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Plants Flashcards

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1
Q

In plants, what does meiosis result in?

A

A reduced second generation (not gametes) - alternation of generations.
Meiosis of sporangia forms spores (n) -> gametophytes -> gametangia -> gametes -> zygote (2n) -> sporophyte -> sporangia.
Simplified in gymnosperms.

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2
Q

What are the sporangia in conifers?

A

Cones.
Woody pine cone = female.
Cone cluster = male (release pollen).

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3
Q

What are spore mother cells?

A

Megasporocyte - female.

Microsporocyte - male.

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4
Q

What are sporophylls?

A

Carpels
(megasporophyll) - have ovules (contains megasporangia -> seeds) and form ovary (-> fruit)
Stamens (microsporophyll) - release pollen (microspores).

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5
Q

How are the embryo and endosperm (seed) formed?

A

Double fertilisation.

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6
Q

What are pollination syndromes?

A

Adaptive significance of flower:
Biotic - birds and insects.
Abiotic - wind and water.

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7
Q

What are the differences between monocots and eudicots?

A 
Monocots:
Flower parts in multiples of 3.
Parallel leaf venation.
Scattered vascular bundles (stem).
1 pore/furrow (pollen).
1 cotyledon (seeds/seedling).
Eudicots:
Flower parts in multiples of 4/5.
Netlike leaf venation.
Vascular bundles in ring.
3 pores/furrows.
2 cotyledons.
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8
Q

Relationship of gymnosperms and angiosperms?

A

Gymnosperms oldest, diverge first, then basal angiosperms (amborella, nymphaeales, magnoliids), monocots then other dicots and eudicots.

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9
Q

What are the basal angiosperms?

A

Same leaf venation and 2 cotyledons like eudicots, but pollen has only 1 pore, like monocots.
3% angiosperms.

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10
Q

What are the eudicots?

A

75% of angiosperms.

Fagaceae (oaks) and asteraceae (daisies).

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11
Q

What are the magnoliaceae?

A 
Many tepals.
Many stamens and carpels.
All parts arranged in a spiral.
Beetle pollinated.
Magnolia have many fruits with one seed each - angiosperm flower but gymnosperm-like seeds.
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12
Q

An example of nymphaeales?

A

Nymphea - water lily.

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13
Q

What are the fagaceae?

A 
Oak and relatives (beech, chestnut).
Dominant, temperate, broadleaf trees.
Reverted to wind pollination.
Catkin inflorescence.
Acorn fruit.
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14
Q

What are KCAG?

A 
K = calix = sepals.
C = corolla = petals.
A = androecium = stamens.
G = gynoecium = carpels, () = fused, _ = superior ovary.
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15
Q

What are the asteraceae?

A 
Daisies (dandelions, sunflowers etc.)
Inflorescence imitates a single flower (pseudanth), actually only 5 petals per flower.
Ancestors similar to gentians.
Calix -> pappus.
Types of flower:
Disc floret - C(5) A(5) Ginferior(2).
Ray floret (female).
Ligulate floret (hermaphrodite).
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16
Q

What are the monocots?

A

22% of angiosperms.
Poaceae (grasses) and orchidaceae (orchids).
Evolved from primitive aquatic magnoliids?

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17
Q

What are the poaceae?

A

Grasses.
Reversion to wind pollination.
KC2 A3 Gsup(2-3).
Spikelet encloses florets.
Florets: palea and lemma (tepals), ovary + stigmas, stamens.
Originated tropical forests, bamboos and rice. Spread (prairies, savannahs) correlated with high crown mammal dentition (herbivore resistance).
Human selection -> cereals.

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18
Q

What are the most diversified groups of angiosperms?

A
  1. Orchids - 24000.
  2. Daisies - 22000.
  3. Legumes - 17000.
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19
Q

What are the orchidaceae?

A

Orchids.
Most specialised monocot family.
Primarily tropical epiphytes.
Asymmetrical, extreme fusion of parts (column).
K3 C2+1 [A1-2 Ginf(3)].
Tiny seeds (like dust).
Insect pollination - highly specialised, eg bee mimicry.

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20
Q

How does fertilisation take place?

