Inquiry Question 2: How does a plant or animal respond to infection?
Investigate the response of a named Australian plant to a named pathogen through the application of physical and chemical defences
A focused answer to the HSC Biology Module 7 dot point on plant defences. Covers the waxy cuticle, bark, stomatal closure, callose deposition, phytoalexins and the hypersensitive response, with a named Australian example (eucalypts and Phytophthora cinnamomi).
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What this dot point is asking
NESA wants you to describe how plants defend themselves against infection, distinguish between physical and chemical defences, and provide a named Australian plant and a named pathogen. Plant immunity is often examined in 3 to 6 mark short responses.
The answer
Plants lack mobile immune cells and circulating antibodies. Instead they rely on a combination of pre-existing structural defences and induced biochemical responses.
Physical defences (passive and structural)
- Cuticle and bark
- The outer surfaces of leaves and stems are covered by a waxy cuticle (cutin and waxes) that resists water loss and pathogen entry. Woody stems have lignified bark, a tough physical barrier that few pathogens can penetrate.
- Cell walls
- Each plant cell is enclosed in a rigid cellulose cell wall. Pathogens must produce wall-degrading enzymes (cellulases, pectinases) to enter.
- Trichomes and thorns
- Hair-like trichomes and physical spines deter macroparasites and reduce pathogen contact.
- Stomatal closure
- Stomata are the main entry point for airborne pathogens. Guard cells detect pathogen-associated molecular patterns (PAMPs) such as flagellin and close the stomatal pore.
Induced physical defences
Callose deposition. When a pathogen attempts to enter, the plant deposits callose (beta-1,3-glucan) into the cell wall at the site of attack, forming a localised plug.
Tylose formation. In xylem vessels, neighbouring cells extrude into the vessel lumen, forming tyloses that block fungal spread through the vascular system.
Chemical defences
- Phytoalexins
- Small antimicrobial molecules (often terpenes, alkaloids or phenolics) synthesised in response to infection. Examples include camalexin in Arabidopsis and the terpene-based oils in Eucalyptus species.
- Reactive oxygen species (ROS)
- Plants produce hydrogen peroxide and superoxide at the infection site, damaging pathogen membranes and triggering further defence signalling.
- Defensive enzymes
- Plants produce chitinases (degrade fungal cell walls), glucanases and protease inhibitors that disable pathogen enzymes.
- Pre-formed antimicrobials
- Many plants store compounds in vacuoles or specialised cells that are released on wounding. Eucalyptus essential oils (cineole, pinene) and tea tree oil (terpinen-4-ol) are antimicrobial constituents of native Australian plants.
The hypersensitive response
The most dramatic plant defence. On detecting pathogen effector proteins, infected cells trigger programmed cell death, killing themselves and the pathogen at the infection site. The result is a small lesion of dead tissue that isolates the pathogen.
A linked response, systemic acquired resistance (SAR), primes the rest of the plant against future infection. Salicylic acid acts as the systemic signal.
Worked example: jarrah and Phytophthora cinnamomi
The jarrah tree (Eucalyptus marginata), a keystone species in Western Australia, is severely affected by jarrah dieback, caused by Phytophthora cinnamomi.
Pathogen. P. cinnamomi is an oomycete (water mould). It produces motile zoospores in moist soil that swim toward root exudates and infect fine roots.
Plant defences.
- Lignified bark and a waxy cuticle on stems and leaves prevent surface infection.
- Infected root cells deposit callose and lignin to seal off the infection.
- Eucalyptus species accumulate phytoalexins (terpenes and phenolic compounds) and produce reactive oxygen species at infection sites.
- Hypersensitive cell death isolates infected root tips.
Despite these defences, P. cinnamomi often overwhelms the plant in wet soils, and jarrah dieback has become one of Australia's most damaging plant diseases. Management focuses on hygiene and quarantine of soil and vehicles in affected areas.
Examples in context
Example 1. Eucalyptus essential oils and resistance to bushfire-associated fungi. Mature Eucalyptus camaldulensis (river red gum) trees along the Murray-Darling produce essential oils dominated by 1,8-cineole (eucalyptol) and alpha-pinene, stored in pellucid oil glands visible in fresh leaves. These terpenes are constitutive chemical defences with broad antimicrobial activity against fungi such as Armillaria luteobubalina, a wood-decay basidiomycete common after fire. When fungal hyphae penetrate the bark, they encounter terpenes that disrupt fungal cell membranes. Trees with higher cineole content show measurably lower mortality from post-fire fungal infections, as documented in CSIRO Forest Health surveys after the 2009 Black Saturday fires. This is an example of constitutive (always-present) chemical defence rather than an induced response.
Example 2. Wheat stem rust and induced callose deposition. Wheat (Triticum aestivum) infected by Puccinia graminis stem rust fungus triggers a localised induced response. Within hours of fungal penetration of the leaf surface, plant cells around the infection site deposit callose (a beta-1,3-glucan) into cell walls at the penetration peg, physically blocking further hyphal entry. If the plant carries a resistance gene matching the fungal effector, it also mounts the hypersensitive response: rapid cell death of the infected and immediately surrounding cells, depriving the biotrophic fungus of living host tissue. NSW DPI variety trials at Wagga Wagga screen wheat lines for these resistance traits, since stem rust epidemics in 1973 and 1989 cost Australian growers hundreds of millions of dollars.
Try this
Q1. Identify two physical defences and two chemical defences used by an Australian eucalypt against a pathogen, naming the pathogen. [4 marks]
- Cue. Physical: waxy cuticle, bark, callose deposits. Chemical: 1,8-cineole essential oils, phenolic phytoalexins. Example pathogen: Phytophthora cinnamomi.
Q2. A study measures callose deposition in barley leaves 6, 12 and 24 hours after powdery mildew inoculation, finding 5, 38 and 62 callose papillae per mm squared respectively. Describe the trend and explain its role in resistance. [3 marks]
- Cue. Increasing deposition over time as induced response builds; physical reinforcement at penetration sites blocks fungal entry.
Q3. Compare physical and chemical defences in Eucalyptus marginata against Phytophthora cinnamomi. (a) Identify one physical defence. (b) Identify one chemical defence. (c) Explain why both are required and why jarrah dieback nonetheless kills susceptible trees. [1+1+3 marks]
- Cue. (a) Bark and suberin layers. (b) Phenolic phytoalexins released after infection. (c) Phytophthora produces enzymes that breach bark and tolerate some plant defences, especially in waterlogged soils where root infection is rapid.
Exam-style practice questions
Practice questions written in the style of NESA exam questions on this dot point, with worked answer explainers. The year tag is the paper they imitate, not the source.
2024 HSC4 marksDescribe a plant disease and its effect on agricultural production. (Name the plant disease.)Show worked answer →
Full marks (4) require describing a named plant disease AND its effects on agriculture. Sample answer: Stone fruit scab, a fungal disease affecting stone fruit (plums, peaches, nectarines). It begins as small dark spots on the fruit that become scabby and may cause the fruit to crack, shrivel and fall off. Effect on agriculture: it downgrades fruit quality and decreases yield, leading to economic losses. Marker feedback: you must name a real plant disease and state a clear, directional effect on agricultural production (e.g. reduced yield/quality), not a vague "it has an impact."
Related dot points
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