HSC Exam Practice

Sample response. A constitutive defence is always present in plant tissues whether or not a pathogen is present — it does not need to be activated. Example: the cuticle (waxy layer on leaf and stem surfaces) is constitutively present and prevents spore germination and waterborne pathogen entry at all times. An induced defence is activated only after the plant detects pathogen presence — it is absent or at very low levels in healthy tissue. Example: phytoalexins are synthesised and released at infection sites within hours of pathogen detection, not before.

Marking notes. 1 mark — correct definition of constitutive defence (always present, not triggered); 1 mark — correct named example of constitutive defence (cuticle, bark, tannins, cell wall accepted); 1 mark — correct definition of induced defence (activated by pathogen detection) with a named example (phytoalexins, PR proteins, stomatal closure, callose deposition accepted).

Sample response. A phytoalexin is an antimicrobial compound produced rapidly at infection sites in plants in response to pathogen attack. For example, resveratrol is produced by grapevines (Vitis vinifera) in response to infection by Botrytis cinerea (grey mould fungus) — it is directly toxic to fungal cells, inhibiting their growth at the infection site.

Marking notes. 1 mark — defines phytoalexin correctly as a plant-produced antimicrobial compound induced by pathogen attack; 1 mark — names a correct organism–pathogen pair and explains the phytoalexin's role as directly toxic / inhibiting the pathogen (resveratrol/grape/Botrytis, or camalexin/Arabidopsis, or Banksia phenolics/Phytophthora accepted).

Sample response. The HR begins when plant R-proteins (receptor proteins) recognise pathogen-associated molecular patterns (PAMPs) from the invading pathogen. This triggers a rapid burst of reactive oxygen species (ROS — hydrogen peroxide and superoxide) at the infection site, which is directly toxic to the pathogen. In response to the ROS signal, infected cells and immediately surrounding cells undergo rapid programmed cell death, collapsing and forming a visible dark necrotic lesion. Surviving cells adjacent to the lesion rapidly deposit callose and lignin to physically seal the dead zone. Simultaneously, salicylic acid produced at the site travels through the phloem, triggering systemic acquired resistance in uninfected parts of the plant.

Marking notes. 1 mark — R-protein recognition of PAMPs initiates the cascade; 1 mark — ROS burst (correctly named, directly toxic + local signal); 1 mark — programmed cell death forming necrotic zone (and why it contains the pathogen — dead cells are unusable by biotrophs); 1 mark — callose/lignin reinforcement to seal the zone AND/OR salicylic acid → SAR. All four steps needed for 4 marks.

Sample response. Phytophthora cinnamomi is an oomycete (water mould), not a true fungus. Its cell walls contain cellulose rather than chitin. Antifungal chemicals such as those targeting chitin synthesis are ineffective against Phytophthora because it lacks the chitin target these drugs are designed to disrupt. Additionally, its motile zoospores spread readily through soil water, making eradication from soil effectively impossible once established.

Marking notes. 1 mark — correctly identifies that Phytophthora is an oomycete with cellulose cell walls (not chitin like true fungi), so chitin-targeting antifungals are ineffective; 1 mark — any additional valid point (soil persistence, zoospore mobility, no eradication possible, OR that oomycetes belong to stramenopiles not fungi).

Sample response. Both SAR and animal immunological memory are defensive priming mechanisms activated after a first exposure, reducing harm from a subsequent infection. They differ in two key ways: (1) Specificity — SAR is broad-spectrum (it activates PR genes against a wide range of pathogens) while animal memory is highly specific (memory B and T cells target the exact antigen that triggered their formation). (2) Duration — SAR lasts days to weeks after the initial infection signal; animal immunological memory can last years to a lifetime. Both are non-heritable — each organism must be individually exposed to activate its own defence memory.

Marking notes. 1 mark — correctly identifies a similarity between SAR and animal memory (both are forms of priming after first exposure; both non-heritable; both speed up or strengthen the response to subsequent infection); 1 mark — criterion 1 comparison correctly stated with specificity direction correct (SAR broad-spectrum, animal memory highly specific); 1 mark — criterion 2 comparison correctly stated with duration direction correct (SAR days–weeks, animal memory years–lifetime). Accept any two criteria from: specificity, duration, mechanism, heritability.