A

Pollen microspores -> microgametophytes and sperm.
Ovule w. megaspores -> megagametophyte (embryo sac) and egg.
Pollen tube delivers sperm to egg inside ovule.

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21
Q

What are the stages of embryo development?

A

Takes place inside ovule.
Stages = shapes:
1. Globular stage.
2. Early heart stage (can see cotyledons).
3. Late heart stage.
4. Mature embryo stage.
After fertilisation -> apical and basal cells.
Apical -> embryo.
Basal -> suspensor.
Embryo has 2 axes: apical/basal and radial ().
Apical/basal pattern of cell division with 2 groups of cells are left undifferentiated - the meristems.
Radial pattern: inside vascular, outside epidermis, cortex between.

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22
Q

Which factors are necessary to form the specific regions of the embryo?

A

Apical - gurke (gk).
Central - fäckel (fk).
^^both housekeeping proteins.
Basal - monopterous (mp), auxin responsive transcription factor.

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23
Q

What are roots made of?

A

Concentric layers of cells.
Central vascular strand - xylem and phloem.
Followed by gate layers - pericycle (with impermeable Casparian strip) and endodermis.
Then cortex and epidermis.
Root cap at end.
Cell-cell communication establishes layers.

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24
Q

What is the root meristem?

A

Where root development happens.
A stem cell niche (stem cells with defined roles) in contact with the quiescent centre - the organiser.
Plethora is expressed in QC and specifies the QC, division zone and elongation zone (gradient).
Plethora prevents the differentiation of the stem cell niche, which would stop root growth.

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25
Q

What happens if a stem cell around the QC is deleted?

A

Neighbour divides to replace it - cell communication.

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26
Q

What are scarecrow (scr) and short-root (shr)?

A

Transcription factors that cause the cortex/endodermis to differentiate.
SHR is produced in the stele but moves through plasmodesmata to cause the differentiation of the endodermis.
SCR is produced in the endodermis.

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27
Q

How do root hair cells (trichoblasts) differentiate?

A

Result from intercellular signals.
Cells in contact with 2 cortex cells -> RHCs.
Non-hair cells only in contact with 1.
Hair is default - GL2 gene determines non-hair, induced by Werewolf (product doesn’t move).
Werewolf also induces a gene whose product CPC is a repressor of GL2 (CPC can move to other cells to inhibit GL2, resulting in RHCs).

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28
Q

How do lateral roots form?

A

By division of pericycle cells, controlled by auxin (initiates growth).
Daughters organised into new root meristem.
Division controlled by mineral nutrient status - lateral roots detect nitrogen.

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29
Q

What is the shoot apical meristem?

A

Remains the same size throughout life of plant.
A pool of undifferentiated stem cells which separates during embryogenesis.
Produce differentiated organs and self-perpetuate.
Three zones:
Central zone - initial cells, slow proliferation, true stem cells, perpetuation.
Peripheral zone - rapid proliferation, leaf primordia differentiate.
Rib zone - vasculature/stem formation.
Three layers:
Tunica:
L1 - epidermis.
L2 - ground tissue, leaf, outer photosynthetic cells.
Corpus:
L3 - vascular tissue, leaf/stem.

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30
Q

What determines how cells in the SAM differentiate?

A

Their position.

However, most of shoot derived from few cells, each with multiple possible fates.

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31
Q

What is WUSCHEL?

A

Maintains initials, prevents differentiation.
Location of WUS expression (outside of central zone) acts as organiser, activates stem cells in central zone (initials).
A transcription factor - moves to the stem cells and binds to the CLV3 promotors to activate transcription. This limits WUS expression - autoregulatory loop.

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32
Q

What is Clavata1?

A

Antagonises WUS.
Promotes differentiation of initials.
Encodes leucine-rich repeat (LRR) transmembrane protein, acts as receptor in interaction with CLV2.
Also a kinase signalling protein.

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33
Q

What is Clavata3?

A

Expressed in initials.
Signals to limit WUS expression and therefore size of central zone.
Ligand for the CLV1/2 receptor.

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34
Q

What is WOX5?

