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From genetics to plant breeding: What do we know and what do we need to know?. James Brown John Innes Centre, Norwich, UK From “ag school” to “life sciences”. Optimism or science fiction?. The plant breeding revolution. Sr2 gene in wheat

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From genetics to plant breeding what do we know and what do we need to know l.jpg

From genetics to plant breeding:What do we know andwhat do we need to know?

James Brown

John Innes Centre, Norwich, UK

From ag school to life sciences l.jpg

From “ag school” to “life sciences”

Optimism or science fiction l.jpg

Optimism or science fiction?

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The plant breeding revolution

Sr2 gene in wheat

Durable resistance to stem rust

CIMMYT, from the late 1940s

Partial resistance to wheat mildew

Durable, polygenic trait

UK breeders, from the late 1970s

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What happened to plant breeding in academia?






  • What happened to partial (horizontal, quantitative) resistance?

  • Major gene (mainly gene-

    for-gene) resistance

    • Tractable

    • Exciting

    • Expensive

    • Superficially promising

    • But not usually useful

Meanwhile in a field near you l.jpg

Meanwhile, in a field near you…


  • Mildew and S.nodorum well controlled

    • Partial, polygenic, durable resistance

  • Yellow rust usually well controlled

    • By partial resistance, despite major genes

  • Control of Septoria tritici improving

  • Control of eyespot could be better

Breeding for

resistance works

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A chasm in plant pathology

Success in understanding

biology of disease

Success in controlling

plant diseases

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“…assessing function in vivo…”

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Looking backwards and forwards

  • What do we know?

    • Plant breeding improves resistance

    • To several diseases (+ yield, quality, etc)

    • Slow and expensive to improve even one trait by GM

  • What do we need to know?

    • Can we predict which resistances are most likely to be effective?

    • How can breeders combine resistances to many diseases?

    • How to breeders combine disease resistance with performance: yield, quality, etc?

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Predicting value of R-genes

  • Increased fitness cost) of virulence

    • Increased effectiveness of resistance

    • Strong theoretical prediction

  • Crosses of barley mildew isolates

    • 6 virulences segregating

  • Reproductive fitness

    • Production of conidia

  • 5 virulences: no fitness cost detected

  • Virulence to Mla13

    • 15°C: no significant fitness effect

    • 10°C: virulent isolates produced 12% fewer spores than Mla13-avirulent

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Costs of virulence: value for breeding

  • For most R-genes, matching virulence has no fitness cost

    • R-genes not predicted to have a durable effect

  • For Mla13, fitness cost depends on environment

    • Might have some durable value

  • How useful is Mla13 in the field?

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Fitness costs in agriculture

  • Survey data on barley mildew virulences

    • NIAB (Sue Slater and Rosemary Bayles)

  • Does fall in frequency of virulence to Mla13 indicate a fitness cost?

    • Rate = 22% per year, ~ 2% per generation

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Modelling evolution of virulence

r = 0.89 (Model 1)

or 0.90 (Model 2)

  • Linkage disequilibrium → hitch-hiking selection

  • Frequency of virulence this year depends on:

    • Its frequency last year

    • LD with other virulences

    • Area of resistant barley

    • (Hovmøller et al. 1995)

  • Mla12 selected by

    barley varieties (Optic)

  • LD of Mla12 virulence

    and Mla13 avirulence

  • Changes due to hitch-hiking, not fitness cost

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Predicting value of R-genes

  • Value of resistance depends on cost of virulence

  • Most R-genes matched by non-costly virulence

     These resistances will not be durable

  • Costs of virulence vary with the environment

     Difficult to predict value

  • Population dynamics dominated by linkage disequilibrium and hitch-hiking selection

     Fitness costs may be almost irrelevant

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Resistance to several diseases

  • mlo barley mildew resistance

    • Increases susceptibility to

      hemibiotrophic fungi

    • Magnaporthe grisea

    • Cochliobolus sativus

    • Kogel & colleagues (Gießen)

  • mlo in ~50% of European spring barley varieties

  • Increase in hemibiotrophic diseases of barley (Rhynchosporium & Ramularia) in last ~15 years

    • Are these two facts connected?

