Securing plant-derived food from the impacts of changing climates on

disease management

RebeccaFordEnvironmentalFuturesResearchInstituteSchoolofNaturalSciencesGriffithUniversity

Cabbage

Wheat

- we rely on relatively few food staples!

PotatolateBlightMildewsonbrassicasp.

Wheatstemrust

Maizestreakvirus

Cassavamosaicvirus

Yamanthracnose

BUT…every plant food is impacted by major biotic constraints (diseases)

Yellowleafspot

Ricebrownspot

Napiergrasssmutdisease

Historically, some have caused mass famine and dislocation of whole populations

• PotatoLateBlight(Phytophthorainfestans)andtheIrishpopulation• Seriesofwetmildwintersinlate1840’s

External environmentrainfall (frequency and volume), temperature, soil conditions, CO2 level, cultural practices, chemicals, vectors

Microclimatehumidity, dew period, temperature, light intensity, radiation, wind speed

Pathogenfitness, virulence, reproduction, dissemination, population size, adaptive potential

Host plantarchitecture, canopy density, resistance genes, additional stress, alternate host

Better management through adaptation

Environment

Genetics

Alternate hosts

Insect vectors

Inoculum reservoirs

Airborne Inoculum

Soil borne

InoculumSoil moisture, soil temperature, root physiology and architecture, possible competition with other microbes, root exudates

Air temperature, wind speed, rain splash, dew period, canopy density, waxes, hairs, cuticle thickness, natural openings, plant fitness, pathogen fitness (virulence)

Presence of alternate host and/or vector

Studies on individual pathosystems – broad conclusions are misleading

Studies of climate change effects on• Pathogen behaviour (population dynamics, pathogenicity, toxic compounds)• Host behavior (physiological, molecular)• Pathogen-host interaction changes (disease reaction R/S)

Revised disease management plans based on • New cultivars• Chemical use• Cultural strategies to alter microclimates

– planting density– planting timing

Where the research is required…..

Disease risk modelling under changed climates

Adapted from Chakraborty and Newton (2011)

Crop Disease and pathogen Predicted influence of climate change on disease

Reference

Barley Powdery mildew – Blumeria graminis

Decrease at higher CO2 Hibberd et al, 1996

Rice Leaf blast – Magnaportha oryzae

Increase at higher CO2 Kobayashi et al, 2006

Soybean Brown spot – Septoria glycines

Increase at higher CO2 Eastburn et al, 2010

Soybean Sudden death syndrome – Fusarium virguliforme

No effect at higher CO2 Eastburn et al, 2010

Wheat Stripe rust – Puccinia striiformis

Increase with higher temperature Coakley, 1979; Chakraborty et al, 1998; Milus et al, 2006

Wheat Crown rot – Fusarium pseudograminearum

Increase at higher CO2, cultivar and soil water dependant

Chakraborty et al, 1998 ; Mulloy et al, 2010

Predicted changes on disease occurrence

Adapted from Luck et al, (2011) Plant Pathology 60: 113-121

Chickpeaandascochytablight

• Australia=largestglobalproducer($1.2bexport2016)• BlightcausedbyAscochyta rabiei• Destroyedtheindustryin1998• Commodityvaluedropped$296min2013(~40%)• Noimmunity,resistanceerosion

Ascochyta rabiei

• Necrotrophic ascomycete fungus

• Wiped out industry in 1998 through loss of yield and grower confidence

• Quantitative resistance

A.rabieipopulationstructure

• Potential to evolve - to overcome host resistance and chemical controls

Ascochytarabieiisaveryfitandbroadlyadaptedclonalpathogen

Resistant sources

In 2009, the population was largely unable to overcome host resistance

Susceptible check

Meanwhile, production systems are adapting

Changed farming practices• Planting density• Row spacing• Raised beds

Transformational changes• Geographical • Chasing the water

Severeepidemics2010-2016

In 2015, the population was significantly more aggressive, able to overcome our best resistant cultivars

Group 4 isolates can kill our best resistance source!

