.
35
36. Summary
• Basal defense reactions to directly invading fungi often operate at the plant cell
wall.
• The invading pathogen is first recognized based on recognition of nonself
molecules and nonself activities at the cell periphery.
• Cell wall–associated defence appears to operate via inhibition of fungal cell wall–
degrading enzymes, secretion of fungitoxic peptides and phytoalexins, and cell
wall strengthening.
36
37. FUTURE ISSUES
• Genetic approaches will identify several genes that are key to nonspecific
disease resistance established at the cell wall.
• Future genetic screenings will provide deeper insight into resistance and
susceptibility to cell wall–penetrating fungal pathogens.
• Genetic redundancies of defence-associated proteins challenge plant
pathologists and will require sophisticated approaches to study gene
function in resistance.
37
The frontline of the plant defence system consists of physical and chemical barriers such as the cell wall, waxes, hairs, antimicrobial enzymes, and secondary metabolites.
If these obstacles are overcome, the pathogen is still confronted by elaborate surveillance systems in which molecular sentinels operate to activate resistance responses.
Most pathogens penetrate plant apoplast to access intracellular nutrients.
Bacterial and fungal pathogens possess a range of enzymatic and/or physical tools.
In plant-microbe interactions, nonself recognition operates via perception of microbial molecules or by surveillance of host cellular intactness.
On recognition, the plant induces apoplastic defence to inhibit microbial enzymes, for cell wall strengthening, or for poisoning the pathogen.
The second layer of defence i.e. HR including cell death restricts pathogens in an area.
Pathogens have evolved more sophisticated virulence strategies to circumvent recognition or to suppress host defence.
Sometime they develop special feeding structures in intact host cells or become actively engulfed for intracellular accommodation.
Cell wall-associated plant defence is important in basal resistance.
Recent evidences has shown how plants defend themselves at their periphery and how microorganisms cope with such defence.
During host invasion, pathogens release nonspecific exogenous and endogenous elicitors, such as oligomeric or monomeric fragments of both the cuticle and the cell wall.
Recognition occurs because the elicitors indicate nonself activity in the apoplast.
Cutin derivatives are able to elicit plant defence responses and prime plants for further responsiveness to pathogen-derived elicitors (Riederer et al., 1998).
Cell wall fragments derived from enzymatic activities have elicitor function or alternative defence-suppressing effects (Kogel, 1992).
Plants recognize nonself activity and nonself molecules such as bacterial lipopolysaccharides or flagellin, fungal chitin, or elicitins from Phytophthora species such as cryptogein in their apoplast.
Receptor-like kinases contribute to detection of conserved nonself molecules (Staskawicz, 2006).
A paradigm of general nonself recognition in plants is perception of bacterial flagellin in Arabidopsis (Jones et al., 2004).
Figure: Bacterial disease resistance is determined by flagellin perception. a, A FLS2 loss-of-function mutation, fls2-17, leads to enhanced disease susceptibility. Left: wildtype and fls2-17 mutant plants were sprayed with Pst DC3000 bacteria or with water and photographed 4 days later. Right: symptoms after 4 days in a series of leaves of decreasing age.
B: Number of Pst DC3000 bacteria extracted from wild-type (open bars) and fls2-17 mutant plants (filled bars) 4 days after infection. Leaves were grouped by age as depicted on the left.
C: A gain-of-function transgene of FLS2 leads to decreased susceptibility in the accession Wassilewskaya (Ws-0), which lacks a functional FLS2 gene. Ws-0 was stably transformed with FLS2p::FLS2-3xmyc or SIRKp::GUS as a control. Plants were sprayed with 5 x 10^8 c.f.u. ml Pst DC3000, or water.
AvrPto, AvrPtoB, AvrE, and HopPtoM, effectors of Pseudomonas syringae, are able to suppress cell wall–associated callose (β-1,3-glucan) deposition (Ammouneh et al., 2006). Bacterial speck Pseudomonas syringae pv. tomato
Fusarium trichothecene toxins contribute to suppression of wall-associated defense in wheat (Maier, 2005).
