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Plant bio
Plant hormones II
| Question | Answer |
|---|---|
| Ethylene | •Control of fruit ripening •Control of leaf and petal senescence •Stress responses |
| Ethylene is a gas | Biosynthesis begins with Methionine • ACS is ACC synthase; ACO is ACC oxidase |
| The receptors negatively regulate the responses | - When not bound to ethylene, the receptor shuts off the ethylene response - When bound to ethylene, the receptor does not shut off the ethylene response |
| Fruit ripening is induced by ethylene | Ethylene is a gaseous hormone that promotes fruit softening and flavor and color development |
| Ethylene promotes senescence | Ethylene promotes leaf and petal senescence Ethylene levels can be managed to maintain fruit freshness, commercially and at home |
| Abscisic Acid (ABA) | • Stomatal aperture • Stress responses |
| ABA synthesis is strongly induced in response to stress | - ABA levels are tightly controlled - ABA levels rise during drought stress due in part to increased biosynthesis and seed germination - ABA can be transported within the plant, from root to shoot and then to guard cells |
| ABA signal transduction affects gene expression | When ABA is present, inactivation of the PP2C phosphatase permits a protein kinase (e.g. SnRK) to phosphorylate and activate ABA-inducible TFs, promoting transcription of ABA-inducible genes |
| ABA regulates stomatal aperture by changing the volume of guard cells via stomata | Guard cells open and close stomata for gas exchange: a fine balance is required to allow CO2 in for photosynthesis and prevent excessive water loss • ABA induced by drought causes the guard cells to close and prevents their reopening, conserving water |
| ABA-induced stomatal closure is extremely rapid and involves changes in ion channel activities | ABA triggers an increase in cytosolic calcium (Ca2+), which activates channels allowing Cland K+- to leave the cell As ions leave the cell, so does water (by osmosis), causing the cells to lose volume and close over the pore |
| Hormonal responses to biotic stress | Bacteria, fungi, viruses – Biotrophic organisms Herbivores – insects, other animals, fungi – Necrotrophic organisms |
| Jasmonates | •Response to necrotrophic pathogens •Induction of antiherbivory responses •Production of herbivore-induced volatiles to prime other tissues and attract predatory insects |
| Jasmonic acid (JA) and its metabolite methyl jasmonate contribute to systemic defence responses | Defence responses are activated in distant tissues |
| Jasomonates stimulate production of volatile signaling compounds | Herbivore-induced volatiles prime other tissues (and other plants) for attack making them unpalatable (indicated in red) |
| JA-induced changes in gene expression | Low JA-Ile: no transcription |
| Jasmonates induce the expression of anti-herbivory chemicals | Wound-induced signals insect oral secretions Protease inhibitors Feeding deterants |
| Salicylic Acid | •Response to biotrophic pathogens •Induced defense response •Systemic acquired resistance |
| Most SA is synthesized in the chloroplast, conjugated in the cytoplasm and sequestered in the vacuole | |
| Salicylates contribute to acquired and systemic acquired resistance | SA is necessary in systemic tissue for SAR, but the nature of the mobile signal(s) is still up in the air It is likely that multiple signals contribute to SAR |
| Grafting studies suggest that SA itself is NOT the mobile signal | - Plants expressing NahG degrade SA and prevent its accumulation |
| - Leaves of rootstock were inoculated with a virus, then upper scion leaves challenged with the virus. Healthy scion leaves indicates SAR and means the mobile signal was produced in the inoculated leaves | |
| Regulation of SA accumulation | SA synthesis is induced by pathogens or stress. Genetic studies have identified some of the signals that transduce pathogen perception to SA synthesis |
| NPR1 itself is activated by binding to SA | NPR1 binds SA, triggering a conformational change that releases its C-terminal activation domain from inhibition to trigger transcription |
| Physical barriers exclude most microorganisms | Some pathogens enter through wounds or stomata |
| PAMP recognition triggers PAMP Triggered Immunity | Pathogen-associated molecular patterns (PAMPs) are conserved molecules like flagellin or chitin They are perceived by extracellular receptors called PRRs (pattern recognition receptors) |
| PAMP perception triggers SA synthesis and defense gene induction – this is called patterntriggered immunity (PTI) | |
| The hypersensitive response involves cell death | Pathogen Response (PR) genes Antimicrobial compounds Strengthening of plant cell walls Programmed cell death Hypersensitive response (HR) |
| The hypersensitive response seals the pathogen in a tomb of dead cells | - The HR kills the infected cells and cells surrounding them and prevents the pathogen from spreading - Without a hypersensitive response, the pathogen can multiply |
Created by:
reub8n
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