BIOSCI 108: Lecture 21 - Responding to Biotic & Abiotic Stress

Abiotic Stressors

Non-living environmental factors that causes stress. Some examples are droughts, floods, temperature changes, soil salinity, UV radiation, heavy metals, and so on

Biotic Stressors

Living organisms that causes stress. Some examples are different pathogens (bacteria, fungi, nematodes, viruses), insects, and herbivores.

Plants use a higher percentage of their genome compared to other organisms in stress response.

Phytohormones

Plant hormones that are crucial in regulating how plants respond to abiotic and biotic stres by regulating various processes.

Some examples are absicisic acid (ABA), ethylene, salicylic acid, and jasmonic acid.

Drought & ABA

Droughts occur when the soil lacks sufficient water to meet the plant’s needs: reducing growth and vitality. Under drought conditions, plants undergo many changes including root elongation, decreased cell division, and closing of stomata.

The closing of stomata occurs and is induced by the release of abscisic acid (ABA) during drought conditions.

ABA will be taken up by swollen (filled with H2O) guard cells and will displace the water, pushing it out of the guard cell. This reduces the turgor pressure and causes it to close.

Flooding & Ethylene

Flooding occurs when the soil is so saturated it lacks air space to provide oxygen for cellular respiration in the root. The plant undergoes many changes: increased gas exchange, increased aerenchyma, and so on.

Aerenchyma are air channels (tubes) that help gas transfer occur more in submerged roots, like a snorkel.

This is induced by ethylene, which causes a localised cortex cell death response which makes more aerenchyma.

Thimomorphogenesis

The changes plants undergo to respond to mechnical stimulations such as winds, touch, and so on. Typically, plants will grow shorter, thicker, and sturdier to withstand the touch stress.

Plant Pathogens & Disease Cycle

There are many different pathogens that causes diseases in plants. Bacteria, fungi, nematodes, oomycetes, and many more are common plant pathogens.

It can cause rotting (bacteria, oomycetes, or fungi), leaf spotting (all pathogens), and tumor-like grown gall (bacteria)

A general disease cycle of pathogens include:

1. Infection of plant

2. Disease development

3. Inoculum production to prepare for dispersal

   1. Dispersal to other plants/other parts of the same plant

Pseduomonas syringae Disease Cycle Example

A bacterial pathogen that causes plant death, a major threat to kiwi fruit trees.

1. They infect the flowers, buds, and leaves of a plant. They can also colonise plant stomata

2. Disease develops, causing leaf spots, wound infections, leaf detachment, and shoot wilting

3. Inoculum production, causing exudates to form for dispersal

4. Dispersal when exudates cankers releases inoculum

Phytophthora infestans Disease Cycle Example

A common oomycete plant pathogen.

1. They infect plants when their zoospores, released by sporangium, swim to plant cells

2. Disease develops, forming cysts on top of the plant and growing mycelium through the plant

3. Inoculum production, the development of oospores that’s ready for dispersal

4. Oospores disperse their spores when met with favourable conditions

Plant Defenses Against Pathogens

They have:

• Physical barriers including cell walls, waxy cuticle, and bark, to prevent pathogen entry

• Immune responses:

  • First layer of defense including the PAMP-triggered Immunity

  • Second layer of defense including the Effector-triggered Immunity which triggers the hypersensitivity response and systemic acquired resistance.

PAMP-triggered Immunity (PTI)

Plants have pattern recognition recpetors (PRRs) that’ll detect and recognise pathogens as they attach to plant cells.

This’ll lead to a signal transduction to the nucleus to trigger the genetic expression of an immune response such as.

Effector-triggered Immunity (ETI) & Salicylic Acid

When the first layer fails and the pathogen is able to inject effectors, it’ll trigger the second layer of defense.

These effectors will be detected by a disease resistant r-protein which triggers a signal transduction to the nucleus to trigger another immune response.

First, it’ll trigger a hypersensitive response which results in the release of antimicrobials and localised cell death at/near the infected area to try and contain it. Before cells die, they also release signal molecules to other plant cells, such as methyl slicylate acid.

Systemic acquired resistance will occur when other plant cells receive the and converts the signal molecule into a hormone, methyl salicylate acid to salicylic acid, to induce defense gene expression.

Plant Defense Against Herbivores

Plants have various defenses against herbivores:

• Physical defenses including spikes, thorns, spines, and hairs (trichomes)

• Chemical defenses including direct chemicals that deter/harm herbivores and indirect chemicals that attract herbivore parasites & predators

  • Direct examples are nicotine, cyanogenic glycoside, and anti-nutritives

  • Indirect examples includes VOCs

However, plants tend to develop strategies that allow them to bybass these defenses (tougher mouths, chemical resistance, and so on)

Trichomes

Trichomes can act as both physical and chemical barriers.

They tend to make plants harder to eat or even harmful.

But, they can also be chemical when they have a glandular tip of chemicals (which can be direct or indirect).

Jasmonic Acid Example

Jasmonic acid is a phytohormone that is released in response to herbivory (wound-induced). The release of jasmonic acid is localised and later on dispersed throughout the plant.

Jasmonic acid induces the production of:

• Terpenoids: toxic & repellent

• Phytoalexins: antimicrobial

• Proteinase inhibitors: interferes w/ digestion

• VOCs: chemical signals to warn neighbouring plants