Plants seem to have evolved recognition tools for nonself patterns, which are indispensable for microbial protein function.
Nonspecific elicitors often derive from the fungal cell wall (Lecourieux et al., 2006).
It is commonly believed that plant defence–related chitinases boost nonspecific defence by releasing elicitor-active chitin oligomers.
In contrast, pathogenic fungi have evolved mechanisms to avoid chitin recognition by chitin-deacetylation (Deising, 2002).
chitin deacetylase is an enzyme that catalyzes the chemical reaction
chitin + H2O > chitosan + acetate Thus, the two substrates of this enzyme are chitin and H2O, whereas its two products are chitosan and acetate.
This enzyme belongs to the family of hydrolases, those acting on carbon-nitrogen bonds other than peptide bonds, specifically in linear amides.
Still poorly understood.
Their association with pectin and glycine-rich cell wall proteins makes them attractive candidates for cell wall guardians that communicate with the cytoplasm (Kohorn, 2001).
Recently, the Arabidopsis RFO1 gene, conferring quantitative resistance against Fusarium oxysporum, has been cloned, and it codes for a wall-associated kinase (Ausubel, 2005). WAK, wall-associated kinases are a family of protein kinases that connect the innermost portion of the cell (the cytoplasm) to the cell wall.
It has been hypothesized that these kinases are important in communication from the inside of the cell (including most importantly the nucleus) to the surrounding environment including other cells.
The WAKs are known to be receptor-like in nature, pointing to a possible role in cell communication.
Signal transduction (also known as cell signaling) is the transmission of molecular signals from a cell's exterior to its interior. Signals received by cells must be transmitted effectively into the cell to ensure an appropriate response. This step is initiated by cell-surface receptors.
Many transcription factors are involved in nonspecific fungal and oomycete elicitor signal transduction leading to defence gene expression (Somssich, 2002).
Transcription factors are proteins involved in the process of converting, or transcribing, DNA into RNA. The function is to regulate - turn on and off - genes in order to make sure that they are expressed in the right cell at the right time and in the right amount throughout the life of the cell and the organism. GTFs are TFIIA, TFIIB, TFIID
Ca2+ influx into the cytoplasm might influence cell wall rigidity due to the role of Ca2+ in noncovalent cell wall cross-linking (Kogel, 2004). Calcium ions are important for cellular signalling, as once they enter the cytosol of the cytoplasm they exert allosteric regulatory effects on many enzymes and proteins.
ROS-induced signalling includes MAP kinases, Ca2+ influx, activation of transcription factors and salicylic acid accumulation (Miedema et al., 2003).
A type of unstable molecule that contains oxygen and that easily reacts with other molecules in a cell. A build up of reactive oxygen species in cells may cause damage to DNA, RNA, and proteins, and may cause cell death. Reactive oxygen species are free radicals. Also called oxygen radical.. Examples include peroxides, superoxide, hydroxyl radical, and singlet oxygen. important roles in cell signalling. during times of environmental stress (e.g., UV or heat exposure), ROS levels can increase dramatically.[2] This may result in significant damage to cell structures.
A mitogen-activated protein kinase (MAPK or MAP kinase) is a type of protein kinase that is specific to the amino acids serine and threonine (i.e., a serine/threonine-specific protein kinase). MAPKs are involved in directing cellular responses to a diverse array of stimuli, such as mitogens, osmotic stress, heat shock and proinflammatory cytokines.
In defence gene expression, phytoalexin production, and both HR and restriction of pathogen-induced cell death (Scheel, 1997)..
NO regulates HR, defense gene expression, penetration resistance, and other resistance responses (Lamb, 2001). (NO) is another signal that activates defense responses after pathogen attack. NO has been shown to play a critical role in the activation of innate immune . Innate immunity refers to nonspecific defense mechanisms that come into play immediately or within hours of an antigen's appearance in the body. These mechanisms include physical barriers such as skin, chemicals in the blood, and immunesystem cells that attack foreign cells in the body.
