AGR2451 Lecture 15– M.Raizada

Review of last lecture “secondary metabolism”

Lecture 15 – “How a plant responds to a pathogen attack”A. Pathogen Strategies A1. Fungi•Irish famine in 1846 and 1847 which caused the emigration of 1 million Irish caused by Phytophthora infestans, a fungal blight disease of potatoes•There are two strategies for infection:I) The fungus establishes a haustorium – a feeding structure inside a living plant cell to take advantage of incoming foodII)The fungus stays in the intercellular spaces (apoplast), and grows onleaked nutrients.

From Biochemistry and Molecular Biology of Plants, page 1106B. Buchanan, W. Gruissem, and R. JonesASPP Publishing, Rockville, MD, 2000

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A2. Bacteriamost bacteria live within intercellular spaces (apoplast) or the xylemmany cause damage by secreting toxins or cell wall-degrading enzymes

A3. Viruses•consist of DNA/RNA surrounded by a protein coat•only 40 families of DNA/RNA plant viruses•viruses must:-replicate inside host-spread from cell to cell and in vascular system•they can travel in the phloem at a rate of 1 cm/hr•viruses also travel between cells through the plasmodesmata. •However, the channels in the plasmodesmata are too small for the viral DNA/RNA to pass through. •How do the viruses overcome this?

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From Biochemistry and Molecular Biology of Plants, page 1107 + 1109B. Buchanan, W. Gruissem, and R. JonesASPP Publishing, Rockville, MD, 2000

A4. Nematodes•1mm long worms•cause major modifications of the root architecture•all possess a hollow feeding tube (stylet) capable of penetrating cells walls•nematode eggs hatch and nematodes migrate to vascular tissue•dormant eggs perceive an unknown chemical signal released by plant roots which causes the eggs to hatch•The nematodes then hijack the cell by releasing secretions through its feeding tube. What do these secretions do?

•in contrast, other nematodes induce mitosis but without the last step of cell wall formation, resulting in giant plant cells

•the syncytial cells and giant cells associate with phloem cells --- the result of these strategies is that the nematodes become alternative sinks for photosynthate!!

From Biochemistry and Molecular Biology of Plants, page 1111B. Buchanan, W. Gruissem, and R. JonesASPP Publishing, Rockville, MD, 2000

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A5. Insects•two categories: those that chew and those that suck sap•eg. thrip and, aphids cause minimal tissue destruction, but use a stylet (mouth part) to drain sap from the phloem

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•eg. locusts chew up entire fields; European corn borer•many insects transmit viruses while feeding

Based on these pathogens, what does a plant need to do protect itself?

B. Plant Defense Strategies •only a small proportion of pathogen infections lead to disease•plants have invested huge numbers of genes/ energy to fight pathogens•must distinguish friend (eg. Rhizobium, friendly mycorhiza) from foes

B1. Preventive Measures – Secondary Metabolites (toxins, bitterness)•many secondary compounds produced constitutively, •compounds may be in vacuole or other compartments, then released into cytoplasm after pathogen attack

From Biochemistry and Molecular Biology of Plants, page 1113B. Buchanan, W. Gruissem, and R. JonesASPP Publishing, Rockville, MD, 2000

B2. The Hypersensitive Response (HR)•within 24 hours of pathogen infection, there can be localized plant cell death – the plant causes its own cells to commit suicide•dead cells contain high concentrations of antimicrobial compounds

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•when you see necrotic flecks on plant cells – these are dead cells at sites of attempted pathogen attack

How is the plant HR response similar to the formation of human toes??

From Biochemistry and Molecular Biology of Plants, page 1087B. Buchanan, W. Gruissem, and R. JonesASPP Publishing, Rockville, MD, 2000

From Biochemistry and Molecular Biology of Plants, page 1133B. Buchanan, W. Gruissem, and R. JonesASPP Publishing, Rockville, MD, 2000

The HR Response (Continued)•within 5 minutes after infection, reactive oxygen species are produced (superoxide O2-, H202 hydrogen peroxide)

The HR response is very species specific. Certain pathogens do not trigger the HR response, whereas others do. What determines this specificity?

