How pathogens attack plants?

Host-Pathogen Interaction

The interaction between a plant host and a pathogen is a complex relationship determined by the pathogen's ability to infect and the host's ability to defend itself.

• Compatible Interaction: 

• This occurs when a pathogen successfully infects a susceptible host, leading to disease. 
• The pathogen can overcome the plant's defenses, grow, and reproduce. 
• Example: Infection of a susceptible wheat variety by the fungus Puccinia triticina, which causes leaf rust.

• Incompatible Interaction: 

• This is a resistant reaction where the pathogen is unable to establish a successful infection. 
• The plant's defenses are strong enough to prevent the pathogen from growing, and no disease symptoms develop. 
• Example: A resistant wheat variety may recognize the Puccinia triticina fungus and trigger a rapid defense response, preventing the infection from spreading.

Pathogen Attack Mechanisms

Pathogens employ a series of strategies to attack and infect their host, which can be broken down into three stages.

A. Pre-Penetration Stage

Pathogens navigate towards a host plant using various cues.

• Chemotaxis: Pathogens are attracted to specific chemicals secreted by the host plant. For example, sugars and amino acids released by a host can attract the zoospores of fungi like Pythium.

• Electrotaxis: Host plants generate a flow of electric currents from their cells, which can guide pathogens.

• Rheotaxis: Pathogens, particularly zoospores, can move through water currents, and if their speed matches the water flow, they can find and attack a host.

B. Penetration Stage

Once at the host surface, pathogens penetrate the plant through natural openings, wounds, or by direct penetration.

1. Natural Openings:

   • Stomata: Bacteria can swim in a film of water on the leaf surface and enter the stomatal cavity. Fungi, like those causing rust, can form a specialized structure called an appressorium that precisely aligns over the stoma before sending a hypha into the leaf.

   • Lenticels: These are pores on fruits, stems, and tubers that provide easy entry for pathogens, such as the bacterium Streptomyces scabies, which causes potato scab.

   • Hydathodes: These pores on leaf margins and tips secrete nutrient-rich guttation fluid, which pathogens like Xanthomonas campestris pv. campestris (black rot of cabbage) can use to enter the plant.

   • Nectaries: Nectar-secreting glands in flowers are exploited by pathogens like Erwinia amylovora (fire blight of apple and pear) for entry.

2. Wounds: 

• Injuries caused by weather, insects, or farming equipment create openings that bypass the plant's natural defenses. 
• Most viruses, for example, rely on wounds created by insect vectors for transmission.

       3. Direct Penetration: 

This method relies on both mechanical pressure and enzymatic degradation to break through the host's surface.

A. Cutinases: 

• The first line of defense a pathogen encounters is the cuticle, a waxy layer on the plant's surface.
• Pathogens secrete cutinases and non-specific esterases to break down cutin, the primary component of the cuticle, allowing the pathogen to reach the cell wall.
• Cutin esterase catalyzes the hydrolysis of ester bonds occurring between free hydroxyl and carboxyl groups of cutin.
• Carboxycutin peroxidase catalyzed the hydrolysis of peroxide groups of cutin. 

B. Pectinases: 

• The pathogen then targets the cell wall. 
• Pectinases are a class of enzymes that degrade pectic substances, which are key components of the middle lamella and primary cell wall. 
• This class includes:
• Pectinmethyl esterases (PME): 
• Causes hydrolysis of methyl ester groups of pectinic acid chain into methyl alcohol and pectic acid.
• Polygalacturonases (PG): 
• Called chain-splitting pectinase. 
• Splits the pectic chain by adding a molecule of water and breaking (hydrolyzing) the linkage between two galacturonan molecules.
• Pectin lyases (PL): 
• Splits the chain by removing a molecule of water from the linkage, thereby breaking it and releasing products with an unsaturated double bond.
  
  
  

C. Cellulases:

• After degrading the pectin, the pathogen uses four main enzymes to break down cellulose, the main structural component of the cell wall, into glucose:
• Cellulase C1: attacks native cellulose by cleaving cross linkages between chains 
• Cellulase C2:  also attacks native cellulose and breaks it into shorter chains
• Cellulase Cx: attacks these short chains and degrades them to the disaccharide cellobiose
• β-(1-4)-glucosidase: attacks cellobiose and degraded it into glucose

D. Hemicellulases:

• The degradation of hemicelluloses, another complex component of the cell wall, requires multiple enzymes such as xylanase, galactanase, and glucanase, which are secreted depending on the specific structure of the hemicellulose in the host plant.