The apoplast contains several lowmolecular- weight and protein antioxidants, which control levels of ROS (Foyer, 2002).
C-PTIO > 2-4-carboxyphenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide
SNP > Sodium nitroprusside
There are three ways by which plants protect their cell walls from pathogenic penetration:
inhibition of cell wall–degrading enzymes
structural remodeling of the cell wall at sites of attempted penetration
killing of potential intruders by antimicrobial means
Plants counter the savage enzyme cocktails by producing proteinaceous inhibitors of cell wall degrading enzymes such as the xylanase inhibitors and PG inhibitor proteins (PGIPs)
PGIPs are not to inhibit pectin degradation entirely, but to shift it toward producing longer OGAs (Oligo Galacturonic acid) that can be sensed as DAMPs (Federici et al., 2006).
Polygalacturonase inhibiting proteins combine a cell wall–protecting function with a function in communication with the symplast by forcing fungal enzymes to release signals (Cervone, 2006).
For Fig 1: Actin filament (green phalloidin-Alexa-488 labeling) reorganization around a CWA (autofluorescence displayed in red) at 20 h after
inoculation of barley with Bgh.
For Fig 2: Formation of the central CWA at 24 h after inoculation is accompanied by neighboring vesicle-like bodies. Structures are brownish stained by 3,3-diamnobenzidine for H2O2
Plant antimicrobial agents are low molecular-weight compounds such as induced phytoalexins and constitutive phytoanticipins, respectively, as well as antimicrobial proteins.
Antimicrobial proteins act synergistically to hinder fungal growth in the apoplast but are insufficient to achieve complete resistance.
Phytoalexins are crucial for penetration resistance together with induced mechanical strengthening of the cell wall. E.g. barley mlo mutants, which are resistant to penetration by B. graminis, overproduce p-coumaroyl-hydroxyagmatine which has antifungal activity and inhibits haustorium formation in vivo.
Cell wall– bound phenolics also accumulate locally to restrict fungal penetration. Ex chlorogenic acids, ferulic acids
Accumulation of soluble and wall-bound indolic metabolites such as indole-3-carboxylic acid or camalexin seems important in interactions of Arabidopsis and other plant species with pathogens.
Toxic compounds are often stored in plants as harmless glucosides. Hydrolytic enzymes cleave the glucosides, and the emerging aglycons poison the pathogen. A glucoside is a glycoside that is derived from glucose. Glucosides are common in plants,. aglycon, is the compound remaining after the glycosyl group on a glycoside is replaced by a hydrogen atom
Sorghum bicolor produces fungitoxic 3-desoxyanthocyanodin flavonoids in a site specific manner when attacked by Colletotrichum species (Nicholson, 1990).
Flavonoids are a group of plant metabolites thought to provide benefits through cell signalling pathways and antioxidant effects
Definitive evidence for the importance of structural and chemical strengthening of the cell wall in penetration resistance is rare.
Cell wall appositions are built in both compatible and incompatible interactions of plants and fungi. Cell wall apposition r cell wall material deposited at sites of microbial attack that differs in chemical and mechanical features from the normal cell wall
Local deposition of chemically modified cell wall material is crucial for penetration resistance.
Lignification makes the cell wall more resistant to mechanical pressure applied during penetration by fungal appressoria.
Lignified cell wall is water resistant and thus less accessible to cell wall–degrading enzymes. Soluble and cell wall-bound phenolics accumulate in plant tissue challenged by fungal pathogens.
NO and H2O2 might thus be potent messengers in cell wall–associated defence.
ROS are key molecules in signaling and the biochemistry of nonspecific plant defence. H2O2 is required for peroxidase-dependent lignification and for protein cross-linking in the cell wall. Attack by fungal pathogens induces peroxidases, which reside in CWAs.