A

Wuschel-like homeobox 5. A gene similar to Wuschel but signals cells around the root QC not to differentiate.
Signals to prevent stem cell differentiation conserved between root and shoot meristems.

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35
Q

What is stm?

A

Shoot meristem-less.
Required to prevent differentiation.
Lethal mutant - stem cells in embryonic shoot meristem differentiate, meristem lost.

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36
Q

What are the KNOX genes?

A 
Knotted homeobox class of genes - STM and related genes, which prevent differentiation into leaves.
Expressed in meristem central zone.
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37
Q

What are ARP genes?

A

Stop (repress) KNOX expression in the leaf primordia, allowing cells to differentiate to form leaves and initiate the SAM (Phan/Phab) to make the shoot.
Ectopic PHABULOSA converts roots to shoots and extra in embryo causes more WUS.

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38
Q

What is the difference between shoot growth and leaf growth?

A

Shoot growth is indeterminate - no limit (KNOX)

Leaf growth is determinate - predefined (ARP).

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39
Q

How do compound leaves form?

A

Extra KNOX.

Leaf primordia cells remain partially indeterminate.

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40
Q

What is TOPLESS?

A 
Makes the SAM shoot.
Represses PLETHORA (root).
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41
Q

Why is the shoot modular?

A

Organ production is sequential.
Leaf primordia are regularly spaced (phyllotaxy), with new primordia arising at the maximum possible distance from previous ones - lateral inhibition.

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42
Q

How does lateral inhibition take place?

A

Withdrawal of an activator - auxin.
Auxin causes differentiation of vascular tissue, which drains it - auxin maxima -> primordia, and withdrawal of auxin -> differentiation.
Local application of auxin generates new phyllotaxy.

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43
Q

What are the cell layers in a leaf?

A

Upper epidermis, palisade mesophyll, spongy mesophyll and lower epidermis (guard cells and stomata).
Mesophyll has vascular bundles - xylem, phloem and bundle sheath.
Each cell type differentiates individually - determined by genetic switches.

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44
Q

What are trichomes?

A

Giant single cells. Protrude from epidermis.

Trichome development activated by transcription factors (without them leaves are glabrous (bald)).

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45
Q

How are guard cells formed?

A

Epidermal cells specialise to become guard mother cells (GMCs), which then divide asymmetrically.
Guard cells inhibit the formation of others in the area (lateral inhibition), creating spacing.

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46
Q

What type of polarity do leaves have?

A

Dorsoventral (upper/lower, adaxial/abaxial).
Phan/Phab (orthologues) required for dorsal/adaxial fate - expressed in adaxial side of primordium (closer to SAM).
Without adaxial side, get needle-like leaves, abaxial all around.

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47
Q

What determines root vs shoot?

A 
Root = Plethora.
Shoot = Phan/Phab.
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48
Q

How are flowers produced?

A

Switch from vegetative to inflorescence meristem to change the type of lateral organ produced.
Involves gene Leafy - extra = advanced flowering.

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49
Q

How are the different floral organs made?

A

One or two classes of homeotic genes required to specify different whorls.
ABC model:
A - sterile sporophyll (Apetala1/2).
B - male/micro sporophyll (Apetala3/Pistillata).
C - fertile sporophyll (Agamous).
Sepals = A.
Petals = A+B.
Stamens = B+C.
Carpels = C.
Agents of Leafy - necessary and sufficient to determine each whorl.
Agamous also turns of floral meristem activity by terminating WUS (central zone).

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50
Q

What would happen in an ABC triple mutant?

A

Floral organs -> leaves.

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51
Q

What happens if Agamous C is comstituively expressed?

A

Overrides A -> extra carpels and stamens (same as A mutants).

52
Q

What do floral homeotic genes encode?

A 
MADS box transcription factors (except AP2).
MADS box proteins act in pairs as dimers so can form different combinations with different functions - eg. an A protein + a B protein combine to make petals.
MADS box proteins have cadasteral activity (territorial). Self-reinforcement and A and C inhibit each other.
B class cue = ring around central zone (appears in embryo).
53
Q

What are barriers

To self fertilisation?

