A Banksia has no white blood cells, no antibodies, no fever response. Yet when Phytophthora cinnamomi invades its roots, it fights back — using chemistry, cell walls, and sacrifice. Plants mount defences as sophisticated as any immune system, just entirely different in design.
Use the PDF for classwork, homework or revision. It includes key ideas, activities, questions, an extend task and success-criteria proof.
Consider this analogy:
"A castle under siege has two lines of defence: the walls and moat that stop attackers getting in, and the soldiers inside who fight those that breach the walls."
Before reading: apply this analogy to how you think a plant might defend itself against a pathogen. What would the "walls and moat" be? What would the "soldiers inside" represent? Write your predictions before reading on.
Come back to this at the end of the lesson.
Wrong: Natural selection means organisms change because they want or need to.
Right: Natural selection acts on random genetic variations; organisms do not consciously adapt.
Core Content
Plants lack the specialised immune cells that animals use to detect and destroy pathogens. Instead, they rely on two integrated defence systems: physical (structural) defences that prevent pathogen entry, and chemical defences that limit pathogen activity once inside. These systems are analogous to the castle analogy — but in plant biology, both layers are active and sophisticated.
When a pathogen breaches initial physical barriers and begins to infect plant cells, one of the most powerful plant defence responses is the hypersensitive response (HR). This response is counterintuitive — the plant deliberately kills its own cells at the infection site to stop the pathogen spreading.
The HR works because most plant pathogens are biotrophs (they require living host cells to survive and reproduce) or hemibiotrophs (living cells initially, then dead tissue). By rapidly killing the cells around the infection point, the plant creates a zone of dead tissue that the pathogen cannot exploit.
Systemic acquired resistance (SAR) is the plant equivalent of immunological memory — though the mechanism is entirely different. After a localised infection triggers the HR, signalling molecules (primarily salicylic acid) travel through the phloem to uninfected parts of the plant.
In those uninfected tissues, SAR activates the expression of pathogenesis-related (PR) genes, producing PR proteins that prime the plant's defences against future infection. The entire plant becomes more resistant — not just the site of the original infection.
SAR can last for days to weeks after the initial infection signal. Unlike animal immunological memory, it is not pathogen-specific — it provides broad-spectrum resistance against a wide range of pathogens. This is both an advantage (broad protection) and a limitation (no targeted antibody-like response).
The HR is a deliberate sacrifice — infected cells die to create a zone the pathogen cannot exploit. A visible necrotic lesion means the response worked.
Phytophthora cinnamomi is an oomycete (a water mould — not a true fungus, but classified similarly as a pathogen) that causes Phytophthora dieback, one of Australia's most ecologically devastating plant diseases. It infects the roots of a vast range of native plants, including Banksia, jarrah, grass trees (Xanthorrhoea), and many heathland species.
Phytophthora spreads primarily through water movement in soil — zoospores (swimming spores) move through water films between soil particles. Human activity (vehicles, boots, contaminated soil on equipment) dramatically accelerates spread into previously uninfected areas.
Zoospores are attracted by chemical signals (root exudates) from living roots. They attach to root surfaces, germinate, and penetrate root cells using enzymatic degradation of the cell wall. Hyphae then grow through root cortex tissue, destroying cells and blocking water and nutrient uptake through the xylem. Above ground, the first visible sign is yellowing and wilting of leaves — a consequence of root failure, not direct above-ground attack.
Most Australian Banksia species have limited resistance to Phytophthora cinnamomi — the pathogen is introduced from Southeast Asia and Australian plants have had limited evolutionary exposure. Banksia species that do show some resistance typically have stronger hypersensitive responses and produce more effective phytoalexins. Research into naturally resistant individuals is ongoing as part of conservation management.
Misconception: The hypersensitive response means the plant is having an allergic reaction to the pathogen.
The hypersensitive response is a deliberate, adaptive defence mechanism — not an allergy. It is a controlled form of programmed cell death (apoptosis-like) that the plant uses to sacrifice infected cells and create a barrier the pathogen cannot cross. An allergy is a maladaptive immune response in animals. The HR is the plant equivalent of deliberately demolishing buildings around a fire to create a firebreak — a strategic sacrifice, not a pathological overreaction.