The presence of H2O2 in CWAs is a biochemical marker that distinguishes non penetrated from penetrated cells in the interaction of barley with B. graminis. The importance of H2O2 for resistance to basal penetration is supported by the observation that enzymatic removal of H2O2 enhances the success of fungal penetration on leaf epidermal cells.
Likewise, H2O2 contributes to cross-linking of proline-rich proteins in the cell wall, which makes it more resistant to cell wall–degrading enzymes.
NO and H2O2 might thus be potent messengers in cell wall–associated defence.
ROS are key molecules in signaling and the biochemistry of nonspecific plant defence. H2O2 is required for peroxidase-dependent lignification and for protein cross-linking in the cell wall. Attack by fungal pathogens induces peroxidases, which reside in CWAs.
The presence of H2O2 in CWAs is a biochemical marker that distinguishes non penetrated from penetrated cells in the interaction of barley with B. graminis. The importance of H2O2 for resistance to basal penetration is supported by the observation that enzymatic removal of H2O2 enhances the success of fungal penetration on leaf epidermal cells.
Likewise, H2O2 contributes to cross-linking of proline-rich proteins in the cell wall, which makes it more resistant to cell wall–degrading enzymes.
In addition to the chemical nature of altered cell wall material that is deposited against an invading pathogen, the speed of deposition and of compaction might be crucial for successful defence.
Wild-type Arabidopsis attacked by B. graminis or Colletrotrichum truncatum builds CWAs more quickly when compared to the syntaxin mutant pen1, which is defective in nonhost penetration resistance to B. graminis.
Callose may still be a defence compound though it is not sufficient for penetration resistance. Callose is a plant polysaccharide. It is composed of glucose residues linked together through β-1,3-linkages, and is termed a β-glucan. It is thought to be manufactured at the cell wall by callose synthases and is degraded by β-1,3-glucanases.
A reduced cellulose content by mutation of cellulose synthase CESA3, involved in primary cell wall formation, leads to production of lignin, and makes Arabidopsis more resistant to different powdery mildew pathogens (Cano-Delgado et al., 2003).
Transport and secretion of defence compounds require dynamic changes in membranes and the cytoskeleton. Cytoskeleton is A microscopic network of protein filaments and tubules in the cytoplasm of many living cells, giving them shape and coherence.
Cytoplasmic reorganization depends on filamentous actin and on microtubules. The direction of polarization and the amount of cell wall–associated defences may thereby depend on local elicitor perception or mechanical pressure.
The cytoskeleton and the endomembrane system are dramatically rearranged and polarized when plants are attacked by fungal pathogens.
An intact actin cytoskeleton is also required for penetration resistance of barley, Arabidopsis, and tobacco to leaf pathogens.
Fungal attack also influences the endomembrane system. Golgi-derived vesicles are likely required for secretion of defence related compounds into the apoplast.
Together, transporter-mediated secretion, Golgi-mediated secretion, and endosome-mediated secretion may collaborate to allocate materials for extracellular defence.
In barley cells attacked by B. graminis, the cytoskeleton rapidly reorganizes from nonpolar to focused polarized patterns during fungal attack. This is particularly evident in nonhost interactions and less obvious in compatible interaction of barley and B. graminis.
Transport mediated by a membrane transport protein. There are three types of mediated transport: uniport, symport, and antiport.
Monolignols are phytochemicals acting as source materials for biosynthesis of both lignans and lignin. lignans are a large group of polyphenols found in plants. Some examples of lignans are enterolignans, enterodiol and enterolactone.
Nonself recognition and effective defense mechanisms are common in plants interacting with most potential pathogens. Therefore, successful pathogens need to bypass or to suppress plant defense in order to be virulent. It is well established that microbial virulence factors are active in suppressing host responses to infection and in reprogramming the host
When haustoria-forming or arbuscule-forming mycorrhizal fungi enter plant cells, the actin cytoskeleton and the endomembrane system reorganize and build pathogenesis-related or symbiosis-related arrays to support pathogenesis.
Hence, an invading fungal hypha does not simply force the host cell to rebuild, but rather the host recognizes the friendly intruder.