A
  1. Flowers mature as male or female at different times.
  2. The shape of the flower allows them to pollinate other flowers, but not themselves easily.
  3. In many species, pollen is not self compatible (S locus responsible - pollen and stigma recognise same genotype).
54
Q

How do fruits develop?

A
  1. Ovary grows.
  2. Dispersal structures or animal attractants develop.
  3. Fruit ripens (senescence), eg. degradation of pectin in tomato cell wall by polygalacturonase.
    (Programmed cell death part of many plant developmental programmes).
55
Q

What are photoautotrophs?

A

Plants.
Use energy from sunlight to make organic molecules from water and CO2.
Photosynthesis.

56
Q

What is light energy proportional to?

A

The frequency of the wave.

57
Q

How are excited electrons generated?

A

Light absorption - changes electronic states.
Light absorbing molecules are pigments (wavelengths that are not absorbed are transmitted or reflected).
When chlorophyll absorbs light, an electron moves from ground state to excited state.

58
Q

What are the photosynthetic pigments?

A
  1. Chlorophyll a.
  2. Chlorophyll b.
  3. Carotenoids.
59
Q

What is the structure of a chlorophyll molecule?

A
  1. Porphyrin ring - light absorbing (Mg centre).

2. Hydrocarbon tail - inside thylakoid membrane.

60
Q

How much incident energy is not absorbed?

A

About half (mostly IR).

61
Q

What happens when chlorophyll absorbs light?

A
  1. The unstable excited electron dissipates its energy via heat or fluorescence.
  2. Photosynthesis - initiates electron transport chain through charge separation. The lost electron is replaced with one from an H2O molecule (solar energy used to split water).
62
Q

What happens after charge separation in PSII?

A

Generates reduced plastoquinone and oxygen (by-product, 1/2O2).

63
Q

Why is oxygen a dangerous by-product?

A

It can recombine partially with electrons to become a reactive oxygen species (ROS).

64
Q

What are stromatolites?

A

Mats of cyanobacteria - beginning of oxygenic photosynthesis.

65
Q

What is the Z scheme?

A

2 photosystems - PSII and PSI, which work in tandem and are asymmetrically distributed.
Light -> electron excitation and charge separation in both.

66
Q

Where do the light reactions take place?

A

The thylakoid membranes.

67
Q

What are photosystems made of?

A

A reaction centre surrounded by light harvesting antennae (accessory pigments).
The antennae transfer excitation to the reaction centre, where charge separation takes place.
PSII = 680 light.
PSI = 700 light.

68
Q

What are the 4 complexes in the thylakoids?

A
  1. PSII (->PQ carrier).
  2. Electron transport chain.
  3. PSI (->PC* carrier).
  4. ATP synthase.
    * plastocyanin.
69
Q

What is chemiosmosis?

A

The movement of H+ ions from the acidic thylakoid lumen to the stroma through ATP synthase, generating ATP.
Electron transport chain pumps H+ ions into the lumen to create the H+ gradient.

70
Q

What is the Calvin cycle?

A

Dark reactions.

CO2 is fixed by rubisco and the cycle produces sugars.

71
Q

What happens at light saturation?

A
  1. Fluorescence.
  2. Non-photochemical quenching (NPQ)
  3. Photochemical quenching.

Strong light causes chloroplasts to emit fluorescence, mostly from PSII.
This can be quenched as electron transport (photochemistry) takes place - photochemical quenching .
Without photochemistry, all light absorbed is emitted as fluorescence.
NPQ happens by means other than electron transport - heat dissipation.

72
Q

How does NPQ work?

A

Correlates with zeaxanthin (a xanthophyll (carotenoid)).
Low NPQ mutant deficient in enzyme that synthesises zeaxanthin.
Zeaxanthin uncouples the reaction centre and antenna.
Change in zeaxanthin level during the day due to synthesising enzyme being activated by a high pH change caused by high light.

73
Q

What are state transitions?

A

Light is redistributed between the 2 photosystems from the one receiving more light to the one receiving less (absorb different wavelengths). Allows them to work in tandem.
Involves the movement of LHCII antenna from PSII to assist light harvesting in PSI. Accumulation of reduced PQ activates an LHCII protein kinase, triggering the movement of the antennae.