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mlo and barley diseases



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mlo and hemibiotrophs

  • mlo increases resistance to

  • but increases susceptibility to

  • Can we predict how it affects other diseases?






Net blotch

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Resistance to several diseases

  • Can we combine resistances to several diseases?

    • Yes: plant breeders do it all the time

  • Can plant pathologists help them?

    • Possibly: but even the best-studied R-genes produce surprises

  • Can we afford to invest in detailed study of all significant R-genes, to have predictive breeding for resistance to multiple diseases?

    • Probably not…

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Making a resistant variety

  • For commercial success, must combine

    • Yield (economic return to farmer)

    • Quality (as required by market)

    • Agronomic properties (standing power, heading date, etc)

    • Resistance to several diseases

  • Septoria tritici

    • Said to be difficult to combine

      good resistance with high yield

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“The Consort Conundrum”

  • Since 1970, varieties susceptible to septoria have been

    • The highest yielding

      • The most widely grown

        • The most widely used as parents of crosses

  • e.g. Norman, Riband, Consort…

  • Why do farmers and breeders like septoria-susceptible varieties?

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Selection for yield and susceptibility

Higher yield than expected

from septoria level


Less septoria than

expected from yield

Yield : in disease-free trials

Septoria : in diseased trials

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Separate yield and susceptibility

  • Senat (resistant) x Savannah (susceptible)

    • In Senat,

    • One gene (QTL) for septoria resistance but lower 1000-grain weight

    • One QTL for septoria resistance but not lower yield

  • Spark x Rialto (both moderately resistant)

    • In Spark, one QTL for resistance and lower yield

    • In Rialto, one QTL for resistance but not lower yield

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No cost of mildew resistance

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Making a resistant variety

  • Can breeders combine yield, quality and resistance?

    • Find genes which increase yield but don’t reduce resistance

    • & vice-versa

    • Natural selection over time (mildew vs. septoria)

  • Can pathologists help them?

    • Developing marker-assisted selection

    • Economic for most important genes controlling most important diseases of most important crops

      • More cost-effective for F1 hybrid breeding

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What do we know works?

  • Selecting for phenotype

    • Genotype may be helpful

    • No genetic model for durable resistance

       Marker-assisted selection may be useful

  • Selecting resistance to several diseases

    • Needs effective trial for each disease

    • e.g. site conducive to disease + virulent pathogens

       Design of pathology tests & scoring systems

  • Breeding for yield, quality, agronomy & resistance

    • Effective trials for all traits

    • Unfavourable linkages broken down over time

       Pathology integrated with plant biology & ecology

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What do we know doesn’t work?

  • Selecting for one gene at a time

    • May have damaging non-target effects

    • Exceptions: mlo, Sr2

  • Developing resistance to one disease at a time

    • Likely to have damaging effects on non-target diseases

  • Focussing on one trait at a


    • Farmers and consumers

      need varieties which

      combine all desirable traits

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When will GM be useful?

  • One gene makes an economic difference

  • One trait is outstandingly important

  • Any trade-offs are less important than that trait

  • When breeding is difficult or impossible

Black sigatoka disease of banana

Late blight of potato

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Research questions for pathology to support plant improvement

  • What is the physiological basis of interactions between resistances to different diseases?

  • When and why is there a trade-off between resistance and yield?

  • Why are many commercially useful traits polygenic?

    • Because genes with ‘major’ effect on one trait more lkely to disrupt phenotype of plant as a whole…?

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With thanks to…

  • Marion Atkinson

    + Susan Slater & Rosemary Bayles (NIAB)

  • Joanne Makepeace

    + Simon Oxley, Neil Havis (SAC), James Burke & Richard Hackett (Teagasc, Ireland)

  • Lia Arraiano

    + Nickerson-Advanta, Elsoms Seeds, Innoseeds, New Farm Crops, Sejet Plant Breeding & SW Seed

  • BBSRC + Sustainable Arable LINK + Home-Grown Cereals Authority + Teagasc

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