Biology · Year 12 · Module 7 · Lesson 8
How Plants Respond to Pathogens
Apply plant defence mechanisms to real data, a Western Australian conservation scenario, and a cause-and-effect chain tracing the hypersensitive response.
1. Interpret resistance data — Phytophthora dieback in WA Banksia woodland
Researchers assessed 180 individual Banksia attenuata plants at a site in the Swan Coastal Plain (WA) twelve months after Phytophthora cinnamomi was confirmed in the soil. Plants were classified as susceptible (dead or severely wilted), partial responders (showing defence symptoms but surviving), or resistant (no visible disease progression). Root tissue was sampled from surviving plants and phytoalexin concentration measured (nmol g−1 fresh weight). The bar chart below shows mean phytoalexin concentration by plant category. 8 marks
Figure 1.1. Mean root phytoalexin concentration (nmol g−1 fresh weight) in Banksia attenuata at 12 months post-infection by Phytophthora cinnamomi, Swan Coastal Plain, WA (n = 180). Adapted from hypothetical trial data after Cahill & Hardham (1994).
1.1 Describe the trend shown in the data across the three plant categories. 2 marks
1.2 Using lesson content, explain why resistant plants show much higher phytoalexin concentrations than susceptible plants in the same infected site. 3 marks
1.3 Predict what the phytoalexin concentration of a partial-responder plant would look like if measured again at 24 months, assuming Phytophthora is still present in the soil. Justify your prediction using the lesson's account of how the pathogen overwhelms defences. 3 marks
2. Trace the cause-and-effect chain — the hypersensitive response
The left column gives four causes. In the right-hand "Effect (so...)" column, write what happens because of that cause during the hypersensitive response. The final "Overall outcome" line asks for the net result for the plant. 5 marks
| Cause | Effect (so…) |
|---|---|
| R-proteins in the plant cell detect pathogen-associated molecular patterns (PAMPs). | |
| A burst of reactive oxygen species (hydrogen peroxide, superoxide) floods the infection site. | |
| Infected cells and immediately surrounding cells undergo rapid programmed cell death. | |
| Surviving cells adjacent to the necrotic zone rapidly deposit callose and lignin. |
Overall outcome (so...): The net result of the entire HR for a biotrophic pathogen is…
3. Compare plant SAR and animal immunological memory
Complete the comparison table below. For each feature, fill in the correct details for Plant SAR and Animal immunological memory. 6 marks
| Feature | Plant SAR | Animal immunological memory |
|---|---|---|
| Triggering signal | Primary exposure to a specific antigen | |
| Specificity | Broad-spectrum (not pathogen-specific) | |
| Duration | Years to lifetime | |
| Mechanism of defence | Clonal expansion of memory B and T cells | |
| Heritable to offspring? | No | |
| One key limitation | Requires prior exposure (or vaccination) |
4. Apply to a conservation scenario — phosphonate treatment in Fitzgerald River National Park
In 2019 park managers at Fitzgerald River National Park (WA) conducted a phosphonate stem-injection program on 300 critically endangered Banksia cuneata individuals threatened by Phytophthora dieback. Phosphonate (phosphite) suppresses Phytophthora growth and also boosts plant immune responses including SAR and PR-protein production, but it does not eradicate the pathogen from soil. A monitoring team recorded disease-progression scores for treated and untreated plants over three years. 5 marks
4.1 Using lesson terms, explain two mechanisms by which phosphonate treatment reduces Phytophthora damage in Banksia cuneata. 3 marks
4.2 Predict whether disease-progression scores in the phosphonate-treated group would be lower, the same, or higher after three years compared to untreated plants. Justify your prediction using lesson content about why treatments cannot cure the infection. 2 marks
Q1.1 — Trend description (2 marks)
Mean root phytoalexin concentration increases progressively from susceptible plants (8 nmol g−1) through partial responders (42 nmol g−1) to resistant plants (118 nmol g−1). Resistant plants show approximately 14.8 times the phytoalexin concentration of susceptible plants at the same infection time-point.
