Plant immunity Study Guide

📖 Core Concepts Plant disease resistance – the plant’s ability to limit pathogen growth compared with a susceptible host. Disease tolerance – plants sustain little damage even when pathogen loads are high. Pre‑formed defenses – always‑present physical barriers (cuticle, cell wall) and antimicrobial chemicals. Induced defenses – activated after pathogen detection; include new antimicrobial compounds, cell‑death responses, and signal amplification. Two‑tiered immune system – Pattern‑Triggered Immunity (PTI) via pattern‑recognition receptors (PRRs) that detect conserved MAMPs/DAMPs. Effector‑Triggered Immunity (ETI) via intracellular NLR (NB‑LRR) proteins that sense specific pathogen effectors. Hypersensitive response (HR) – rapid, localized cell death that restricts pathogen spread; common to both PTI‑amplified and ETI. Quantitative vs. qualitative resistance – many small‑effect genes (QTL) give partial, durable protection vs. single major R‑genes that give strong, strain‑specific resistance. Systemic Acquired Resistance (SAR) – whole‑plant, long‑lasting immunity induced by a local infection; mediated by salicylic acid (SA) and mobile signals (MeSA, azelaic acid, pipecolic acid). --- 📌 Must Remember Disease triangle = pathogen + host + environment → disease outcome. PTI → ion fluxes, ROS burst, MAPK cascade, callose deposition. ETI → NLR activation → strong ROS, HR, amplified PTI outputs. Gene‑for‑Gene: R‑gene ↔ pathogen avirulence (Avr) gene; resistance only if both are present. Vertical (strain‑specific) resistance = single R‑gene; Horizontal (broad‑spectrum) resistance = many QTL. Durability rule: quantitative resistance ≈ more durable because pathogens must overcome many loci simultaneously. Key hormones – SA → biotrophs/SAR; JA + ethylene → necrotrophs/chewing insects. Core effectors are conserved across pathogen populations and are prime targets for resistance‑gene discovery. Loss‑of‑function susceptibility genes (e.g., MLO, eif4e, Os‑8N3) confer resistance when knocked out. --- 🔄 Key Processes Pathogen detection (PTI) MAMP/DAMP binds PRR → PRR autophosphorylates → activates MAPK cascade → ROS burst, Ca²⁺ influx, transcription of defense genes. Effector delivery & ETI Pathogen injects effectors → NLR either directly binds effector or guards a host protein altered by the effector → NLR oligomerization → HR & amplified defense signaling. Hypersensitive Response NLR activation → rapid Ca²⁺ & ROS → programmed cell death in infected cells → containment of pathogen. SAR induction Local infection → SA accumulation → NPR1 monomerization → transcription of PR genes; mobile signals travel via phloem to prime distal tissues. RNAi‑based resistance (HIGS) Plant expresses dsRNA → Dicer → siRNA → loaded into RISC → silences essential pathogen gene (cross‑kingdom RNAi). --- 🔍 Key Comparisons Pre‑formed vs. Induced Pre‑formed: always present (cuticle, antimicrobial peptides). Induced: synthesized after detection (phytoalexins, PR proteins). PTI vs. ETI PTI: recognizes conserved patterns, moderate response. ETI: recognizes specific effectors, strong/rapid response (often HR). Vertical vs. Horizontal resistance Vertical: single R‑gene, strain‑specific, less durable. Horizontal: many QTL, partial, more durable. Direct vs. Guarded NLR recognition Direct: NLR binds effector. Guarded: NLR monitors a host “guardee” that the effector modifies. --- ⚠️ Common Misunderstandings “Resistance = no pathogen” – resistance limits growth; tolerant plants may harbor high pathogen loads. “All PRRs trigger ETI” – PRRs only initiate PTI; ETI requires intracellular NLRs. “RNAi only works against viruses” – HIGS can silence fungal, oomycete, and even insect genes. “Loss‑of‑function in a susceptibility gene always harms the plant” – many MLO or eif4e mutants show normal growth while gaining disease resistance. --- 🧠 Mental Models / Intuition “Layered castle” – imagine the plant as a fortress: walls (cuticle/cell wall) = pre‑formed; watchtowers (PRRs) detect invaders → alarm (PTI); elite knights (NLRs) recognize the enemy’s secret emblem (effector) → decisive strike (ETI/HR). “Signal amplification cascade” – small MAMP detection → big ROS/ Ca²⁺ wave → massive transcriptional reprogramming; akin to a microphone (MAMP) turned up to a megaphone (HR). --- 🚩 Exceptions & Edge Cases Adult Plant Resistance (APR) – quantitative resistance that only appears after the seedling stage; not effective early in development. Non‑host resistance – a plant species is completely immune to a pathogen because the pathogen lacks compatible effectors, even if PTI is functional. Cross‑talk – SA can suppress JA signaling; pathogens that trigger SA may indirectly weaken JA‑mediated defenses. --- 📍 When to Use Which Breeding decision – use major R‑genes for rapid, high‑impact control in low‑pathogen‑diversity regions; stack multiple R‑genes or combine with QTL for durability. Genetic engineering – transfer PRRs (e.g., EFR) for broad bacterial resistance; edit susceptibility genes (MLO) when a loss‑of‑function is known to be non‑detrimental. RNAi deployment – choose HIGS when the target pathogen’s essential gene is known and sequence‑conserved across isolates. Stacking strategy – combine NLRs with different effector specificities + quantitative QTL to hedge against pathogen evolution. --- 👀 Patterns to Recognize MAMP → rapid ROS + Ca²⁺ spike within minutes of inoculation → indicates PTI activation. HR lesions (localized necrosis) appearing 12‑24 h post‑infection → hallmark of ETI. Elevated SA + NPR1‑dependent PR gene expression in distal leaves after a primary infection → SAR in action. Pathogen isolates that overcome a single R‑gene but still cause reduced disease → quantitative resistance at work. --- 🗂️ Exam Traps Distractor: “PRRs are intracellular.” – False; PRRs are membrane‑localized. Trap: “All NLRs directly bind effectors.” – Incorrect; many NLRs act via guarded (indirect) recognition. Misleading choice: “Loss‑of‑function of MLO confers resistance to all pathogens.” – Only to powdery mildew; not universal. Near‑miss: “RNAi only silences plant genes.” – In HIGS, the siRNA silences pathogen genes, not plant genes. Confusion: “Quantitative resistance is always weaker than qualitative.” – While each QTL has small effect, together they can provide strong, durable protection. ---