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Summary - Class notes - Plant-Microbe interactions
1488322800 Plant Microbe Interaction
Pest: insects, mites, nematodes, fungi, bacteria, viruses.
Abiotic: drought, temperature, nutrition, salinity
In Finland: dryer in summer, wetter in winter (in future) +- 2-7 degrees higher temp.
World population will keep growing. Need for technology to supply food.
Poor people have the least resources ánd bad surroundings (dry etc)
Eat more plants and less meat.
Sweet potato+ potato is relatively more grown: can be grown in dry season, doesn't have a lot of diseases, uses less water than other crops. You can probably survive for months on potato's.
Disease reduces yield by 10%! Tomato in niguragua has millions of white flies -> farmers use pesticides -> unhealthy tomatoes. Should try to grow resistant crops now that are tolerant plants (no severe symptoms)
Chemical control: fungisides, but not possible for virus, limited for bacteria.
Insecticides affect also useful or non-harmful species !
Economical problem: no pesticide = maybe pests = less yield. But pesticides also cost money.
We need health (uninfected) seeds.
Plant growth promoting rhizobacteria, compete with pathogens, are beneficial for the plant (fixate nitrogen) and eat sugars/root exudates. Plants doesn't experience abiotic stress because the ethylene stress signal is broken down by rhizobacteria enzymes.
You can control yield losses of a certain bacteria (streptomyces turgidiscabies) with another (non-pathogenic)-streptomyces.
There are many new techniques for engineering plants. Such as: cisgenesis crispr-cas9
Outcome is the same: ust a plant with a mutation and therefore maybe disease-resistance. So regarded as non-transgenig? (In Sweden this is the case)
In developing countries more biotech crops are growing than in industrialized countries.
80% of soybean is transgenic, 30% maize, 75% cotton, 24% canola.
"When we have learned the technology, we do the applications we need" - Dr. Patrick Rubaihayo
1488409200 Defense mechanisms of plants
Disease not always related to microbes, can be abiotic.
Pathogens can be necrotroph (fungus botrytis), biotroph (oomycete hydroperonospora) or hemibiotroph (baceria pseudomonas). Hemibiotrophs may switch from biotroph to necrotroph.
Disease is still the exeption! Plants have defense!
Preformed physical barriers: epidermis, bark, wood, cell wall
Preformed chemical barriers: secondary metabolites
Cuticula protects leaf against desiccation, herbivores, pathogens
Trichomes: physical and/or chemical barrier
Thorns and spines in some plants against herbiovers
Stomates prevent water loss... how in response to enemies? Still under investigation
Cell wall: primary with cellulose (microfibrils) and secondary with pectin and glycan
Cell wall strengtening defenses
- pathogen-induced ROS borst (Reactive Oxygen Species)
- Callose deposition
Special cells: Ideoblasts ('crazy cells') : Stinging cells, stone cells, pigmented cells with bad taste, etc.
- terpenes (primary in sugars, proteins, amino acids..) Vooral in coniferen en bijvoorbeeld laurierblad
- Phenolic compounds
- nitrogen containing coumpounds (alkaloids) like nicotine and cocaine (cyanogenic glycosides, glucosinolates)
Pathogen might not recognize host: also resistance (non-host resistance)
- Pamp-triggered immunity (for instance flagellum of bacteria recognized by plant leading to first layer in defense)
In response, bacteria may excrete effectors to break down this defense
now, plant activate next layer of defense -> avirulence factors. Strong and efficient.
This is effector-triggered immunity
HR-response might happen, effective against biotrophs (but might help necrotrophs)
Some resistance genes exist against nematodes and insects
SAR - Systemic Acquired Resistance (may move in plant) is long-lasting and effective against many pathogens. Which signal is responsible? Definitely at least Salicylic acid. Mainly defense against biotrophs.
Jasmonic Acid and ethylene are mainly against necrotrophs
Induced Systemic resistance (ISR) triggered by beneficial microorganisms in rhizosphere.