Q1.2 — Why resistant plants have higher phytoalexin concentrations (3 marks)
Phytoalexins are induced defences — synthesised only after pathogen detection. Resistant Banksia plants have R-protein recognition systems that more efficiently detect Phytophthora PAMPs [1], triggering a faster and higher-magnitude phytoalexin production response at infection sites [1]. Susceptible plants either fail to recognise the pathogen efficiently or produce phytoalexins at concentrations too low to be effective, because Australian Banksia species have had limited evolutionary exposure to this introduced oomycete [1].
Q1.3 — Prediction at 24 months (3 marks)
The phytoalexin concentration in partial responders is likely to decrease (or the plant may die) at 24 months [1]. Even though partial responders initially mount some defence, Phytophthora spreads through soil water and can establish new infection points simultaneously at multiple root sites [1]. The plant's localised phytoalexin production is overwhelmed as new infections exceed the rate at which the plant can mount effective defences, and continued cortex destruction impairs water and nutrient uptake, weakening the plant's capacity to sustain the metabolically expensive induced response [1]. Accept: prediction of eventual decline with mechanism referencing the multi-site soil-spread.
Q2 — Cause-and-effect chain (5 marks)
Effect 1: The defence cascade is initiated / the hypersensitive response begins [1].
Effect 2: The ROS burst is directly toxic to the pathogen and amplifies local alarm signals, triggering programmed cell death in infected and surrounding cells [1].
Effect 3: A necrotic lesion (dead zone) forms — biotrophic and hemibiotrophic pathogens cannot exploit dead tissue, so the infection is contained [1].
Effect 4: The necrotic zone is physically sealed; healthy cells are protected from further pathogen movement [1].
Overall outcome: The pathogen is contained within a dead zone it cannot use to reproduce, at the cost of a small cluster of host cells. The visible necrotic lesion is evidence of a successful HR — the infection has been contained and the rest of the plant is protected [1].
Q3 — SAR vs animal memory comparison (6 marks, 1 per blank)
SAR — Triggering signal: Localised infection → salicylic acid signalling (through the phloem).
Animal — Specificity: Highly specific — memory cells target the exact antigen (pathogen/strain) that triggered the original response.
SAR — Duration: Days to weeks after the initial infection signal.
SAR — Mechanism: Salicylic acid activates PR gene expression throughout the plant; PR proteins (chitinases, glucanases, protease inhibitors) prime defences; phytoalexin production primed.
Animal — Heritable?: No — each individual must be exposed (or vaccinated) to form their own memory.
SAR — One key limitation: Broad-spectrum (not targeted like an antibody); lasts only days to weeks (not lifetime); does not prevent infection — it primes the plant to respond faster.
Q4.1 — Two mechanisms of phosphonate (3 marks)
Mechanism 1: Phosphonate directly suppresses Phytophthora growth — it inhibits the oomycete's metabolism, reducing the rate at which hyphae invade root cortex cells [1].
Mechanism 2: Phosphonate boosts the plant's induced immune responses, specifically triggering SAR and upregulating PR-protein production (chitinases, glucanases) and phytoalexin synthesis throughout the treated Banksia [1]. This means that even where Phytophthora zoospores do establish new infection points, the plant's phytoalexins and PR proteins are primed at higher baseline levels, slowing pathogen spread [1].
Q4.2 — Prediction for treated group (2 marks)
Disease-progression scores in phosphonate-treated plants would be lower than in untreated plants over three years [1], because phosphonate both directly suppresses Phytophthora and boosts SAR. However, scores would not remain at zero — phosphonate cannot eradicate the pathogen from soil, so zoospores continue to be present and re-infect roots. Over time, as treatment effects diminish and re-infection pressure accumulates, progression is expected to resume unless treatment is repeated [1].