Some new isolates are REALLY nasty

The worst isolates are used to select for best resistance…

• …but PBA Seamer derives its Resistance from ICC3996

• And we are always one season behind the pathogen

• And we are selecting in today’s climate

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Increase in frequency of high risk Isolates 2013-2016

ICC3996

Gen090

HatTrick

Seamer

n= 102 (2013)n= 100 (2014)n= 101 (2015)n= 38 (2016)

• 10.5% of 2016 isolates screened are highly aggressive on PBA Seamer compared to 53% on PBA HatTrick

We are already finding isolates able to cause significant disease on PBA Seamer (2016)

Weneedtounderstandthepathogen-host-climateinteraction

Temperature

AntagonistsChemicals

Water and % RH

[CO2] Solar radiation

Host defence responses

[SO2][ozone]

12-16 hours = spore germination

24-36 hours =direct penetration

16-24 hours =stomatal penetration

5-7 days =disease symptoms

We are building a picture of the plant-pathogen interactions

Crop-pathogen recognition and defence - transcriptomics

We know how long the fungus stays outside the plant –climatic interaction, fungicide to choose (prophylactic)

Germ

tube

length(µ

m)

= PG – 4

= PG – 3

= PG – 2

= PG – 1

= LOW

Informed disease management

• Pathogen specific• Host specific• Region specific• Climate prepared

Butaretheylisteningwhentheycanmakethismuch?

Acknowledgementsandsomepublications

• Mehmood Y, Sambasivan P, Kaur S, Davidson J, Leo AE, Hobson K, Linde CC, Moore K, Brownlie J, Ford R (2017). Evidence and consequence of a highly adapted clonal haplotype within the Australian Ascochyta rabiei population. Frontiers in Plant Science. 8: 1029.

• Leo A, Linde CC, Ford R (2016). Defence gene expression profiling to Ascochyta rabiei aggressiveness in chickpea. Theoretical and Applied Genetics. 129: 1333-1345.

• Leo AE, Ford R, Linde CC. (2015). Genetic homogeneity of a recently introduced pathogen of chickpea, Ascochyta rabiei, to Australia. Biological Invasions. 17: 609-623.

• Elliott VL, Taylor PWJ, Ford R (2013). Changes in foliar host reaction to Ascochyta rabiei with plant maturity. Journal of Agricultural Science 5 (7): 29-35.

• Elliott VL, Taylor PWJ, Ford R (2011). Pathogenic variation within the 2009 Australian Ascochyta rabiei population and implications for future disease management strategy. Australasian Plant Pathology 40: 568-574.

• Leo AE, Ford R, Linde CC, Shah RM, Oliver R, Taylor PWJ, Lichtenzveig J (2011). Characterization of sixteen newly developed microsatellite loci for the chickpea fungal pathogen Ascochyta rabiei Molecular Ecology Resources Primer Database. http://tomato.biol.trinity.edu/manuscripts/11-2/(for mer-10-0345.pdf) [database numbers 45147-45161].

• Bian XY, Ford R, Han TY, Coram TE, Pang ECK and PWJ Taylor (2007). Approaching chickpea quantitative trait loci conditioning resistance to Ascochyta rabiei via comparative genomics. Australasian Plant Pathology 36: 419-423.

• Phan TTH, Ford R, Taylor PWJ (2003). Population structure of Ascochyta rabiei in Australia based on STMS fingerprints. Fungal Diversity 13: 111-129.

• Phan TTH, Ford R, Taylor PWJ (2003). Mapping the mating type locus of Ascochyta rabiei, the causal agent of ascochyta blight of chickpea. Molecular Plant Pathology 4(5): 373-381.

• Flandez-Galvez H, Ford R, Ades PK, Pang ECK, Taylor PWJ (2003). QTL analysis for ascochyta blight resistance in an intraspecific population of chickpea (Cicer arietinum L.). Theoretical and Applied Genetics. 107: 1257 – 1265.

• Phan HTT, Ford R, Bretag T, Taylor PWJ (2002). A rapid and sensitive PCR assay for detection of Ascochyta rabiei, the cause of ascochyta blight of chickpea. Australasian Plant Pathology 31: 1-9