74
Q

What is solar tracking/avoidance?

A

Adapting to light by physical movement.
Eg. leaves angle towards Sun, or chloroplasts within a cell move to avoid strong light.
Increase efficiency or minimise damage.

75
Q

When are ROS intentionally produced?

A

When the electron transport chain is saturated (reduced ferredoxin).
O2 is reduced to O2- (superoxide) -> H2O2, +H2O +ascorbate -> spent ascorbate + H2O.
Water-water cycle or Mehler reaction.
O2->H2O2 = superoxide dismutase.
Ascorbate and peroxide reaction = ascorbate peroxidase.

76
Q

Which part of the photosystems is photodamage limited to?

A

PSII D1 subunit.
Toxic photoproducts result of excess photons.
If D1 doesn’t contain damage, result is photoinhibition.

77
Q

How does acclimatisation affect photodamage?

A

When exposed to increasing light:
Sun leaf has better defence mechanisms and does not suffer photoinhibition.
Shade leaf defence mechanisms fail much more quickly and leaf suffers photoinhibition.
Differences in leaf anatomy and chloroplast components:
Sun leaf can photosynthesise at higher light levels where shade leaf would be saturated.
Sun leaf chloroplasts have more rubisco and fewer antennae than shade leaf, and more PSI as PSI harvests less light (long term solution to compared to short term state transitions, also signalled by imbalance in electron transport) - this takes time (acclimatisation).

78
Q

How does low temperature affect plants?

A

Similar stress to high light.
At low temp. biochemistry is slower, causing same imbalance as high light in summer.
NPQ always engaged as in summer midday.

79
Q

What is photorespiration?

A

The C2 cycle.
Rubisco fixes O2 instead of CO2 about 25% of the time.
Produces phosphoglycolate instead of phosphoglycerate. This is salvaged, involving peroxisomes and mitochondria, but CO2 is lost.
Overall, oxygen uptake and CO2 loss - like respiration.

80
Q

Why does rubisco fix oxygen?

A

Rubisco has carboxylase and oxygenase activity.
When rubisco evolved, there was far more CO2 and far less O2 in the atmosphere.
Increased O2 -> increased oxygenase activity.

81
Q

Why is O2 fixation by rubisco a problem in hot/dry conditions?

A

Plants close their stomata to reduce water loss:
1. Reduces CO2 uptake.
2. Allows O2 to accumulate.
3. CO2 less soluble than O2 at high temperatures.
= too much O2, not enough CO2 for rubisco.

82
Q

How does C4 photosynthesis concentrate CO2 for the Calvin cycle?

A

In C4 plants, mesophyll and bundle sheath cells have different functions.
Light reactions take place in mesophyll cells and CO2 is fixed by PEP carboxylase (-> oxaloacetate -> malate).
The Calvin cycle takes place in bundle sheath cells, where malate is decarboxylated to release CO2 (and pyruvate, which returns to mesophyll cell).
As well as changes in biochemistry and chloroplast composition, development - mesophyll cells must be in contact with bundle sheath cells.

83
Q

What is the cost of C4 photosynthesis?

A

Uses 5 ATP instead of 3.
Only worth it at high temperatures.
Benefit = can also cope with limited gas exchange.

84
Q

How do CAM plants cope with drought?

A

Close stomata during the day and store CO2 overnight.
Night:
Stomata open, PEP carboxylase fixes CO2 and it is stored as organic acid (requires water).
Day:
Stomata close, CO2 released from acid for Calvin cycle.

85
Q

How do plants avoid photorespiration?

A

Separating light harvesting (O2 generating) and CO2 fixation - C4 and CAM plants.

86
Q

What are hormones?

A
  1. Coordinate responses of groups of cells.
  2. Synthesised at 1 location and act at another.
  3. Act at catalytic concentrations - must trigger second messengers and signal transduction pathways.
  4. Morphogens.
87
Q

What is phototropism?

A

Bending of plants towards light (blue), caused by lateral auxin transport.

88
Q

Auxin controls the development of what?