Misconception: Systemic acquired resistance is the same as immunological memory in animals.
SAR and immunological memory are analogous but mechanistically different. SAR is triggered by salicylic acid signalling and activates broad-spectrum PR gene expression — it is not pathogen-specific. Animal immunological memory involves the clonal expansion of antigen-specific memory B and T cells that produce highly targeted responses on re-exposure. SAR also lasts only days to weeks, while animal memory can last a lifetime. The analogy is useful but the mechanisms are fundamentally different.
Misconception: Phytophthora cinnamomi is a fungus.
Phytophthora is an oomycete — also called a water mould. Oomycetes superficially resemble fungi (they produce hyphae and spores) but are evolutionarily distinct, belonging to the stramenopiles rather than the fungal kingdom. Their cell walls contain cellulose (not chitin as in true fungi), and they produce motile zoospores that move through water. This distinction matters for treatment: antifungal drugs targeting chitin are ineffective against oomycetes, which is one reason Phytophthora is so difficult to manage.
Systemic Acquired Resistance (SAR) Pathway
Activities
Researchers investigated the defence responses of two Banksia species — one showing field resistance to Phytophthora cinnamomi (Species A) and one highly susceptible (Species B) — by infecting seedlings and measuring defence indicators over 72 hours.
Write your responses here or in your book.
A student wrote the following explanation of how plants respond to pathogen infection. The passage contains four factual errors. Identify each error, explain why it is wrong, and write the correct information.
"When a plant is infected by a pathogen, it responds using both physical and chemical defences. Physical defences include the cuticle, which is made of cellulose, and stomatal opening, which allows defensive chemicals to be released onto the leaf surface. Chemical defences include phytoalexins, which are always present in plant tissues before infection occurs, and salicylic acid, which signals local resistance at the infection site only. The hypersensitive response involves the plant producing extra nutrients to feed cells near the infection, creating a zone of healthy, fortified cells that the pathogen cannot penetrate. Phytophthora cinnamomi is a fungus that spreads through airborne spores in dry conditions."
Write your responses here or in your book.
You were asked to apply the castle analogy — walls and moat versus soldiers inside — to plant defences against pathogens.
The mapping works well. The "walls and moat" are the plant's physical (structural) defences: the cuticle (outer wall), cell wall (inner fortification), stomatal closure (closing the gates), and bark (the moat — a zone the pathogen must cross). These are largely constitutive — always in place, whether an attack is occurring or not.
The "soldiers inside" are the chemical and cellular responses activated when a pathogen breaches the physical barriers: phytoalexins and PR proteins (chemical weapons deployed against the invader), the hypersensitive response (soldiers sacrificing themselves to create a firebreak), and systemic acquired resistance (dispatching messengers to alert the rest of the castle to prepare).
Where the analogy breaks down: unlike soldiers, the HR doesn't fight the pathogen directly — it removes the resource the pathogen needs (living cells). It's less "soldiers fighting" and more "burning your own stores to deny them to the enemy." Also, SAR is more like a general alertness upgrade across all soldiers than a specific counter to the known attacker.
If you predicted something like "thick walls prevent entry, internal chemicals fight what gets through" — you had the essential structure exactly right.
