Plant diseases

Question 1

Plant pathology

Answer 1

interaction between plants and plant pathogens (not by herbivores/insects or malnutrition/abiotic stress)

Question 2

Phytopathology caused by

Answer 2

Viroid/virus – replicate inside host cell

Viroid example: Coconut Cadang-Cadang
- killed >30M coconut palms in Philippines since 1927 (no treatment / control)

Virus example: Papaya Ring Spot Virus
- Hawaiian papaya production decreased 94% in 1950s
- treat w/ transgenic RNAi plants – put viral genome element into host so silences RNAs of viruses

Bacteria - prokaryote, Gram(-)/(+)

Example: Olive Tree Quick Decline Syndrome
- > 500 woody and herbaceous hosts
- Very limited disease control options.

Fungus- filamentous, a/sexual cycles, spores

Ascomycete example: Rice blast
- Magnaporthe oryzae
- 10-15% rice loss
- Spore lands on surface of the rice epidermis
- The germination tube extends punching through the cell.
- Hypha grow (feeding structure-> feed on cell contents)

Basidiomycete exampe: Wheat stem rust
- Puccinia graminis
- wheat loss 10-70% annually
- treat w/ fungicides + resistance breeding – but new virulent Ug99 Uganda 1999 strain is quickly spreading so need more resistance breeding

**oomycetes **- filamentous, a/sexual, not related fungi

Example: Potato late blight disease
- Phytopthora infestans
- Irish potato famine = 1.5 million people died of starvation (pesticides, hygiene, resistance breeding treatment)

Question 3

Pathogen life styles

Answer 3

Biotroph: colonize and feed from living host tissues (e.g. rusts)

Necrotroph: kills host and feasts on dead tissue (e.g. grey mould fungus on strawberries)

Hemibiotroph: biotroph only initially until they kill the tissue and then become necrotroph

Saprotroph: lives on decaying tissues (does not kill)

Question 4

Entry mechanisms into the host

Answer 4

1. Stomata eg. P. syringae
2. Lenticels (raised pore in woody plant stems that allows gas exchange)
3. Hydratode (at end of each vein where water come outs) eg. X. campestris
4. Wounds (from gardening, wind) eg. X. aeopodis
5. Lateral roots (small cavity when root forms allows entry) eg. F. oxysporum
6. Nectarthode (pore in base of flower) eg. E. amylovorum
7. Haustoria (punches haustoria through leaf surface) eg. E. necator powdery mildew on grape
8. Appressoria (appressorium punches hyphae through epidermal cell then grows) eg. Stem rust
9. Killing host cells eg. Rhizopus microsporus

Question 5

host manipulation: Phytohormones

Answer 5

Change growth/ block immunity

Gibberellin GA– GA is plant elongation hormone so makes plants taller + spores easier spread by wind (e.g. G. fujikoroi fungus)

Auxin – auxin induces plant tumour growth by increasing cell division – tumours make space for pathogen to grow in (Ustilago maydis fungus)

Auxin + cytokinins – A. tumefaciens infects plants and transforms host w/ T-DNA via T4SS type 4 secretion system. T-DNA encodes mRNA for these hormones which make tumours (resources and space)

Question 6

host manipulation: Phytotoxins

Answer 6

Coronatine – reopens stomata to allow entry into host as usually hosts close stomata when recognise flagellin / pathogen (e.g. P. syringae bacterial hemibiotroph-> infect tomato)

Syringolin A - blocks host proteosome and signalling + makes host susceptible -> allows wound entry (e.g. P. syringae)

Rhizoxin – targets β-tubulin + blocks microtubule formation (fungus has mutant β-tubulin so resistant to own effects) (e.g. R. microsporus fungal necrotroph)

Question 7

host manipulation: small RNAs

Answer 7

target + degrade host mRNA

Example: Botrytis cinerea fungus – small RNAs enter host via exosomes + block / degrade specific transcripts (cross-kingdom RNAi)

Question 8

What are effectors?

Answer 8

What are effectors?
- Pathogen-derived molecules that manipulate the host cell-> include phytohormones, phytotoxins, and small RNAs but mainly talking about the proteins.
- Often interfere with immune signalling (biased view-> immune signalling is the most well studied)

1. Often secreted outside the pathogen cell (have SP, no TM)
2. Expressed (only) during (early stages of) infection
3. Often under positive selection (Ka/Ks>1)
   a. Beneficial mutations for virulence
4. Often no homology to annotated proteins

Question 9

Appoplast effectors

Answer 9

secreted into extracellular space / apoplast

Non-enzymatic apoplastic effectors
- Unrelated, small, stable, secreted proteins
- Acting as inhibitors and preventing degradation and recognition of pathogen by plants.

Enzymatic effectors:
- degrade host cell wall (although this allows detection of damage by host)

Question 10

Cytonuclear effectors

Answer 10

Act inside plant cell + delivered by T3SS for bacteria, or haustoria for fungi / oomycetes

Effectors targeting immune kinsase
- interfere w/ kinase signalling cascade involved in immune signalling after pattern recognition receptor (many effectors act redundantly on same immune pathway)
- Example: P. syringae

TALE transcription factors
- Example: SWEET gene epression by TALE = sucrose exporter that exports sucrose into apoplast (not usually active in mesophyll cells + only in phloem companion cells to load sucrose into phloem)
- Pathogen can take up sugar from apoplast

Opines
- T-DNA from Agrobacterium expresses opine which can only be metabolised by pathogen