RNA-silencing-degradation of specific viral RNA, triggered by DS-RNA molecules... Maybe also in immunity to other pathogens!
They are roundworms, occur in all habitats, are parasites or free living (+- 25000 species)
Largest nematode up to 9 meter. In whale-placenta. Most up to 1 cm.
All are aquatic: they need water to move, keep body functioning, but NOT TOO MUCH water.
They are bilateral symmetric, have a hydrostatic skeleton, are unsegmented and the body is filled with fluid. Tube (digestive system) in tube (body).
Have nervous system (no eyes/ears) and reproductive system
They have 6 stages: egg-juvenile 1-juv 2-juv 3-juv 4- adult. In some juv 2 hatch from egg.
Bad conditions stops development. Dauer stage. in some daur larvae obligate. Often J1, J2. Different mouth parts (stylet to penetrate plant cells or fungi, tube feeds on bacterica, sphere for omnivores, wide with 'teeth' for predatory)
Plant parasytic nematodes can be considered free living (some species are obligate plant parasites)
Herbivorous nematodes have many effects on plants like modify cell function/development, cause cell death, cause wounds and so entry for eg. bacteria.
Symptoms usually uncrlear.... Slow growth, death, wilt, root deformaties, reduced yield...
on average 12,3% crop loss due to nematodes
Chemical control of nematodes is effective, but now banned.
Looking into the plant-nematode interaction
root feeders: endoparasites in roots ectoparasites on roots. Also seed feeders and stem/leaf feeders
Pinewood nematodes make holes in the cappilary, trees can't transport water.
Sedentary (endoparasites) like cyst nematodes and root knot nematodes
Migratory can be endo-or ectoparasites.
See picture for scale of size of different pathogens. Kinda big are nematodes.
Steps of feeding: orientation, probing, penetration, secretion, salivation, ingestion of host cytoplasm, retraction. (1 week or few hours on 1 place).
May transmit TOBRA viruses (may cause spraying in potato, brown stripes)
May transmit NEPO viruses
they lose the virus when they mold, stylet also molds
They can produce many enzymes (cellulase, xylanase, arabinase...)
Migratory nematodes move ghrough cortex. Cyst nematodes go through endodermis
Cyst nematodes can be in the soil for years (as cyst). They form a syncytium (feeding cell).
Males leave the root to mate with females. Females stay in 1 place and turn into cyst. root knot nematodes lay an egg mass. Root swells. they also initiate a feeding cell: giant cell.
Syncytium formed by dissolving cell walls. Giant cell formed by interference in mitosis: cells don't split/make cell walls. Both are multinucleate.
Development of feeding cells
1. Cell wall + membrane modification (expansins, water channel proteins, etc)
2. rearrangement of cytoskeleton
3. Nuclear changes
4. Signal transduction pathway & transcription factors
In nematodes, it is not known yet which PAMPs are recognized by the Plant
effectors are known, ongoing research
the nematode mimics plant proteins on its cuticle (so plant doesn't recognize them, or targets these proteins and then the nematode sheds skin)
Nematode also produces enzymes to deal with plant defense
Resistance against nematodes... Not available for all, mostly for the specialized, sedentary nematodes.
The plant genes that make it resistant are being used in breeding programms
Thicker cell walls
3 classes of resistnace genes: TIR/L2/HS1PRO-1
Mi-gene (against root-knot): necrosis near invading nematode- No giant cell
H1-gene (feeding cell starts, but necrosis around, so they die or become male)
Identify genes involved in plant parasitism
- look at proteins in seretions
- antibodies against these
- this is only the genes that are active and encode for small transcrips so you
- isolate the glands of nemetodes. check the RNA
- expressed sequence tags ESTs
- completely sequence genome
- RNA interference (RNA-i) < another lecture on this
Nematodes can have benefits. More nitrogen for plants, bio-control by feeding on other nematodes or fungi or insects.
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