A
  1. Embryos.
  2. Shoots.
  3. Roots.
89
Q

How is auxin transported?

A

From top to bottom via vascular tissue. Reversed in peripheral tissue.
Efflux carriers (PIN1) transport auxin out of vascular cells. Located on only one side of cell - controls direction of auxin movement.
Polar localisation of PIN1 happens early in embryogenesis.

90
Q

What is the first signal that causes polar localisation of PIN1?

A

Gravitropism.

PIN proteins transported to lower side of cell.

91
Q

How does auxin cause extension?

A

Acts at membranes to cause the cell wall to stretch.
Auxin activates a membrane H+ pump, lowering the cell wall pH.
Low pH activates expansins, which loosen xyloglucan binding in the cell wall.

92
Q

What is apical dominance?

A

Axillary bud growth - controlled by auxin.

93
Q

How does auxin control phyllotaxy and leaf formation?

A

Primordia emerge at auxin maxima.
As primordia differentiate, they draw in auxin (L1), becoming auxin sinks.
Auxin is then withdrawn by veins (differentiation triggered by auxin) - leaf formation.
PIN1 is located in the L1 cell layer of meristems, and directs auxin flow towards maxima. This polarity is determined by auxin gradients - positive feedback.

94
Q

What does modelling the PIN/auxin positive feedback loop predict?

A

Phyllotaxy - the positions of new leaf primordia.

95
Q

How does auxin act?

A

Activates expression of many auxin-regulated genes.

  1. These genes have auxin response elements (AREs).
  2. Auxin response factors (ARFs) bind AREs.
  3. ARFs are normally inhibited by AUX/IAA.
  4. When auxin is present, AUX/IAA inhibitors are targeted for degradation (ubiquitination).
  5. TIR is the auxin receptor that triggers ubiquitination.
96
Q

What is ethylene?

A 
A gas hormone.
Controls:
1. Ripening.
2. Abscission (w. auxin).
Also signal of attack - triggered by injury/pathogens.
97
Q

How is ethylene produced?

A

From methionine by ACC synthase and ACC oxidase.

98
Q

Why is there a burst in respiration at ripening?

A

Ensures even ripening.

99
Q

How does ethylene work?

A

ETR1 encodes a sensor histidine kinase, which is the ethylene receptor.
Ethylene is an inhibitor of ETR1, which is an activator of CTR1, which is an inhibitor of EIN3, which produces the responses.
Histidine kinases are common environmental sensors in bacteria

100
Q

What is the ethylene triple response?

A

Results in etiolated seedlings:

  1. Inhibits root elongation.
  2. Shortens hypocotyl.
  3. More curved apical hook.
101
Q

What is cytokinin?

A

Causes cell division.
Cause plant organ differentiation (with auxin).
Synthesised in roots and promotes shoot and leaf differentiation.

102
Q

How does agrobacterium infection cause crown gall tumours?

A

Agrobacterium injects T-DNA containing genes for the synthesis of growth factors auxin and cytokinin, as well as for tumour growth.

103
Q

How does cytokinin work?

A

Sensor histidine kinase receptor (like ethylene) and cytokinin-dependent response regulators.

104
Q

What does gibberellin do?

A

Promotes stem elongation and germination (inc. mobilisation of seed reserves).

105
Q

How does gibberellin work?

A

DELLA protein (encoded by GAI gene) represses growth (stops transcription of growth genes).
Gibberellin targets DELLA for destruction (ubiquitination) through its receptor
GID1.
Gibberellin signalling poised but repressed in absence, like auxin.

106
Q

Why do dominant and recessive DELLA gene mutations produce different phenotypes?

A

Dominant mutations prevent ubiquitination, so growth is constitutively repressed even in presence of GA - dwarf mutants.
Recessive mutations result in loss of DELLA, so growth is constitutively active even in absence of GA - tall mutants.

107
Q

How were semi-dwarf wheat varieties produced to avoid famine (1960s, green revolution)?

A

Reduced height wheat due to dominant GAI mutations.

108
Q

How are hormones balanced in the SAM?

A

Contrasting balances in different zones.

109
Q

How can the location of the QC be predicted?