Sample response. Most Australian Banksia species have had very limited evolutionary exposure to Phytophthora cinnamomi, which is introduced from Southeast Asia. As a result, their R-protein recognition systems did not co-evolve with this pathogen's PAMPs, leading to delayed or inefficient recognition even in individuals that eventually do mount a response. Furthermore, even where phytoalexins and HR are triggered, the pathogen spreads through soil water and can establish simultaneous new infections at multiple root sites faster than the plant can produce localised containment zones. Finally, phytoalexin concentrations in most susceptible Banksia species may be too low to effectively inhibit Phytophthora at the point of contact.

Marking notes. 1 mark — identifies limited co-evolutionary history as the primary reason (no co-evolution with this introduced oomycete → inefficient R-protein recognition); 1 mark — identifies multi-site simultaneous infection overwhelming localised defences (zoospore spread through soil water); 1 mark — identifies insufficient phytoalexin concentration OR delayed HR as a specific mechanistic limitation in susceptible individuals.

Sample response (a) — 2 marks. SAR-primed plants show a rapid, large increase in PR-1 concentration over 96 hours, reaching approximately 4.8 arbitrary units (a.u.) at 72 hours before slightly declining to about 4.6 a.u. at 96 hours. Control plants show a much slower and smaller increase, reaching only approximately 1.9 a.u. at 96 hours. At 72 hours, the SAR-primed plants have approximately 3.2 times the PR-1 concentration of control plants (4.8 vs 1.5 a.u.).

Marking notes (a). 1 mark — describes the contrasting trend correctly (SAR-primed rises rapidly and to a much higher peak; control rises slowly and to a lower level); 1 mark — supports with at least two specific values from the data (accept ±0.2 a.u. tolerance).

Sample response (b) — 3 marks. The SAR-primed plants received a low-dose pre-treatment of Pseudomonas syringae seven days earlier. This local infection triggered salicylic acid production at the inoculation site, which travelled through the phloem to the rest of the plant, including the uppermost leaf [1]. In those leaves, salicylic acid activated PR gene expression — turning on the genes encoding PR-1 protein (and other PR proteins) — without the plant needing to establish a new infection there [1]. When the high-dose challenge was then applied to the uppermost leaf, the PR-1 gene was already primed and could respond rapidly and at high amplitude. The control plants received no priming signal, so PR-1 gene expression at the uppermost leaf was at baseline, and the plant had to mount a response from scratch when challenged — resulting in a much slower and lower PR-1 accumulation [1].

Marking notes (b). 1 mark — correctly identifies SA signalling from the initial low-dose infection as the priming mechanism; 1 mark — explains that PR genes were upregulated in the uppermost leaf before challenge (primed state); 1 mark — explains why this leads to faster/higher PR-1 production on challenge vs the unprimed control (starting from a higher baseline / faster gene expression).

Sample response (c) — 2 marks. Control plants still show a gradual increase in PR-1 because the high-dose challenge itself triggers a local infection at the uppermost leaf, activating pattern recognition (R-proteins detecting PAMPs of the pathogen) and initiating an induced defence response including PR-gene expression [1]. This is an uninduced initial response — the same signalling cascade the SAR-primed plants experienced 7 days earlier — but starting from a low baseline at the point of challenge rather than a primed baseline, which explains why the increase is slower and reaches a much lower peak [1].

Marking notes (c). 1 mark — identifies that the high-dose challenge itself triggers PR gene expression via the normal pathogen-detection cascade (R-proteins / PAMPs); 1 mark — explains why it is lower and slower than the primed response (no prior SA priming, starting from a lower baseline).