Assessment
5 random questions from a replayable lesson bank — feedback shown immediately
1. Distinguish between constitutive and induced plant defences. Give one example of each and explain how each type contributes to plant protection against pathogens. (3 marks)
1 mark: constitutive defence defined with example | 1 mark: induced defence defined with example | 1 mark: explanation of how the two types are complementary
2. Describe the sequence of events in the hypersensitive response (HR) in plants. In your answer, explain why programmed cell death is considered an adaptive defence rather than a sign of disease. (3 marks)
1 mark: HR sequence correctly described (recognition → ROS burst → programmed cell death → cell wall reinforcement) | 1 mark: salicylic acid signalling and SAR | 1 mark: explanation of why cell death is adaptive, not pathological
3. Investigate the response of Banksia to infection by Phytophthora cinnamomi. In your answer, describe how the pathogen causes disease, explain both the physical and chemical responses the Banksia mounts, and explain why these responses are often insufficient to prevent plant death in susceptible species. (4 marks)
1 mark: mechanism of Phytophthora infection in Banksia roots | 1 mark: physical responses | 1 mark: chemical responses including HR if present | 1 mark: explanation of why responses are insufficient in susceptible individuals
Answers
SA1: Constitutive defences are always present in plant tissues regardless of whether infection is occurring — they do not need to be activated. An example is the cuticle: a waxy layer covering leaf and stem surfaces that physically prevents spore germination and the entry of waterborne pathogens at all times. Constitutive defences contribute to plant protection by providing an immediate, continuous barrier that pathogens must overcome before any infection can begin. Induced defences are activated only after the plant detects pathogen presence — they are not present (or present only at low levels) in healthy tissue. An example is phytoalexins: antimicrobial compounds synthesised and released at infection sites within hours of pathogen detection. Induced defences contribute by providing a targeted, high-concentration response exactly where it is needed. Together they are complementary: constitutive defences provide the first barrier that reduces pathogen entry, while induced defences provide a second, more powerful response against any pathogens that succeed in breaching the initial barrier. Neither alone is as effective as both operating in combination.
SA2: The hypersensitive response begins when plant receptor proteins (R-proteins) detect pathogen-associated molecular patterns (PAMPs) from an invading pathogen. This recognition triggers a rapid burst of reactive oxygen species (ROS — including hydrogen peroxide) at the infection site, which is directly toxic to the pathogen and acts as a local alarm signal. In response to the ROS burst, infected cells and immediately surrounding cells undergo rapid programmed cell death — collapsing and turning brown, forming a visible necrotic lesion. Surviving cells adjacent to the lesion rapidly deposit callose and lignin, reinforcing their walls to physically seal off the dead zone. Simultaneously, salicylic acid produced at the site travels through the phloem to uninfected parts of the plant, activating systemic acquired resistance — expression of pathogenesis-related (PR) genes throughout the plant. Programmed cell death is adaptive rather than pathological because most biotrophic pathogens require living host cells to survive and reproduce. By deliberately killing infected cells, the plant creates a zone of dead, nutrient-poor tissue the pathogen cannot exploit. The necrotic lesion is evidence of containment — the plant has sacrificed a small cluster of cells to save the rest. An absence of necrosis in susceptible plants means the pathogen is spreading freely, which is the worse outcome.
SA3: Phytophthora cinnamomi causes disease in Banksia through root infection. Zoospores — motile swimming spores — are attracted by chemical signals (root exudates) released by living roots, and move through water films between soil particles. They attach to root surfaces, germinate, and penetrate root cells by enzymatically degrading the cellulose cell wall. Hyphae then grow through the root cortex, destroying cells and blocking xylem vessels — preventing water and nutrient uptake. Above ground, the first visible symptom is yellowing and wilting, as the plant suffers water and nutrient stress despite having above-ground tissue that is not directly infected. Physical defence responses include deposition of callose and phenolic compounds in root cell walls at infection sites — reinforcing the wall to slow hyphal penetration — and in some species, growth of proteoid cluster roots away from infected zones to maintain some nutrient uptake capacity. Chemical defence responses include production of phytoalexins (antimicrobial phenolic compounds) at infection sites, and in resistant individuals, a hypersensitive response involving programmed death of infected root cells to create a necrotic containment zone. These responses are often insufficient in susceptible Banksia species because: (1) most Australian Banksia have had limited evolutionary exposure to Phytophthora, meaning their R-protein recognition systems may not efficiently detect the pathogen's PAMPs, resulting in delayed or absent HR; (2) even where phytoalexins are produced, their concentration may be too low to effectively inhibit the pathogen; and (3) Phytophthora spreads rapidly through soil water, meaning the plant's localised root defences are rapidly overwhelmed as new infections establish at multiple points simultaneously.
Defend your ship by blasting the correct answers for How Plants Respond to Pathogens. Scores count toward the Asteroid Blaster leaderboard.
Play Asteroid Blaster →