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From Biochemistry and Molecular Biology of Plants, page 1094B. Buchanan, W. Gruissem, and R. JonesASPP Publishing, Rockville, MD, 2000

From Biochemistry and Molecular Biology of Plants, page 1128B. Buchanan, W. Gruissem, and R. JonesASPP Publishing, Rockville, MD, 2000

The HR Response (continued)•disease resistance (due to Avr/R interaction) -- pathogen infection is prevented or stopped•disease tolerance = plants are infected, but the plant restricts the biochemical process that causes symptons, so tissue damage is minimal even though plants are heavily infected

•How does the R/Avr recognition system explain why it is so easy for a pathogen to gain resistanct to a plant?

•So, how do plants respond to the rapid evolution of the pathogen genes?

•as part of the HR response, the surrounding cells create a “penetration plug” which consists of sugar and lignin polymers

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What are plant “lesion-mimic” mutants?

From Biochemistry and Molecular Biology of Plants, page 1090 + 1135B. Buchanan, W. Gruissem, and R. JonesASPP Publishing, Rockville, MD, 2000

B3. Pathogenesis-Related (PR ) proteins•PR proteins are enzymes including chitinases, glucanases = enzymes that degrade fungal walls•within minutes - hours after pathogen attack, PR transcription is induced•Aspirin (Salicylic Acid) is a plant signalling compound that mediates the switching on of many PR genes•there are also hundreds of very small proteins (called defensins) which are induced and lead to pathogen cell wall and other damage. Defensins are produced by birds, insects and mammals as well.

B4. Phytoalexins •low molecular weight antimicrobial compounds that accumulate at site of pathogen infection•these must be induced by infection (**not constitutive)•includes flavonoids

B5. Post-transcriptional gene silencingWhat is this?

How does the virus fight back?Can encode an enzyme to suppress the plant degradation factors!!

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B6. Systemic acquired resistance (SAR) 8within hours after pathogen exposure, defense responses are seen in tissues far from the invasion site and even neighboring plants. How is this possible?

•this is a sort of immunity mechanism that plants have --- if a part of aplant is pre-exposed to a pathogen, other parts become protectedprotection is mediated through the turning on of specific PR proteins (eg. fungal cell wall degrading enzymes)

•an identical response occurs after mechanical wounding due to insects – the long-distance signal is via an 18 amino acid peptide (systemin) which travels through phloem to upper unwounded leaves within 60-90 minutes

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From Biochemistry and Molecular Biology of Plants, page 1144B. Buchanan, W. Gruissem, and R. JonesASPP Publishing, Rockville, MD, 2000

Conclusion-disease resistance is a complex series of biochemical reactions involving many genes, many proteins, toxins and other compounds

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From Biochemistry and Molecular Biology of Plants, page 1143B. Buchanan, W. Gruissem, and R. JonesASPP Publishing, Rockville, MD, 2000

.Improving Disease Resistance

How can plant disease resistance be improved?

C1. Genetic Engineering/Breeding of New R genes•perhaps can engineer new R genes for specific pathogen recognitionwhat are some technical problems with:Breeding?

Genetic engineering?

C2. Special case – the Bt toxin•Bacillus thuringiensis produces toxins; since 1930s sprayed to control coleopteran and lepidopteran insects eg. larvae of European corn borer•the BT toxins create holes in the membranes of the cells in the insect digestive tract thus causing death attractive for genetic engineering because BT toxin only affects a few insect speciesthe toxin is a protein

From Biochemistry and Molecular Biology of Plants, page 1154B. Buchanan, W. Gruissem, and R. JonesASPP Publishing, Rockville, MD, 2000

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