Sample response. Plants defend themselves against pathogens using two integrated layers: physical (structural) defences that prevent entry, and chemical/cellular defences that limit spread once inside. Physical defences are primarily constitutive — always present. The cuticle (a waxy layer covering leaf and stem surfaces) physically prevents spore germination and entry of waterborne pathogens. The cellulose cell wall blocks hyphal penetration and can be reinforced with callose and lignin at infection sites. Stomata close on detection of pathogen signals, blocking a primary airborne entry point. Tyloses — outgrowths from xylem parenchyma cells — block xylem vessels against vascular wilt pathogens. Together, these physical defences form a first barrier that reduces the probability of infection without requiring metabolic activation.

When pathogens breach physical barriers, plants deploy chemical and cellular defences. Constitutive chemicals (tannins, phenolics) are toxic to many pathogens and are released when cells are damaged. Induced chemicals include phytoalexins (antimicrobial compounds produced rapidly at infection sites — e.g. resveratrol in grapevines), pathogenesis-related (PR) proteins such as chitinases that degrade fungal cell walls, and a reactive oxygen species (ROS) burst of hydrogen peroxide and superoxide that is directly toxic to invaders.

The hypersensitive response (HR) is the plant's primary cellular defence once infection has been detected. It is initiated when R-protein receptors detect pathogen-associated molecular patterns (PAMPs). The cascade proceeds: R-protein recognition → ROS burst (toxic, alarm signal) → programmed cell death of infected and surrounding cells → formation of a necrotic lesion → callose/lignin reinforcement sealing the dead zone → salicylic acid signalling → whole-plant systemic acquired resistance (SAR). The adaptive significance of the HR lies in its strategic sacrifice: most plant pathogens are biotrophs or hemibiotrophs that require living host cells to reproduce. By rapidly creating a zone of dead cells, the HR denies the pathogen the resource it needs. The visible dark lesion is evidence of containment, not failure.

Despite these mechanisms, plant defences have important limitations, illustrated by Banksia and Phytophthora cinnamomi in south-western Australia. This oomycete (not a true fungus — cellulose cell walls, not chitin; motile zoospores; evolutionarily distinct from fungi) was introduced from Southeast Asia. Most Australian Banksia species have had no co-evolutionary history with it, so their R-protein systems do not efficiently recognise its PAMPs — recognition is delayed or absent, meaning HR is mounted too slowly if at all. Phytophthora also spreads through soil water, establishing simultaneous new infections at multiple root sites faster than localised HR can contain them. Phytoalexin concentrations in susceptible Banksia species are insufficient to inhibit the pathogen effectively. The result is progressive root cortex destruction and xylem blockage, leading to above-ground wilting — not because the plant mounts no defence, but because the defence is too slow, too localised, and too low-concentration to match the spread rate of an evolutionarily novel pathogen. SAR, triggered in survivors, provides broad-spectrum priming but is not heritable — seeds do not carry activated SAR. Management (phosphonate injection, hygiene protocols) can suppress the pathogen and boost SAR, but eradication from soil is not achievable.

Marking criteria.

• 1 mark — Describes two or more physical defences correctly and identifies them as constitutive/structural (cuticle, cell wall, stomatal closure, bark, tyloses accepted).
• 1 mark — Identifies the constitutive vs induced distinction for chemical defences AND names at least one induced chemical defence with its mechanism (phytoalexin, PR protein, ROS burst).
• 1 mark — Correctly sequences the HR (R-protein recognition → ROS → programmed cell death → necrotic zone → callose/lignin seal → SA → SAR).
• 1 mark — Explains the adaptive significance of the HR: programmed cell death deprives biotrophic/hemibiotrophic pathogens of living host cells, containing the infection at the cost of a small cluster of cells.
• 1 mark — Names Phytophthora cinnamomi and Banksia (or another valid Australian example) and correctly identifies one specific defence limitation linked to this system (co-evolutionary gap, multi-site infection, insufficient phytoalexin concentration).
• 1 mark — Evaluates a second limitation in depth (multi-site soil spread overwhelming localised HR; SA-SAR being non-heritable; or phosphonate management being suppressive not curative) with correct mechanism.
• 1 mark — Reaches a clear overall analytical conclusion linking the two layers of defence to the broader point that even sophisticated plant defence mechanisms can be overwhelmed by introduced pathogens against which there has been no co-evolutionary selection.