A

Located at the site of an auxin maximum.

Predictable using the known action/localisation of PIN proteins.

110
Q

How does auxin organise the root meristem?

A 
Activates PLETHORA (max. in the QC), which prevents the stem cell niche from differentiating.
Via MONOPTEROUS, an ARF.
111
Q

How does TOPLESS repress PLETHORA in the shoot?

A

Co-repressor of AUX/IAA, which represses ARFs (eg. monopterous).
Repressing auxin response represses PLETHORA.
The SAM is then maintained by cytokinin.

112
Q

How do cytokinin, WUS and CLV3 interact?

A

CK inhibits CLV3 and activates WUS.

CLV3 inhibits WUS and WUS activates CLV3.

113
Q

What types of plant pathogens are there?

A 
Fungi - eg. powdery mildew.
Bacteria - eg. crown gall.
Viruses - eg. tomato mosaic.
Nematodes - eg. root nematode.
Affect 25% of crops.
114
Q

What are generic defences?

A

Plant detects elicitors:
Fragments of own cell wall (oligogalacturonides).
MAMPs (microbe associated molecular patterns - eg. chitin, flagellin.
Elicitation triggers gene expression and production of new proteins (PR) or secondary metabolites (phenolics).
First line of defence - non-host immunity.

115
Q

What are PR proteins?

A

Pathogenesis proteins.
Produced as part of first line defence against a pathogen.
Eg. chitinases or defensins.

116
Q

What are phytoalexins?

A

Plant antibiotics, effective against microorganisms or insects.
Eg.
Glucosinolates - cruciferous veg.
Cyanogenic compounds - produced by different compartments mixing when cells are disrupted.

117
Q

What are pathogenesis factors?

A

Pathogen weaponry.

Eg. bacteria have injection apparatus (Hrp) which they use to inject Avr proteins (avirulence).

118
Q

What are Avr proteins?

A

Host specific, they suppress elicitation and first line defence.

119
Q

What is the second line of defence?

A

Gene for gene resistance.
Plants specifically recognise Avr proteins through their own R (resistance) proteins.
Recognition -> more vigorous response, as R gene activation triggers an oxidative burst.
Avr and R genes result in pathogen specific resistance - gene for gene interaction.

120
Q

How do oxidative bursts limit the spread of infection?

A

Cause:
Death of the cell (hypersensitive response HR).
Increased PR expression in surrounding cells.

121
Q

How does an HR protect the rest of the plant?

A

Triggers:
Sealing of phloem.
Production of ethylene for abscission.
Production of PR proteins in distant tissues (mobile signal).

122
Q

What are host and non-host interactions?

A 
Non-host = species incompatibility, immune, eg. barley powdery mildew and wheat.
Host = species compatibility, disease depends on gene for gene resistance - Avr and R proteins (resistant or susceptible).
123
Q

What type are R proteins?

A

Most include a leucine-rich repeat (LRR) and some also a kinase motif, while others associate with kinases.
One class are LRR-RKs (receptor kinases).
Genetic signal receptors are also LRR-RKs.
Homologous to components of innate immune system in animals.

124
Q

Why are R genes continuously replaced?

A

They have a limited useful life - pathogen Avr gene can be lost or mutate.
Arms race.
R genes can be used to genetically engineer resistance.

125
Q

Why do plant roots have symbiotic relationships with mycorrhiza?

A

The hyphae harvest phosphate for the plant and receive organic carbon.
Phosphate is the hardest macroelement for plants to obtain.
Symbiosis may be intra or extracellular.

126
Q

Why do plants have symbiotic relationships with bacteria (nodulation)?

A

Nitrogen in the soil is often a nutritional limiting factor. Some bacteria can fix nitrogen from the atmosphere, so association with nitrogen fixing bacteria = source of nitrate.
Nodules on the roots harbour the bacteria.

127
Q

How do plants respond to N fixing bacteria?

A 
NOD factors (rhizobium) detected by symbiosis receptor-like kinase (SYMRK).
Common mechanism with mycorrhiza symbiosis - nodulation using pre-existing mechanism (LRR-RKs)

Biology (6 decks)

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