Stress Damage rewatch 23 Flashcards
Describe Stress
-adverse force or influence that tends to inhibit normal systems from functioning optimally
-any external constraints that limits fitness/productivity below the genetic potential of the plant
→ lack of an essential element
→ factor that results in physical or chemical damage to plant body or metabolism
Mechanical damages caused by wind
Stem lodging in barley happens mostly in grasses, towards maturity, the wind breaks the stem
Root lodging in wheat where the wind moves the roots from the soils as they don’t provide anchorage anymore.
Stem breakage in Norway spruce
Uprooting in Sitka spruce
High Temperature affects membrane fluidity
Phospholipids move around the membrane; this movement increases with temperature.
Increase in membrane fluidity affects the activity of transmembrane proteins.
High temperatures disrupt membrane structure.
High temperatures disrupt chloroplast internal organisation
Temperature affects protein folding.
high temperature leads to protein aggregation
we don’t know the consequences of high fluidity as their movement is always changing
Cold-induced membrane damage
Close proximity between plasma and chloroplast membranes in cold conditions can lead to fracture-jump lesions and hexagonal II phases.
Some consequences of cold stress occur upon thawing when membrane damages prevent expansion of the cell.
destabilization as lack of fluidity in membranes, two sets of membranes close to each other they sort of merge together which is not good they called fracture jump lesions the consequences are
lose volume of water
plasma membrane makes folds, then if water goes back to cell, the cell goes back to normal shape however if some parts are fused you can’t unfold the extrusions so the cell won’t go back to normal volume therefore the water can’t flow back in and cell will die.
Ice crystals also form in apoplast, which can get into the cell which will damage the cell and potentially the plasma membrane
Loss of cell turgor → Collapse of the cell wall
low temperatures may also affect protein folding and prevent them from doing what they need to do.
Desiccation affects protein stability
Water stresses (drought, salt stress, cold) can lead to low water potential and cellular desiccation.
During cellular desiccation, the binding between proteins and other molecules increases, favouring destabilisation of proteins.
desiccation leads to molecular crowding, there are some compound that are destabilizers that of they get close they can interact with it and make it lose its shape and destabilase it and prevent it from functioning normally.
Reactive Oxygen Species: a major source of stress damage
They are a very reactive form of oxygen that is extra reactive because they have extra electrons
singlet oxygen–> dioxygen (triplet oxygen)–>superoxide radical–>peroxide ion–>hydrogen peroxide–>then fenton reaction to create a hydroxyl radical (IMPORTANT)
Sites of production of ROS are;
Mitochondria
Complex I: NADH dehydrogenase segment
Complex II: reverse electron flow to complex |
Complex III: ubiquinone-cytochrome region
Enzymes: Aconitase, 1-galactono-y lactone, dehydrogenase (GAL)
Chloroplast
PSI: electron trans port chain
Fd, 2Fe-2S, and 4Fe-4S clusters
PSIl: electron trans port chain QA
and QB
Chlorophyll pigments
Plasma membrane
Electron transporting
oxidoreductases
NADPH oxidase, quinone
oxidase
Endoplasmic reticulum
NAD (P)H-dependent electron transport system
* flavoproteins
* cyt b5
* cYt P450
Apoplast
Cell-wall-associated oxalate oxidase
Amine oxidases
Cell wall
Cell-wall-associated peroxidase diamine oxidases
Peroxisome
Matrix: xanthine oxidase (XOD)
Metabolic processes: glycolate oxidase, fatty acid oxidation, flavin oxidases, disproportionationof
O2radicals
Stress-induced production of ROS in chloroplasts
ROS are generated when the light reactions are running at a higher rate than the carbon fixing reactions: there isn’t enough NADP+ for electrons to reduce and the electron transport chain overflows.
It can be bad to have too many NADPH as you also do need NADP+
Both light reactions should run at the same time
If the light dependent reaction is working faster due to excess light then loss of electrons and they will start to create oxygen reactive species.
If the Calvin benson cycle is slowed down. It can be slowed by not having enough CO2 perhaps due to drought/low temperature/salt stress (cold is the worst as it willa slos slow down the enzymes that are in the calvin cycle. It will not regenerate enough NADP+ for electrons to jump on to.
High temperature is strange as it can make enzymes go faster in calvin benson cycle so it can catch up eith ligt dependant recation however it may have a negative effect on the nezymes as they my denature.
What happens to eletrons that cant go to calvin. Excited can have excited chrophyl to create singlet oxygen . Oxygen could also be made into superoxide radical. If it happens, on the ttroma side there is an enzyme thats is superocide demutase tat turn it into hydrogen peroxude. (H2O2 is least reactive HOWEVER it can move to other parts of the cell.
Photorespiration may alo happen (increases with heat ) oxygenation of RUBP. ???
Stress-induced production of ROS in peroxisomes
water stress heat= Increased photorespiration
Stress-induced production of ROS in mitochondria
Both low and high temperature decrease the efficiency of ROS scavenging enzymes in mitochondria, resulting in increased ROS concentrations.
More ROS can happen if scavenging system isn’t working properly.
ROS damage: lipid peroxidation
Poly-unsaturated fatty acids (PUFAs) get oxidized by ROS
Lipid radicals can react with and damage other cellular components.
Phospholipid peroxidation decreases membrane fluidity, increases membrane permeability and impairs the activity of transmembrane proteins.
Lipid peroxidation damages the cell membrane, resulting in ion leakage.
Electrolyte leakage is measured by placing leaf disks in a water bath and measuring the conductance of the solution.
Lipids (polyunsaturated fatty acids) are the target of ROS as easy to steal electron, they also steal an oxygen form the lipid so water occurs but the instability has been transferred to the fatty acid. This leads to a chian freaction. The unstable lipid reacts with oxygen and creates a lipid peroxy radical
initiation step
propagation step
termination step
termination will be two radicals will react to create a fatty acid dimer.
Thes elipid radicals may damage other things and at the end the fatty acids wont do the same thingsan dthis may increase fluidity and mermeability nd will not be good for protind in the membrne.
malondialadheyde is like a marker of lipid peroxidation
ROS damage: protein oxidation
Oxidation affects protein biological activity and increases chances of degradation.
Specific damages of ROS on photosynthesis: photoinhibition
Among the first victims of ROS production in chloroplasts is the photosynthetic apparatus.
The D1 protein in the core of PSII is a major target of photodamage.
The decrease in photosynthetic efficiency due to PSII damage is called photoinhibition.
Specific damages of ROS on photosynthesis
Chlorophyll and carotene concentration in leaf disks of cucumber leaves after varying times at 1°C in dark or high light conditions.
Photosynthetic pigments are damaged by oxidative stress and degraded.
fewer pigments less light being harvested so less ROS being made.
ROS damage: DNA damage
Oxidative damage to DNA leads to mutations.
Sodium-specific indirect damage (salt stress specific)
The reasons for the specific toxicity of Na+ is currently being debated.
It is agreed that Na+ disrupts K+ homeostasis, indirectly leading to K+ deficiency.
It has been claimed that low K+ /Na+ ratio impairs the functionality of enzymes depending on K+ but there is evidence against this.
may disrupt potassium transporters