E. Ligninases:

• Lignin is a tough, complex polymer that provides structural support to the plant. 
• Most pathogens cannot degrade it, but a group of fungi known as white rot fungi produce powerful enzymes called ligninases to break down and utilize lignin.

F. Proteases and Peptidases:

• These enzymes are produced to degrade the structural proteins and glycoproteins embedded in the plant's cell wall, further weakening the host's defenses.

C. Post-penetration Stage

This stage involves:

• Infection and colonization
• Growth and reproduction of the pathogen
• Development of symptoms
• Dissemination of pathogen for spread of infection

Pathogens can cause disease by producing toxins or manipulating the plant's own growth hormones.

1. Pathotoxins

Pathotoxins are proteinaceous, highly poisonous substances produced by pathogens, and they play a critical role in the development of plant diseases.

These toxins are effective even at very low concentrations and are known for their ability to bind tightly to specific sites within the plant cell.

Some pathotoxins are also unstable or react so quickly that they are difficult to isolate and study. 

These are poisonous substances that directly damage host cells. 

Their mechanism of action may involve:

• affecting the permeability of the cell membrane 
• inhibiting enzymes and subsequently interrupting the corresponding enzymatic reactions
• acting as antimetabolites

Toxins can be of two types: 

• Host specific toxin 
• Host non-specific toxin 

Host-Specific Toxins

• These toxins are highly selective, only causing disease in specific host plants that are susceptible to the pathogen. Their production is essential for the pathogen's ability to be virulent, and they are typically not produced outside host cells in laboratory cultures.
• Example: Victorin, T-toxin, etc.

 

Host Non-Specific Toxins

• In contrast to host-specific toxins, these toxins affect a wide range of plant species and are not necessary for the pathogen's virulence on a specific host. They can often be produced in vitro (in a lab setting) and can cause milder symptoms like chlorosis or necrosis. 
• Example: TAB-toxin, Tentoxin, etc.

 

 Comparison between host-specific and host-nonspecific pathotoxins

Feature	Host-Specific Toxins	Host Non-Specific Toxins
Specificity	Highly specific to a particular host plant.	Affect a wide range of host plants.
Virulence	Essential for the pathogen's ability to cause disease (virulence).	Not essential for the pathogen's virulence.
Production	Not typically produced in vitro (laboratory cultures).	Can be produced in vitro.
Toxicity	Highly toxic and effective at very low concentrations.	Generally, less toxic than host-specific toxins.
Examples	Victorin (Cochliobolus victoriae), T-toxin (Cochliobolus heterostrophus).	Tabtoxin (Pseudomonas syringae), Tentoxin (Alternaria tenuis).

2. Altered Growth Regulators

Pathogens can manipulate plant hormones for their own benefit.

• Auxins: Pathogens can increase auxin levels by inactivating the IAA oxidase enzyme. This can lead to the formation of tumors, galls, and hairy roots, such as the crown gall disease caused by Agrobacterium tumefaciens. Conversely, a decrease in auxin synthesis can result in stunted growth.

• Gibberellins: The fungus Gibberella fujikuroi produces excessive gibberellins, causing rice seedlings to grow tall and spindly, a disease known as "foolish seedling disease."

• Cytokinins: Some pathogens produce cytokinins, which can lead to excessive cell division and gall formation, or witches' broom symptoms. A reduction in cytokinin production can cause dwarfism. 

• Ethylene: Pathogens can alter ethylene levels, leading to premature yellowing (chlorosis) and senescence of leaves and fruits. Ex: Pseudomonas solanacearum infection in bananna 

 3. Polysaccharides in pathogenesis

Exo-polysaccharides appear to be necessary for several pathogens to cause disease symptoms by:

• being directly responsible
• indirectly facilitating pathogenesis by promoting colonization
• enhancing survival of the pathogen.

Example: Vascular wilts 

4. Suppressors of plant defense

Some pathogenic fungi produce substances called suppressors that act as pathogenicity factors by suppressing the expression of defense responses in the host plant. 

 Example: Puccinia graminis tritici